Eggs: Are they better for you raw?

Eggs are one of very few animal foods that you can store at room temperature for weeks with absolutely no processing. How perfect. A single chicken egg can supply a variety of proteins in the proportions that you need, all safely delivered in a hard, bacteria-resistant shell. Again, how perfect.

Starting in the 1950s with Steve Reeves— Hollywood’s Hercules—and continuing with Sylvester Stallone’s character Rocky Bolboa and The Governator, Arnold Schwarzenegger, generations of muscle-seeking citizens have downed large quantities of raw eggs as part of their training regimes. Much of the thinking that raw eggs are the ideal source of calories can be traced back to 1904, when raw-foodists Molly and Eugene Christian wrote that, “An egg should never be cooked…and that in its natural state it is easily dissolved and readily taken up by all the organs of digestion.”

Yeah, raw eggs are slimy, and there’s a campaign today to convince you that they’re also dangerous. But what if the raw eggs in front of you are safe and you’re not grossed out by a little slime? Does cooking an egg really make it less nutritious than if it were raw? Some Belgian researchers claim to have the answer.

In a set of experiments, some gastroenterologists analyzed the fate of egg protein after it was consumed by various test subjects. For the most accurate results, the researchers fed hens a diet rich in “labeled” atoms of stable isoptopes of carbon, nitrogen, and hydrogen. The researchers could then measure how much of this labeled protein  remained in the food collected in the ileum, at the end of the 35 feet or so of the test subject’s small intestine. Any protein that traversed the entire length of the small intestine was not absorbed. This protein was essentially metabolically useless because from this point on, bacteria in the colon digest the protein for their own selfish needs.

When the eggs were cooked, 91 to 94 percent of the cooked proteins were absorbed before in the small intestine, but only 51 to 65 percent of the raw proteins were absorbed. In other words, 35 to 49 percent of the protein from raw eggs was not absorbed and metabolized. In short, the researchers determined that cooking increased the available protein value of eggs by as much as 40 percent. The denaturation of proteins through the application of heat weakens the internal bonds of the proteins, making the three-dimensional structure more accessible to digestive enzymes, which in turn increases the amount of protein absorbed.

It’s worth pointing out that cooking also takes eggs from an essentially liquid form to a more solid food. As discussed in the earlier post on food texture and calorie burn, the human digestive process then has to take the solid eggs “back to” a liquid form to maximize protein absorption. This process is metabolically expensive and results in increases thermogenesis and increased calorie burn. Hell yeah.

A strict diet of pay attention is what it’s all about. eatNAKED friends, and live well.

Is food texture more important than calories in preventing weight gain?

Is a calorie just a calorie? Whether from a wheat bagel or a Snickers bar, is 300 calories, regardless of the source, just that: 300 calories? The experts say yes. This thought process then leads to the positive-caloric-balance hypothesis as an explanation of weight gain and obesity. In short, eat more calories than your body uses and you will gain weight. Seems logical.

These same researchers will quickly point to the first law of thermodynamics (the law of energy conservation) to bolster a cause and effect that implies that any change in body weight must equal the difference in the amount consumed versus the amount expended. This energy balance equation looks like this:

Change in energy stores = Energy intake – Energy expenditure

To this day, nearly a century of obesity research has been based on this simple formula. However, most obesity researchers and public health officials rely only on the right side of the equation (Energy intake – Energy expenditure) to explain obesity, conveniently ignoring the left side (Changing in energy stores). These experts correctly assume that a positive caloric balance is associated with weight gain, but they assume without justification that positive caloric balance is the cause of obesity. Any adult female can attest to the role of hormones in weight gain—a gain that is unrelated to caloric balance. This is made more clear during pregnancy, when hormone-driven evolutionary forces promote hunger, weight gain, and lethargy—all to assure that sufficient calories are available for the newborn. This and other misconceptions of weight gain and obesity have lead to over a century of misguided obesity research that continues to this day.

In a series of blog posts beginning with this one, we will lay out some basic evolutionary, biological, and cultural adaptations (and maladaptations) that may provide some insight into weight gain and overall health and well being.

To cook or not to cook (if so, how long?)

With all due respect to the raw food movement, cooked food just tastes better. And from an evolutionary perspective, the application of heat to our food has played a significant role in the success of our species. But are we cooking our food a little too much and for too long?

Cooking makes a food more digestible than the same food without the benefit of cooking. In carbohydrate-rich foods, the application of heat to a moisture-rich food (e.g., a potato) causes hydrogen bonds in the glucose polymers to weaken, causing the tight crystalline structure to loosen and gelatinize. As long as water is present in the food or the cooking environment, the starch will gelatinize. Once consumed, the gelatinized starches are more easily cleaved by our digestive enzymes, thus more digestible. The same process occurs in meats through denaturation of proteins through the application of heat.

From an evolutionary perspective, we may be cooking some of our food a tad too much for cultural and culinary reasons, and in the process affecting some time-honored physiological requirements of the human body—specifically, the role of the stomach in energy balance, satisfaction, and hunger.

