And, of course, there’s another significant motivator—the same one that got former President Bill Clinton inspired to change his diet a few years back: the ubiquitous desire to live a long, full, and healthy life.
For the former president, after a lifetime of eating whatever seemed good at the time, undergoing two heart surgeries, and taking stock of a family history of heart disease, Clinton finally decided to make some serious life changes, including moving to an almost completely vegan diet, in 2010.3 Sometimes you just have to be pushed into making a total change and, just like Clinton, radically change your nutritional lifestyle. Even if you’re properly motivated, accessibility and the affordability of nutritious and healthy foods can come with substantial obstacles, but ones that are worth working to overcome.
Okay, what have we learned so far? Find good food, eat like your recent ancestors—but not as much—get physically active, and then listen to your body for telltale clues that you’re on the right path.
If only life were so simple. Far from being a utopian solution, eating strictly like your ancestors will not work for everyone. We are, after all, genetically unique. In fact, as we saw with Jeff the Chef and Cindy who has OTC deficiency, not taking stock of what we individually inherited can even turn deadly. Each of us should be eating in a way that more closely matches our distinctive genetic inheritance.
As we’re about to discover, this is far from a modern problem—something that our seafaring ancestors would have no trouble recognizing, either.
***
Enshrined in nutritional lore is the story of how British sailors suffered horribly from bleeding gums and easy bruising—a condition known as scurvy—because of the lack of fresh fruits and vegetables aboard maritime ships. Back before we’d figured out electrical refrigeration, the best sailors could hope for was a combination of cured and dried meats and some crusty bread. For men stuck at sea for months at a time, this led to some pretty nasty nutritional deficiencies—and, curiously, not all sailors suffered equally from them.
Today, we know that citrus fruits are rich in vitamin C, which for most people is good for preventing the sorts of deficiencies that some of those sailors faced. Back then, they just knew that lemons and limes could keep their teeth in their mouth and the other symptoms of scurvy at bay.
Interestingly, the rats on those ships didn’t have that same problem. Neither did the cats that were often kept on board to do battle with the rodent marines. So why were the rats and cats not losing their teeth as well?
From aardvarks to zebras, most of our mammalian cousins have working copies of the genes that can manufacture vitamin C naturally within their bodies. But humans (along with guinea pigs, of all things) have a genetic inborn error in metabolism, a mutation that renders us incapable of doing the same thing. This makes us completely dependent upon our diets to get our daily supply of vitamin C.
Some small groups of seafarers appear to have figured out the magic of citrus fruits centuries earlier, but it wasn’t until the end of the eighteenth century that the British Admiralty, encouraged by a Scottish physician named Gilbert Blane, had its sailors drink lemon juice to combat scurvy. And on return trips from the empire’s Caribbean territories, where limes were more plentiful, the ships were loaded with the lemon’s green taxonomic cousin—which is how British sailors became known as limeys.4
Once we figured that out, though, it was only natural to want to determine the minimum amount of lemons, limes, oranges, and the like we need each day to stay healthy (after all, the famously bureaucratic Brits needed to know just how many citrus fruits to pack for a long voyage at sea). This is the root of modern nutritional science, which to this day is based on the idea that we can math our way to a healthy diet. Hence the “reference daily intake” (formerly known as the recommended daily allowance) that is used to determine—down to the gram, milligram, and microgram—the daily values of food we all supposedly need to live healthy, active lives. Many of these values have been derived from what’s needed for the average person to overcome a symptomatic deficiency and not what’s optimal for us as utterly unique individuals.
Which is why we don’t all need the same amount of vitamin C. As we move toward what’s individually optimal, we’ll have no choice but to look at our genes. In a study that focused on the genes that help get vitamin C into our bodies, researchers found that variations in a transporter gene called SLC23A1 affected the level of vitamin C completely independent of our diet.5 And even with a corresponding higher intake of vitamin C, some people, it seems, will always have lower levels of vitamin C no matter how many citrus fruits they eat. Discovering which version of the transporter gene we inherited can have a tremendous impact on our understanding of the amount of vitamin C that gets successfully absorbed into our bodies.
Direct dietary advice is not, however, all we need. We are discovering that some of the differences in our genetic inheritance, for instance versions of another gene involved in vitamin C metabolism, SLC23A2, have been associated with an almost threefold risk of spontaneous preterm birth.6 It’s been suggested that this might be related to vitamin C’s role in the production of collagen, which helps provide the tensile strength a mother needs to keep her baby inside her body,7 again underscoring the importance of taking our genetic inheritance seriously when it comes to nutrition.
So, given that generalized dietary advice can be wrong when it comes to the individual, you may rightly be wondering how much is the right amount of citrus. And what’s the right diet for you? And what foods should you avoid? The answers to those questions are going to be different for everyone, not only because of the genes you’ve inherited but because, more importantly, what you eat can completely change how your genes behave.
***
This year, tens of millions of Americans will attempt to change their diet.
And most of them will fail.
