Some people can devour three-egg omelettes slathered with cheese and indulge in one chocolate bar after another without gaining even a kilo or showing any spike on the cholesterol count. Others seem to get obese just by staring at a fatty food.
No prizes for guessing what’s behind this scandalous dietary injustice: the culprit lies hidden in the genes. Your genetic make-up not only determines how your body metabolises the nutrients you consume, but also your susceptibility to obesity and other related diseases.
In the new nutritional realm, the battle of the bulge no longer remains simple. And those classic one-size-fits-all dietary approaches — focussing on certain proportions of carbohydrate, fat, protein, minerals or vitamins — seem inadequate for your well-being.
The latest eat-right mantra, called nutritional genomics or nutrigenomics, redefines your dietary requirements based on your unique genetic signature. A spinoff of the Human Genome Project, this new field of research studies how genes and diets interact. Within the next few years experts on nutrigenomics will be able to precisely tailor a diet for you. It’ll keep you trim and prevent or delay the onset of a possible illness as well.
Diets tailored to fight disease
“With more personalised nutritional genomic information,” says Jose Ordovas, director of the Nutrition and Genomics Laboratory at Tufts University in the US, “we will be able to use diet as a primary disease prevention tool, in a precise way.” The scenario conjured up by experts like Ordovas seems more like a page out of a sci-fi novel: A doctor pricks your finger, draws a little blood, and after a quick analysis, pulls out a print-out showing tailor-made dietary recommendations. Some people may be advised to refrain from eating omelettes, while others may be told to stuff themselves with lots of them.
We have long known that food plays an important role in our gene expression. Much before modern genetic studies, scientists used biomedical tests to detect genetic disorders such as phenylketonuria (PKU) which makes people vulnerable to brain damage if they eat certain types of protein (called phenylalanine). Just keeping out those protein from their diet enabled PKU-patients keep a range of anomalies —such as mental retardation, epileptic seizures, and abnormal brain wave patterns — at bay. Studies on PKU helped geneticists realise that all dietary chemicals don’t serve as raw materials for producing energy for the cell. Instead, the moment they are ingested they bind with certain proteins involved in “turning on” certain genes. In other words, there are food chemicals which act as a trigger to specific gene expressions.
As scientists learnt more about the human genome they found that many illnesses, including cancer, diabetes, obesity, heart disease etc., are the result of interactions between a number of genes and diet. It has been estimated that there are at least 150 gene variants that can give rise to type 2 diabetes, 300 or more that are associated with obesity. In the case of cancer, there are countless such genes. Diet is responsible for one in three cases of cancer.
It’s evident that a lot of individual genetic variation influences our propensity to a number of chronic illnesses. How does a scientist pin down a specific genetic makeup' “Right now, we know only about a few switches and how to turn them on or off,” says Ordovas. “But there are plenty of more switches that we don’t know about yet.”
Those known switches involve the commonest types of genetic variability called single nucleotide polymorphisms or SNPs (pronounced ‘snips’). These are places in the genomic code that vary by a single genetic ‘letter’ among individuals. Snips may determine differences in appearance, such as hair and eye colour, predisposition to illnesses, and how people respond to drugs or food items.
Disease-markers on genes
Several such snips of importance to nutrition have been identified in the last few years. For instance, common polymorphisms in genes that control the metabolism of the nutrient called folate (found in leafy green vegetables and citrus fruits) have been linked to conditions such as Down’s syndrome, neural tube defects and cancer. If the mechanisms by which these polymorphisms disturb folate metabolism and alter disease risk can be pinned down, it should be possible to develop dietary or therapeutic strategies for “at risk” individuals to restore the dietary equilibrium. Polymorphisms have also been identified in genes involved in fat metabolism that are important in determining an individual’s low density lipoprotein (LDL) or bad cholesterol level — a marker of heart disease risk.
It’s not a surprise that several genetic markers have got a strong ethnic influence. Although the finding evokes an ethical outcry, there are indeed several gene variants which follow from the fact of whether you have a Caucasian, African, Hispanic or Asian origin. And in several cases diets play an important role in such genetic expressions.
For instance, a change in a single gene (or a genetic polymorphism) that arose nearly 10,000 years ago allows people of Caucasoid (North European) ancestry digest milk in adulthood, whereas most southeast Asians are intolerant to the milk-chemical lactose when they grow up .
According to Jim Kaput, founder of NutraGenomics, a biotechnology company, as humans evolved, and our bodies interacted with food available in each of the continents, our genes got naturally selected for the food variants. In other words, changes in genes have occurred in the human population as evolutionary responses to changes in diet. Some of these changes in the genes do not allow people to shift to any diet they choose. The most famous of the gene variants is the “thrifty-genotype”, acquired by the Asians who had been migrating to North America across the Bering Strait about 30,000 years ago.