It was not that long ago that all of our foods were minimally processed. In short, more crunchy, more grainy, and definitely less refined. There is no doubt that our ancestors would marvel at the sleek and gelatinized angel hair pasta of today and the pasty softness of a steamed carrot torpedo. While convenient and tasty, our modern processing (in the case of the finely milled flour in the pasta) and cooking techniques (“hyper” steamed veggies) have moved digestion from the stomach to the stovetop. All the extra cooking in our modern lifestyle has slowly eliminated—or at least reduced—the role the human stomach evolved to play in digestion. And herein lies the discordance between our modern lifestyle and its nifty technological tools and cultural preferences, with our evolution-determined physiology and specifically, energy balance.

The carrot-like tuber your ancestors ate either raw or minimally cooked has been replaced by foods with a texture like baby food. This texture comes from weakened glucose polymers caused by the application of super-efficient cooking techniques. The modern cooked carrot is easily digested and therefore rapidly moved through the stomach. It’s safe to say that modern humans are experiencing some of the fastest rates of gastric emptying in human history. Gone are the days when minimally processed foods stayed in the stomach for two, three, or even four hours. There’s no longer a need for food to stay in the stomach; the stovetop started the digestion well ahead of ingestion, greatly speeding the work of gastric enzymes.

This effect is nicely captured in the widely popular Glycemic Index (GI). The GI ranks foods according to their effect on blood glucose levels. High GI foods, like highly processed donuts and sugary soft drinks, cause a rapid rise in blood glucose and subsequent insulin levels. Not good. Foods that are processed less generally have a lower GI.

But cooking has a significant and often unappreciated effect on the GI of a food. A raw carrot, which takes some crunching to break down, is transferred to the stomach, where some time-honored digestion takes place in a natural and slow way. Thus, a raw carrot has a low GI (about 16). However, a peeled and boiled carrot is easy to chew and rapidly processed in the stomach, as it has been predigested on the stovetop. This cooked carrot has a higher GI, around 60. This translates to rapid gastric emptying and subsequent rapid absorption—resulting in elevated glucose and insulin levels. Not good.

So what does this have to do with weight gain? Aside from some issues related to elevated levels of insulin in the blood—which has a dramatic impact on fat metabolism (something we will cover in a subsequent post)—the processed carrot versus the unprocessed carrot is tinkering with some evolutionary processes related to thermogenesis, and may be playing an unrealized role in our national epidemic of obesity. This is nicely demonstrated in an elegant study recently published by Japanese researchers. (Hang in there, almost to the point!)

In this study, a team of Japanese scientists divided 20 rats into two groups of 10 at four weeks of age. Over the next 22 weeks, both groups ate a nutritionally identical diet of rat chow. However, for one group of rats, the hard-to-chew pellets were injected with a tiny bit of air, making them softer and easier to chew. This is more or less similar to our raw versus steamed carrot discussion above.

The air-injected pellets were more like breakfast cereal and required about half as much force to chew and break down. The hard and the  soft pellets were the same in how they were cooked, in their nutrient composition, and in their water content. Based on the “calorie is a calorie” argument and the first law of thermodynamics discussed above, rats reared under identical conditions and consuming the same nutrition should grow at the same rate and size and with the same amount of body fat and overall weight. But they did not.

Even though the rats had identical energy intake throughout the 22-week experiment, the rats which consumed the soft pellets slowly become heavier. It was gradual at first, but the rats fed soft pellets weighed about 6% more than the harder pellet eaters and had 30 percent more abdominal fat—enough to be classified as obese. The difference documented was due to the cost of digestion.

Before and after feeding, the researchers measured the body temperature of each rat.  At every meal the rats experienced a rise in body temperature, but the rise was less in the soft pellet group. The difference in temperature was most significant between the groups within an hour of ingesting a meal, when the stomach is churning and secreting. The researchers concluded that the softer diet resulted in obesity simply because it was less costly to digest. Increased heat during digestion burns calories at a faster rate, similar to the weight loss we experience when we’re sick with a fever.

We all know that weight gain does not happen over night. It’s a slow process that takes place over long periods of time and can fluctuate dramatically. And because this is a slow and gradual process, we also know the body is constantly trying to regulate energy intake to energy expended. The body strives for balance, not an imbalance. This is why you are hungry after vigorous physical exercise; your body wants to replace the calories you just burned. This also explains why a lumberjack needs 5,000 to 8,000 calories a day, but an advertising executive might only need 2,500 or so. If exercise were the answer, then all meter maids would be thin. But they are not.

Weight gain among a given population has more to do with tinkering with evolutionary processes than with sloth or one’s willpower. It’s uniquely biological. If the experts are correct in that small changes, like 90 minutes of exercise a week or 100 calorie snacks are the answer, then paying attention to the level of processing of our food discussed in this blog should have at least as much merit in fighting the obesity epidemic.

We are not advocating a raw food diet—oh hell no! That’s a sure way to guarantee you don’t get sufficient nutrients and will surely bore yourself and your loved ones to near death—literally. And raw beef is downright dangerous. We are suggesting that you take a closer look at the amount of processed food you eat. Think, before you steam rice for 15 minutes, that maybe 12 minutes would be enough— making it a little crunchier and therefore a tad harder for your stomach to break down. This will, in turn, elevate your body temperature slightly as your stomach churns and burns calories. You might also consider doing the same with steamed broccoli. In addition, don’t cut off and throw away the stalks and eat just the yummy crown. Cut that fiber-rich stalk into thin slices and steam away. By increasing the fiber in your meals, you will also give your stomach a chance to do its job as well.