In part, that’s because without knowing what diet is genetically right for them, some of those folks are essentially flying blind—and many are doing things that are counterproductive to their goals.8
But even for those in the majority, for whom the advice to eat a reasonable diet and get vigorous exercise is still the best medicine, there’s another problem: Dieting is hard.
For most of human history, food was far from plentiful. To mitigate this scarcity, coupled with the rare times that food became bountiful, we’ve all inherited genes that favor overeating. And in the past, if there happened to be any caloric leftovers from those rare big meals, our bodies would eagerly pack them away as body fat. Like a caloric savings account, storing what we didn’t use came in handy when scarcity returned. And for most of human history, we’ve known more paucity than plenty.
Today we’re faced with a complex problem, a glaring mismatch between what we’ve inherited and the current environment we find ourselves in. First off, given our sedentary lifestyles, we don’t need anywhere near the same amount of calories to get by as in the past. We’ve sentenced machines to do most of our hard labor for us and get us around from place to place. And secondly, combine that with the abundance of cheap available calories, and it’s easy to understand why obesity rates are soaring today as never before in human history. It’s not just the amount of foods we’re consuming, either. As we’ll come to see, our food choices are far from optimized for our genetic inheritance.
Thanks to the science known as nutrigenomics, we’re starting to figure out what to leave off the individualized contemporary menu. For example, you’ll no longer need to wait to get bloated, write a food diary, and have diarrhea to find out that you are lactose intolerant. The genetic test that would give you that information is already commercially available. And if you’re an early adopter you might have already looked beyond single gene testing, say for lactose intolerance, and decided to go all the way and get your exome or even your entire genome sequenced.
Which can then be used for twenty-first-century genetically based dietary advice. You can use this i
nformation to decide whether your next cappuccino should be caffeinated. This decision would come about by finding out what version of the CYP1A2 gene you’ve inherited. Different versions of this gene determine the rate at which your body breaks down caffeine. You may be a fast or slow metabolizer of one of the world’s oldest stimulant drugs.
Having a different version of the CYP1A2 gene and consuming caffeinated coffee can have far more wide-ranging effects than just keeping you up at night. Again depending on the version of CYP1A2 you’ve inherited, you’re likely to experience a consequential unhealthy spike in your blood pressure. This is thought to happen if you’ve inherited a copy of the CYP1A2 gene that breaks down caffeine slowly. On the other hand, if you’ve inherited two copies of the same gene that burn through caffeine quickly, your blood pressure is not likely to be affected in the same way.9
Let’s start putting together pieces of what we’ve learned so far about our genomes and nutrition, because things are about to get a lot more interesting. As we’re learning, our lives are not functioning in a genetic or environmental vacuum, with only single-gene interactions. We previously spoke about how our genomes are continually responsive to how we behave and what we eat. Like Toyota and Apple, employing JIT or just-in-time forms of production, our genes are constantly being turned on or off. And this happens through genetic expression—where genes are induced to make more or less of a product.
An example of how our lives can affect our genes in interesting ways can be seen in smokers who drink coffee. Have you ever wondered why people who smoke tobacco seem to have no problem consuming very large quantities of coffee?
The answer has to do with genetic expression.
Our bodies actually use the same CYP1A2 gene to break down all sorts of poisons. Given its noxious contents, it’s no surprise that tobacco is a very loud genetic call to action, and in this regard smoking induces or turns on the CYP1A2 gene. The more this gene is turned on, the more easily your body can break down caffeine in coffee. Don’t get me wrong—I’m not suggesting that you take up smoking so you can drink more coffee and still fall asleep at night. I’m just saying that smoking changes the way your body breaks down caffeine, which can turn a genetically slow metabolizer into a faster one.
Anyway, if coffee doesn’t agree with your genetic makeup, you’re always welcome to brew yourself some green tea. And before you sit down to enjoy some sencha or matcha, just a quick reminder that nothing we do is without some type of genetic consequence.
In the case of green tea it’s been suggested that it may play a role in preventing some forms of cancer. More recently, researchers gave breast cancer cells one of the potent chemicals found in green tea called epigallocatechin-3-gallate, and they noticed two very important results. The breast cancer cells began killing themselves through a cellular process called apoptosis, and those cells that didn’t, still showed much slower growth. This is exactly what you want to see happen if you’re looking for new treatments for rogue cancerous cells.
When the details were worked out as to how the cancer cells were coaxed to change their behavior, it became clear that epigallocatechin-3-gallate can promote positive epigenetic changes—those on and off modifications to DNA that work to help regulate gene expression. These are important and crucial steps in trying to control cells when they decide to stop obeying our bodies’ collectivist biological manifesto. When cells cease to work together cooperatively and go on a malignant rampage, you end up with cancer.
The more we study the interplay between our genes and what we eat, drink, and even smoke, the more apparent it becomes just how important these interactions are to the maintenance of our health.
And from studying monozygotic twins who have inherited the same genomes and are eating similar diets, we’re now uncovering the crucial missing piece to our nutritional puzzle.
Which is why it’s time that I introduce you to your microbiome.
***
The human gut is a mind-bogglingly complex example of microbial biodiversity.