The multi-grain crust at NAKEDpizza is a great starting point, far better than the over-processed offerings at other pizza places as well. Live long. EatNAKED, friendos.

Can our cooling bodies be playing a role in obesity?

The human body temperature more or less hovers around 98.6 °F (37.0 °C), although this varies throughout your day according to how active you are, what you eat, and so forth. The weight loss we experience when we exercise is related to, among other things, our increased body temperature. A higher core body temperature increases the rate of moisture evaporation and burns more calories. This is why our appetites increase following prolonged exercise or physical activity—for example, a burly lumberjack working outside all day may burn twice as many daily calories as an accountant, and that lumberjack will need to replace those calories just to maintain his original weight.

We have all lost weight while lying flat on our backs after catching some nasty bug. True, some of this has to do with reduced appetite and loss of fluids, but much of it has to do with our increased core body temperature, which rapidly burns through our stored calories: fat deposits in adipose tissue. Depending on the severity and length of your illness, body temperatures in the range of 99 to 101 degrees can increase the number of daily calories burned by 5 to 20%. Staggering when you think about it.

This “infection” burn rate for calories, when viewed through the lens of our evolutionary past, becomes interesting—or at least it should—for those of us fighting the bulge at home or in guiding public health policy.

Before the age of infection-fighting drugs and antibiotics—and you can include antimicrobial soaps as well—our ancestors battled infection and its temperature-raising, calorie-burning effects on a daily basis. When I say ancestors, I’m talking about our pre-agricultural predecessors, not the old world folks who created a freakish relationship with the microbial world through crowded cities and tainted water and food supplies—all of which resulted in average life expectancy of a little more than 20 years.

If modern medicine has given us anything, it has been lower core body temperatures through reduced infection rates. While high fever and infection get all the attention, it’s the “low grade” infections and “slightly” high temperatures that should interest obesity researchers and public health officials. We have all heard that 3,500 or so calories equal a pound of body weight. That is, burn 3,500 calories on the treadmill or running around the park and you will lose one pound. Now think for a minute. The effects of a low-grade infection that raises your core body temperature from our current average of 98.6 degrees to, say, between 99.0 and 99.6 degrees on a more or less permanent basis. Without boring you with the math, this modest increase in body core temperature will increase our resting metabolic rate (the amount of energy one burns just sitting on the couch and not eating, as digestion burns calories, too) by 2 to 7 percent, depending on a dizzying number of variables. Imagine for a moment that your body automatically burned (needed) 2 to 7 percent more calories on a daily basis, and that your increased body temperature was not noticeable and did not affect your daily routine. For someone on a 2,500 kcal daily diet, an increased burn rate from a slightly elevated core body temperature (from a constant low grade infection) might result in an additional 100 or more calories burned in a day. Using the less than perfect assumption that 3,500 calories burned equals one pound lost, you would carve almost a pound from your frame every month if you just went about your daily routine. And in a year, well, you get the idea.

So what was the low-grade infection that our ancestors experienced? While there were a number, the most likely characters were various parasitic worms (e.g., helminths) that lived deep in our ancestral gastrointestinal tract. The presence of these parasites sends our immune system into action causing body temperatures to rise. Because the parasites compete with “us” for nutrients in our intestinal tract and “can” cause a great deal of problems if they get out of hand, the World Health Organization and modern medicine spend a lot of time trying to eradicate them from our species. These efforts are especially intense in developing countries, where dirty water and minimally processed meats easily transmit these parasitic infections. An estimated 40 million Americans have some form of parasitic infection. That said, much of the world’s population lives in a symbiotic relationship with our evolutionary hitchhikers. In fact, intestinal parasites are used to combat some autoimmune diseases.

Anyone in the livestock industry will tell you that administering antibiotics to your herd or flock will result in weight gain. In other words, reducing low-grade inflammation and general infection reduces calories burned and thus increases weight. Might our overuse of antibiotics and antimicrobials have reduced our “natural” low-grade inflammation just enough to tip the scales against us? Makes you wonder.

Did our ancestors really live longer than us?

British nutrition researcher Geoffrey Cannon recently restated in the journal of PUBLIC HEALTH NUTRITION a widespread affirmation that “Paleolithic people usually did not survive into what we call later middle age.” His underlying point, which is widely shared among researchers and the public at-large, is that our ancestors did not live long enough to develop cancer, heart disease and other chronic illnesses. All of which forms the basis for the near universal belief that ancient hunter-gatherers (our ancestors) really were not healthier or fitter than us moderns, and therefore their ancient dietary practices have little relevance to modern health, well-being, and longevity.

On the initial point, Cannon is correct. The average life span of our ancestors was short, compared to that of modern humans in developed countries where one can expect to live into their 60s, 70s and possibly early 80s, on “average.” Conversely, a Neanderthal living in ancient Europe was lucky to live past her teens, and if you lived to your mid-thirties you might have been considered old in Ancient Egypt. More recently, the average life expectancy in the United States in 1900 was 47.3 years. By 1935, that age had risen to 64 years and today that number hovers in the 70s for both women and men (though women can expect to live a few years longer, on average).

The first problem with this line of thinking is that the “average life span” math is misleading and tells us very little about the health and longevity of an individual, but rather gives us an average age of death for a given group or population. For example, a couple that lived to the ages of 76 and 71, but had one child that died at birth and another at age two ([76+ 71 + 0 + 2] / 4), would produce an average life span of 37.25. Using this methodology it is easy to see how one would come to the conclusion that this group was not very healthy.

However, the precept that diet played a significant role in the abbreviated average life span of our ancestors is simply not true. There are few among us that believe our so-called “westernized diet” of highly processed grains and added sugars and fats are an optimal diet for anyone – past or present. Our soaring rates of obesity and an ever-growing list of acute and chronic diseases – occurring in alarming frequency among younger sections of the population – speak to the discordance.

It is useful to point out that our species reached our current anatomical and physiological standing nearly 200,000 years ago. That is, while components of what we discern as hallmarks of behaviorally modern human beings, such as language, art, trade networks, and advanced weapons, have only occurred within the last 50,000 years, the hardware has been in place for 150,000 years. While we may drive around in hybrid cars today, we do so in very ancient bodies and with a genome that was selected, for the most part, on a nutritional landscape very different than the one on which we find ourselves today.

Before the advent and widespread adoption of agriculture, which depending on where you lived occurred between 1,000 and 9,000 years ago, humans organized in highly mobile groups of dozens or a few hundred individuals. Archaeological data and analysis of burial populations reveal that life was harsh and dominated by warfare, strife, destruction, human trophy taking, and the all-to-often practice of infanticide. All of these facts of ancient life, in conjunction with the lack of simple antibiotics and modern surgical practices, resulted in shorter average life spans than many of us enjoy today. As agriculture took hold around the globe and groups settled down and built more permanent communities and ultimately socio-politically complex civilizations, the more homogenous and centralized food and water supply was easily contaminated by human waste. While war and even larger massacres continued throughout the agricultural revolution, tiny microbial killers took their share of victims, especially among the young and undernourished, further reducing the cyclical nature of the average life span. As European ships set sail just a few centuries ago, new ills and evils further reduced the average life span of populations they encountered – albeit punctuated.

As war, contaminated water, killer microbes, and illness pulsed through humanity over time, our basic underlying physiological and nutritional parameters have changed little in the last few hundred thousand years. Our modern genome is in fact an ancient one and natural and cultural selection has built it to last. Under optimal nutritional conditions, such as those our genome evolved on, us modern hunter-gatherers can live healthy and long lives. We need only look to the modern Hunza of northern Pakistan or the southernmost Japanese state of Okinawa to witness the longevity that our ancient genome is selected for. With the threat of war and violence greatly reduced, and upon a sound footing of a safe food supply, our ancient bodies can be healthy well beyond “our best-before date” Cannon writes about. Based on a low-calorie, high-fiber plant-based diet, a significant portion of the population enjoy healthy and active lives into their 80s, 90s, and often beyond 100. Incredibly, the aged portions of these populations have lower rates of obesity, heart disease, diabetes, hypertension, high cholesterol, cancer, and other chronic diseases compared to western populations.

The modern world owes much to antibiotics and advanced surgical procedures of the last half-century, resulting in dramatic increases in average life span for much of the developed and developing world. Though horrific events in Darfur and other African regions remind us how significant gains in average life span can easily be erased. In Iraq, a male or female could expect to live to an average age of 66.5 in 1990, but today following years of foreign occupation and endless violence, life expectancy has dropped to a mere 59 for both sexes – and slightly younger for males. The self-confidence that comforts us today as we review the average life span of our ancestors is misguided and tenuous when viewed through the captivating haze of modern medicine that literally props most of us up into our golden years. I doubt our ancestors would call this living. While we may live longer than our ancestors, we are in fact dying slower. So rather than rest on our perceived cultural and medical success as it pertains to our longevity, we should challenge ourselves and our genomes to maximize our health for optimal longevity. For those not trusting of the past and the nutritional landscape upon which we evolved, our genetic cousins, the Hunza and Okinawans, have shown us a way forward.

What do pirates and Eskimos teach us about vitamin C deficiencies and the common cold?

In 1753 a Scottish naval surgeon named James Lind set out to solve why British sailors and various pirates suffered from scurvy on long voyages. Scurvy results in spots on the skin, spongy gums and bleeding from almost all mucous membranes, and general weakness. In some cases this can get you thrown over board – well before you succumb to the illness.

Lind discovered that by adding citrus to the standard sea fare “of water gruel sweetened with sugar in the morning, fresh mutton broth, light puddings, boiled biscuit with sugar, barley and raisins, rice and currants,” scurvy could be cured or prevented. It would be many years later before we learned that scurvy was caused by vitamin C deficiency. In the early part of the twentieth century, vitamin C would play a central role in the research into vitamin-deficiency diseases and the birth of our modern supplement craze of today.

Once James Lind had demonstrated that by consuming fresh fruits and vegetables containing vitamin C you could cure or prevent scurvy, it was logically assumed that fruits and vegetables were necessary for a balanced diet. But some critical thinking is missing from this line of thinking. While vitamin C may prevent or cure scurvy and hence balance the deficiency, it does not technically tell us that vitamin C deficiency is caused by a lack of fresh fruits and vegetables. This is made all the more interesting when you consider that Inuit and Eskimos living on a vegetable- and fruit-free diet at the turn of the century never suffered from scurvy. Something else must be going on.