Two of the main players in this huge little ecosystem are the phyla Bacteroidetes and Firmicutes.10 If you add up all the species belonging to each of these groups, you’ll come up with several hundred different types of microbes—and everyone’s microscopic menagerie is a little bit different.
To the microbes living within you, the 30 feet of plumbing from your mouth to your anus is a veritable planet. Its twists and turns, if mimicked in roller-coaster form, would humble even the most experienced thrill seeker. And the difference in conditions, from one part to the next, is like going from the bottom of the sea to the inside of a volcano to the lushest of rain forests.
It’s probably not surprising, then, that the gastrointestinal system is one of the most complex structures our bodies construct during fetal development. To give you an idea of the developmental Cirque du Soleil required, at one point in our fetal development, our intestines actually grow out and into the area inhabited by our umbilical cord. To make it back safely into the abdominal cavity, the intestines need to twist and turn, stuffing and coiling themselves like a snake back into a charmer’s wicker basket. Which is why it doesn’t take much to throw the process off. If the intestines get trapped on their way back into the body, an omphalocele—a sort of intestinal and umbilical herniation—can form. If the intestines do make it safely into the abdomen but the body wall fails to close properly, gastroschisis can occur. This is the name given to the condition that results when parts of the intestines remain on the outside of the body during development, poking out through a crack or crevice. Because the intestines and the amniotic fluid are not meant to meet, the exposed intestines are usually damaged and need to be surgically removed and reconnected.11 And those are just a few of the many things that can go wrong in the development of a system that, later on, will house a jungle of physiological and microbial flux.
So while it’s not always pleasant to think about, it turns out that knowing a bit more about what’s happening inside our intestines might be one of the more novel things we can do to stay in touch with our personal health.
To understand this better, let’s take a trip to China, where scientists at Shanghai Jiao Tong University recently turned the dietary science world on its ear.
Here’s what happened: When studying the gut of one morbidly obese person (who at 385 pounds was about the size of the average sumo wrestler), the scientists noticed an abundance of bacteria that belong to the genus known as Enterobacter. Now, lots of people have some Enterobacter in them, but in this particular patient, it made up 35 percent of the bacterial forms in his system. That’s a lot. So to better understand what was happening, the researchers took a strain of the bacteria from the patient and introduced it to mice that had been raised in a completely germ-free environment.
And, well, nothing happened.
That could have been the end of the experiment. But the Shanghai scientists then decided to see what would happen if they had the Enterobacter-infected mice eat a diet that more closely mirrored the high-fat diet the patient had been eating. Essentially, they drove their furry little companions over to McDonald’s and gave them a double cheeseburger, large soft drink, and fries—lots of fat and lots of sugar. And, surprising to absolutely no one, the mice got fat.
But here’s the fascinating thing: Per basic scientific procedure, the scientists also kept a control group of mice that consumed the exact same high-fat diet as their counterparts but weren’t infected with Enterobacter. And those mice stayed skinny as rails.12
So was the obese man’s diet the problem? Certainly. But that, by itself, may not be the only reason why he was so heavy.
With time we may come to appreciate how genetics, diet, plus the presence of a specific combination of microbes could be helping us tip the scales.
Now we certainly can’t “catch” obesity—but we can spread bacteria. And if that type of bacteria is one that potentially contributes to an unhealthy reaction to fats, then the effect coul
d be the same.
But it’s not just weight gain that we need to be thinking about when it comes to the effect our personal microbiomes—the menagerie of microbes and their DNA that inhabit our bodies inside and out—are having on our health. It’s also our hearts.
You’ve likely heard that red meat and eggs are bad for your cardiovascular system. What you might not know, though, is that it’s not only the saturated fat and cholesterol alone, which we’ve long assumed causes an increased risk of heart disease. Rather, the risk may be heightened by a compound called carnitine that is prevalent in those foods. By itself, carnitine doesn’t appear to be at all harmful. But when met by the bacteria that make up the microbiome living in most people’s guts, it’s turned into a new chemical compound called trimethylamine N-oxide, or TMAO, that, when introduced to our bloodstream, appears to be bad for our hearts.13
So far, the health effects that can be caused by microorganisms that make up the human microbiome have gotten a lot less attention than the human genome. This is going to change as it becomes more apparent, that one’s microbiome is just as important as what one eats and the genes one gets. Even monozygotic twins with identical genomes don’t always have identical microbiomes, especially when they don’t weigh the same.
Which is why, as we’re learning about the importance of being stewards of our genetic inheritance, it might be sensible for us to take more of an interest in the welfare of our microbiome as well. One of the easiest ways for us to do that is to consider alternatives to the indiscriminate use of antibacterial products like soaps, shampoos, and even toothpaste. Also, it would be prudent to discuss with your physician the absolute need for an antibiotic prescription before rushing to fill it. As we’ve learned time and time again, a political regime change that is accomplished by force, or a microbial one caused by medication, can often have unforeseen and long-standing consequences.
Inheritance: How Our Genes Change Our Lives--and Our Lives Change Our Genes Page 10