Harvard anthropologist turned-Artic-explorer Vilhjalmur Stefansson was one of the first professional observers to note the overall good health of these rugged, arctic people. Subsisting almost exclusively on a diet of caribou, fish, seal meat, rabbits, polar bears, birds and eggs, the diet was greater than 50%-75% fat and the rest protein with very small amounts of carbohydrates. Vitamin C was not on the menu. Many naysayers at the time had argued that the Inuit and Eskimo had become “adapted” to a diet that lacked such things as vitamin C. However, this would not explain why traders, explorers and people like Stefansson who lived among the Eskimo for often years and ate this diet never suffered from scurvy. (Note that meat does contain small amounts of vitamin C – evidently, enough to prevent scurvy!).

Turns out, the vitamin C molecule is similar in configuration to glucose – the sugar in the body that is generated from dietary sugars and processed carbohydrates in our diet – and competes with glucose in cellular-uptake. Said differently, when glucose and vitamin C are circulating in our blood, glucose is greatly favored and vitamin C is “inhibited” and thus left circulating and not utilized efficiently. Therefore, by increasing blood sugar (glucose) levels – such is the case in our sugary, high-fructose corn syrup, processed carb diet of today (just like the pirates and sailors) – vitamin C uptake will drop accordingly. Glucose also impairs the reabsorption of vitamin C by the kidney, resulting in the loss of vitamin C in the urine. Though these mechanisms are not controversial, they are rarely mentioned by public health officials and never mentioned in those snazzy “drink Florida orange juice” commercials touting the need for vitamin C. Damn you Tom Selleck!

On top of all that, research has shown that vitamin C supplements do not provide nearly as much protection as other measures – like frequently washing your hands – in preventing the soon to be common cold of the cooler season ahead. Don’t be fooled by the common myth that vitamin C provides any meaningful protection against colds. Whether it is caused by a mild cold or the flu, a runny nose and sore throat are signs of a viral infection. Many people are absolutely convinced that vitamin C provides protection against respiratory infections. Yet research has shown that vitamin C does not prevent infection, and that high doses can even be harmful!

Researchers at the Australian National University and the University of Helsinki found that after following more than 11,000 people over several decades that took a daily dose of at least 200 milligrams of vitamin C (ascorbic acid), did little to reduce the length or severity of a cold.

So, even though a 1970s Nobel Prize-winning chemist named Linus Pauling popularized the regular use of vitamin C in the “cure of common colds” – encouraging us to take 1,000 milligrams daily – you might want to rethink the monetary costs of doing so in these trying financial times.

Take Home Message: Even though vitamin C deficiency can be cured or prevented by eating fruits and veggies, it does not explain why you are deficient. The Eskimos taught us this. In addition, there is very little evidence to suggest that vitamin C has a significant effect on reducing your chances of “catching” a cold or reduce suffering once you have gotten the sniffles. It may be that you get enough vitamin C in what ever diet you may be consuming, but if that diet includes crappy highly-processed pizza from the “other” guys and any appreciable amounts of other processed carbs (sugar, lots of bread, and so forth), then you may need to eat a few more oranges and some select veggies and, of course, a few slices a week of our tasty prebiotic multi-grain pizza fortified with probiotics.

*Note we are NOT saying to stop eating vitamin C containing fruits and veggies, just chatting about the vitamin C craze in general and the adverse effects of our so-called modern diet of highly processed carbs.

So go the Pimas, so go the rest of us

Anyone familiar with the American Southwest may have heard of the Pima Indians of south-central Arizona. The Pima are the modern descendents of the famous desert Hohokam who occupied vast swaths of south-central Arizona from roughly 200 BC to AD 1450. Famous among archaeologists for their massive and intricate canal systems built to deliver water to the arid and ecologically defiant agricultural fields of the parched Southwest, the Hohokam are a true success story of the ancient world.

While history paints the Hohokam as masters of their ancient environment, medical researchers fear our modern environmental landscape may be undermining their modern Pima Indian descendants.

In the 1960s epidemiologists started noting an alarming trend among the 11,000 or so Pima Indians living in the Gila River Indian Community just east of Phoenix, Arizona. For some unknown reason, a startling number of Pima were developing type 2 diabetes.

Diabetes affects tens of millions of Americans, resulting in the death of more than 300,000 people annually. It’s also the leading cause of end stage kidney disease, adult blindness and amputation. The prevalence of diabetes among African Americans is nearly 70% higher than in Caucasians. Like obesity, diabetes dominates our national discussion on health care.

But for the Pima, type 2 diabetes and its complications are acutely devastating. With the prevalence of diabetes estimated at 5.1% of the global population, and 7.9% of the US population, the 38% recorded among the Pima of central Arizona gives them the distinction of being the most diabetes-prone group on the planet.

Once the trend started rearing its ugly head in the 1960s, researchers saw not only a looming health crisis among the modern Pima, but also an opportunity to study the disease in a genetically ‘pure’ group, as many of the Pima married within their own community. Importantly, they had multiple generations within families in which to follow the development of the disease and the genetic predisposition. With millions in funding from the National Institutes of Health (NIH) and the blessing and cooperation of the Pima, the Phoenix Epidemiology and Clinical Branch of the NIH was established.

It is now several decades and 100 million dollars later, and researchers are still grappling with the Pima diabetes enigma.

So why are the Pima prone to diabetes? Diabetes research in general has determined that lifestyle (diet, smoking, physical activity, etc) and genetic factors clearly play a role. For example, there seems to be a significant correlation between ones weight and predisposition to developing diabetes and suffering from its complications. But among the Pima, given the genetic isolation of the group, it seems genes may play a major causal role in individual susceptibility. Or does it? A new study may shed some light.

If you happen to be thumbing through the latest issue of the journal Diabetes Care, you would have come across a fascinating study by researchers who examined and compared adult Pima Indians of central Arizona with their genetic cousins, the Mexican Pima of northern Mexico (see map here). As mentioned above, the Pima of central Arizona are descended from the ancient Hohokam, who originally migrated to southern Arizona from what is today northern Mexico (several hundred kilometers to the south). Based on genetic, linguistic, and archaeological data, this migration is thought to have occurred a little over 2,000 yrs ago. Not all of the ancient population migrated and settled in southern Arizona, however, some stayed behind to farm the highlands of Mexico. This situation has provided a unique opportunity for researchers studying diabetes and other diseases among the Pima of southern Arizona. On the one hand, you have Pima who have embraced the modern western civilization and its lifestyle (diet) as it swept over them, and on the other, you have genetically identical ‘cousins’ who essentially stayed on the farm.

The Mexican Pima live in remote areas of the Sierra Madre Mountains and enjoy few modern amenities. Much of these communities only recently became accessible by road. The Mexican Pima are primarily farmers and work manual labor jobs, such as those available in local saw mills. Almost every aspect of daily life includes physical activity.

In contrast, the Pima of southern Arizona, who were traditionally farmers, “enjoy” a typical US lifestyle of computers and TVs, with low levels of occupational physical activity. They have ready access to automobiles and mechanized farm equipment for those who still farm. Indeed, two very different worlds.

The researchers set out to test the following question by examining adults among the genetically similar but environmentally different sets of Pima: “Do type 2 diabetes and obesity have genetic and environmental determinants?” In other words, does environment (diet, obesity, physical activity, and other risk factors) play a role in the development of diabetes when you hold the genetic pool relatively constant? If genetics played a major role in the southern Arizona Pima’s astounding rate of type 2 diabetes, you would expect to see elevated levels in the Mexican Pima.

To add an additional variable to their study, the researchers also included Mexicans living in the same environment as the Mexican Pima in the Sierra Madre Mountains. The Mexicans (not of Pima heritage), are a mix of local Indians and Spanish. Like the Mexican Pima, the Mexicans live a rural and physically demanding life as farmers and ranchers.

Using Spanish-speaking interviewers and medical technicians, the data was collected. A brief medical history and  physical activity questionnaire was completed on each participating individual, followed by measurements of blood pressure, and a 75-g oral glucose tolerance test. The entire sequence was performed on 193 adult male and female non-Pima Mexicans and 224 Mexican Pima near the town of Maycoba in the Sierra Madre Mountains of northern Mexico. In addition, obesity was assessed by BMI (weight in kg divided by the square of the height in meters), body fat was measured, and waist-to-hip ratio was determined. On top of all that, a 24-hour dietary recall was conducted to determine what everyone was eating.

Using the data collected from these two groups, researchers compared the obesity, diet and prevalence of diabetes to some 888 Pima from southern Arizona. The prevalence of diabetes among the three groups is presented graphically below.

The prevalence of diabetes between the two genetically similar Pima groups is striking. Among the Mexican Pima men, 5.6% had diabetes, along with 8.5% of the women. Compare this to the Pima Indians of Arizona where 34.2% of the men have diabetes and 40.8% of the women. Among the non-Pima Mexicans (no shared heritage with the Pima), 5% of the women were diabetic and none of the men. That last part is worth repeating: none of the non-Pima Mexican men had diabetes!

In other words, age- and sex-adjusted prevalence of diabetes in U.S. Pima Indians was 5.5 times higher than their Mexican cousins and 16 times higher than the non-Pima Mexicans. The researchers also point out that the differences seen between the two Mexican groups was not significantly different (i.e., basically the same).

The differences between the prevalence of diabetes among the Pima Indians of Arizona versus the non-Pima Mexicans and Mexican Pima was also paralleled by differences in obesity, physical activity and diet.

BMI, percent body fat, waist and hip ratios were about the same among the two Mexican groups, but significantly different from the U.S. Pima Indians. The average non-Pima Mexican weighed in around 158 pounds (72 kg), with the average Mexican Pima at 145 pounds (66 kg). However, the average U.S Pima Indian male weighed 215 pounds (98 kg). While the women in all three groups weighed less, they followed much the same trend with U.S. Pima Indian females weighing, on average, about 200 pounds (91 kg).

As you may already sense, the levels of moderate to heavy physical activity among the groups was higher for the non-Mexican Pima and the Mexican Pima compared to the U.S. Pima Indians. For example, the average U.S. Pima Indian women spent 3.1 hours a week on moderate to demanding physical activity compared to 22 hours per week recorded for her Mexican Pima cousin.

As for diet, nothing glaring jumps out between the non-Mexican Pima and Mexican Pima – other than a remarkably low percentage of calories derived from fat, ~25%. In the current study, the researchers did not collect dietary data on the U.S. Pima Indians. Previous studies, however, reveal that percentage of calories from fat for U.S. Pima Indians was much higher than the 25% recorded for the Mexicans groups.

The dietary fiber measured in the diet among the non-Pima Mexicans and the Mexican Pimas deserves some special mention. No matter if they were male or female, non-Pima Mexican or Mexican Pima; they consumed greater than 50 grams of dietary fiber a day. Compare this to the 12 to 15 grams a day the average U.S. Pima Indian, or the average American for that matter, are consuming.

Given the similar genetic background between the U.S. Pima Indians and the Mexican Pima, the nearly fivefold increase in diabetes among the U.S. Pima can only be attributed to differences in lifestyle and environments.

While researchers continue to look for genes that make someone of a distinct genetic group susceptible to diabetes and other diseases such as heart disease, the current study among the westernized and nonwesternized Pima has taught us that obesity and physical activity have more to do with the likelihood that you will develop diabetes, regardless of your genetic makeup.

The take home message from the current study is profound: the genetic likelihood that you will develop type 2 diabetes is NOT inevitable and is CLEARLY preventable if you balance a reasonable amount of energy intake with energy expenditure and follow a diet low in westernized, highly processed foods.

However, the escalated levels of diabetes among the U.S. Pima and the increase of prevalence with age (for example, 77% of the U.S. Pima > than 55 years of age have diabetes) hint at some underlying genetic discordance with the modern food supply and environment. This is what keeps millions of tax dollars flowing into the genetic-arm of modern medical studies among the U.S. Pima Indians of southern Arizona.

I would add to the current study that the dramatic shift (drop) in dietary fiber in the U.S. Pima Indian diet from that of their Hohokam and earlier ancestors (who consistently consumed >100 grams of dietary fiber from a diverse variety of plants), has dramatically influenced the amount of insulin secreted throughout life contributing to the metabolic condition of insulin resistance – a complication associated with type 2 diabetes. This metabolic condition, which I call The Human Hybrid Theory, potentially affects all modern humans who have shifted away from a diversity and quantity of dietary fiber that our ancestors once enjoyed and that our genome was selected upon.

It is worth noting that the non-Pima Mexican men, a group that recorded the highest consumption of fiber at 56 grams a day, not a single case of diabetes was noted. Not one.

Are government recommendations for daily fiber intake too low? an evolutionary perspective

Modern humans are the latest in a diverse line of species within the genus Homo that evolved on a nutritional landscape very different from the one we find ourselves on today. During the ~ 2.5 million years since the first member of our genus made an appearance in the fossil record, humans subsisted on an extraordinary diversity of wild plants and animals from a dynamic environment that literally changed at a glacial pace. It is only within the last 5,000 to 10,000 years that our food supply has begun to include domesticated plants and animals. For more than 99 % of human history, our genome and its nutritional and physiological parameters were selected during our non-domesticated foraging life-way conditioned, in no small way, by a diet that included large amounts of dietary fiber from a significant diversity of sources.

Even though this important reality underlies the basic evolutionary biological principles of modern human nutrient requirements, it is all but missing from policy and research discussions on recommended intake of dietary fiber throughout the world. Even more startling, much of our discussion on the health benefits of fiber, at least in the U.S. and U.K., often refer to the mechanical actions of fiber (stool bulking, for example) and nearly ignores the critical role of dietary fiber as a nutrient base of sorts for the trillions of microbes living throughout the human gut.

It’s safe to say that our current chronic low-intake of dietary fiber in the western world (~12 to 15g/d) – coupled with our overuse of antibiotics and the increase in multiple antibiotic resistance in pathogens – has started a large-scale genetic “re-engineering” experiment on the slowly evolved and critical symbiotic relationship between humans and our little evolutionary hitchhiking friends, with limited discussion of its outcome on public health.

As you read this, there are millions of tiny microbes swimming around in the fluid surrounding your eyeballs. But you can’t see them. There are millions more under your fingernails, on your hands, arms, legs and just about every imaginable section of your fleshy real estate. There are millions more lining your moist nasal passage, many more maneuvering about your liver, heart, lungs, pancreas and trillions more have been living throughout your continuous gastrointestinal tract – from mouth to anus – from the moment you enter this world. But this is good news.

The bad news is as we fill our shopping carts and pantries with the latest neatly boxed and wrapped goodies of industry, we continue down a path that began some ten thousand years ago with the emergence of agriculture – an event that eventually, along with steel roller mills in the 1880s, farm subsidies in the 1970s, and the divergent interests of food sellers and public health, may be leading us on a path to one of the greatest unintended consequences in human history by tinkering with the health of our intestinal microbes. Current dietary advice would be well served by an appreciation that the average human is a complex super-organism, rather than a single individual.

The archaeological and ethnographic record serves as an interesting reminder of the magnitude of the shift in the diversity and quantity of fiber in human diet.

Along the shores of the Sea of Galilee in modern-day Israel, a remarkably well-preserved collection of plant remains recovered from the 23,000-year-old archaeological site of Ohalo II  provides an extraordinary window into a broad-spectrum diet that yielded a collection of >90,000 plant remains representing small grass seeds, cereals (emmer wheat, barley), acorns, almonds, raspberries, grapes, wild fig, pistachios, and various other fruits and berries. Owing to excellent preservation, a stunning 142 different species of plants was identified, revealing the rich diversity of fiber sources that was consumed by the site inhabitants.

In Australia, Aborigines are known to have eaten some 300 different species of fruit, 150 varieties of roots and tubers, and a dizzying number of nuts, seeds, and vegetables. Recent analysis of over 800 of these plant foods suggest the fiber intake was estimated between 80 to 130 g/d – possibly more – depending on the contribution of plants to daily energy needs.

In semi-arid west Texas, a nearly continuous 10,000-year record of ancient foraging reveals a plant-based diet that conservatively provided between 100 to 250 g/d of dietary fiber. Analysis of hundreds of preserved human feces (coprolites) recovered throughout the 10,000-year archaeological sequence reveal a significant diversity of plants were consumed.

While the diversity and quantity of fiber varied spatially and temporally in the past, our ancestors clearly evolved on a diet that included daily intake of fiber from a huge diversity of sources that far exceed those recorded among populations in recent intervention and prospective studies concerned with the role of fiber in human health. These modern studies invariably group people with fiber intakes hovering around 20 g/d as the “high fiber” group, when in reality these high fiber or upper quintile groups are in fact low from an evolutionary perspective. Therefore, from an evolutionary perspective we should not be surprised when analytical hair splitting of these minute amounts of fiber does not yield the desired protective role one might suspect going into the study.

The potential protective role of dietary fiber among these modern studies may further be complicated by the lack of diversity as much as the quantity. According to data compiled by the Economic Research Service, United States Department of Agriculture in 2007, 57% of all vegetables consumed by Americans are limited to five sources (potatoes, tomatoes, leafy greens, lettuce, and onions). Unfortunately, the most consumed vegetable in America, the potato, is often in the form of oil-soaked french fries or potato chips. For fruit, five sources (apples, bananas, grapes, strawberries, and oranges) account for 71% of the total intake. From an evolutionary perspective, this minimal diversity, even when coupled with the handful of whole grains and beans/legumes consumed, translates into a striking shortfall in the physical and chemical diversity of fiber once consumed by humans and subsequently utilized by the hundreds of bacterial species that inhabit the human gut. We have changed the rules of the game between “us and them” in such a way as to possibly disrupt the organic harmony that evolved in this symbiotic relationship to a nutritional tipping point.

The emergence of prebiotics as a “super fiber” of sorts is just one example of the importance of diversity of fiber in the human diet. The steady clip of scientific papers demonstrating the health benefits of prebiotics is fascinating as we are literally peaking under the evolutionary curtain of our nutritional past.

Unlike probiotics, which are live microbial organisms that are naturally present in the human body, prebiotics are literally food for probiotics. While many fibers claim to be prebiotics, true prebiotics selectively stimulate the growth of certain probiotics known to be beneficial to humans, such as bifidobacterium and lactobacillus, while not promoting the growth of less useful or even harmful strains, such as clostridium.

Even though prebiotic fibers are present in more than 30,000 edible plants throughout the world, American and European diets only include 1 to 3 g/d – sometimes a little more, sometimes a little less. When we look into the archaeological record, like the west Texas example discussed above, we see daily consumption (though variable seasonally) of 10, 15 and often more than 20 g/d from desert plants such as agave, prickly pear, sotol, wild onions and so forth. Dozens of peer-reviewed studies have shown that test subjects who consumed between 5 to 20 g/d of prebiotic fiber, mainly in the form of inulin and fructo-oligosaccharides derived from chicory roots, were able to stimulate the growth of “good” bacteria and increase calcium absorption, blunt hunger, relieve symptoms of irritable bowel syndrome, reduce biomarkers of some cancers, reduce inflammation through various mechanisms, improve immunity, and fortify our natural defenses against many food-borne pathogens. And the list goes on.

It would be a mistake to look at the science and health benefits emerging from clinical benefits of prebiotics as a new discovery of some magic bullet. More correctly we are simply witnessing a rediscovery of the importance of the diversity of fiber in human diet and, specifically, the role these particular fibers play in the health and well-being of gut bugs.

The exciting science behind prebiotics coupled with the underlying biological reality that humans are still designed to ferment a large and diverse quantity of fiber (~50 to 90 g/d, minimum), and that much of our health is tied to the maintenance of a healthy population of gut bacteria, should serve as a wake up call for new therapeutic approaches to health. We don’t need yet another diet for us, but desperately need a diet for our entire “super-organism’ – both us and them.

Even though humans evolved from nothing more than a run-of-the-mill large mammal on an open savannah of other large mammals, to something of a geological force in an evolutionary blink of an eye, we owe much of our current success as a species to these tiny microorganisms. They require little more than a safe place to live and a steady flow of the quantity and diversity of fiber that they and their microbial ancestors evolved on.

Continuing to ignore our shared nutritional past with our tiny friends and adhering to the very human-like notion that we are somehow separate from nature will only result in progression of many human diseases to levels that will require the medical community to seek new vernacular to describe the public health hardships that potentially lie ahead. Fiber anyone?