These genes were believed to offer the ancient migrants an ability to store fat and metabolise it thriftily amid the chill of the Arctic environs. The genes allowed these people pile on calories from seal fat, caribou meat and fish even though they ate little vegetable or fruit so that the excess body fat could keep them warm in the sub-zero temperature and hunt for food.
But the traits which helped the Inuits — the descendants of those Asian migrants — survive the Arctic wilderness thousands of years ago, suddenly put them in evolutionary disadvantage in the 21st century. They no longer need to chase reindeer in dog-sledges or hunt for seals in the freezing water. Travelling in snowmobiles, living in electrically heated homes and eating American fast-food only adds extra calories that rarely get used up. In the changed scenario, the thrifty-genotype goes haywire paving the way to diabetes, obesity and cardiovascular diseases.
The scenario gets even more complicated in the Pima tribe —descendants of the same Asian migrants — of Arizona in the US who suffer one of the highest rates of diabetes in the world. Sedentary lifestyle and loads of junk food have made Pimas vulnerable to a number of obesity-related diseases. However, another group of Pima, which lives in Mexico, leads more or less a healthy life — courtesy their traditional diet and an active lifestyle.
| Modern lifestyle: An Inuit family in Tula, Greenland
Whenever people moved away from their traditional environments and adopted a drastically changed diet, the genes rebelled. This is how the Masais of east Africa developed high blood pressure and high blood sugar after abandoning their traditional lifestyle. More than 60 million Chinese became overweight in just about a decade. And south Asians turned vulnerable to diabetes and cardiovascular diseases when they adopted a high-fat and high-protein junk diet, as opposed to their traditionally frugal food habits.
According to scientists working on nutritional genomics, a tailor-made diet can compensate for the obsolete genes like the thrifty genotype that we have inherited from our primitive ancestors. For instance, Ordovas’ team at Tufts is now teasing apart genetic factors that contribute to obesity. He thinks he will be able to carve a specific diet for overweight people so that they can successfully lose weight. “We are in the process of identifying diet-regulated genes and appropriate nutritional interventions that will allow individuals to better manage their health and well-being,” echoes Kaput of NutraGenomics.
Several such projects in nutritional genomics are sprouting around the globe. In the US, the National Institute of Health has helped set up a Centre of Excellence for Nutritional Genomics at the University of California, Davis. Raymonds Rodriguez, the director of the centre, hopes that nutritional genomics will usher in a new era of consumer genetics.
Huge marketing boom
Food companies indeed have lapped up the idea to market the so-called functional foods that address specific needs of populations. For instance, the British company Sciona has already begun selling genetic screening and personal diets for obesity management. “In order to improve the accuracy of the diets we prescribe to patients, we have introduced into our obesity clinics a genetic test for polymorphism in genes involved in nutrition metabolism and have treated 70 patients so far,” gloats Sciona’s website. Unilever, the famous Anglo-Dutch conglomerate, has forged an alliance with Perlegen, a genetics company based in California which has categorised 1,586,383 SNPs in 71 Americans of European, African and Han Chinese ancestry. “This knowledge can lead to new product [read food] development and a htching of products to consumer populations,” announces Perelgen’s website.
Following the footsteps of Sciona and Unilever, other food companies are earmarking substantial amounts of their R&D budgets for ‘functional’ foods. According to the US market research firm Aroq Limited, the global functional food market is expected to grow by 14 per cent annually and it will reach $167 billion by 2010.
Is this sudden boom based solely on science' Will it be ethical to market food tainted by the ethical divide' Several geneticists as well as nutritionists warn against such a headlong rush into nutrigenomics until the staggering complexity among genes, and between genes and environments, are completely unravelled. “Food interactions are usually far more complicated,” said Dr Muin Khoury, director of the Office of Genomics and Disease Prevention at the US Centers for Disease Control and Prevention, to Newsweek. “Metabolism involves huge numbers of genes interacting in uncountable ways.”
Even Kaput thinks that nutrigenomics needs many more epidemiological and controlled animal studies in labs to pin down specific dietary constituents as the main culprits inducing or contributing to chronic diseases. But then results of such studies on animals too often do not resemble those conducted on humans.
Even more concerned are ethical experts. “Nutrigenomic testing and the labelling of foods for specific populations on the basis of their genetic makeup could become highly important public health tools,” says Peter A. Singer, director of the Joint Centre for Bioethics in Canada. “But this research raises many ethical concerns now associated with genetic screening.”
Experts like Singer fear that personal genetic profiles can be misused by insurance companies to charge higher premiums or altogether exclude people from their plans. Potential employers also may gain access to information which could cost a person a job.
Notwithstanding these hurdles, a whole new economy is all set to boom centred on diet-gene interactions. Won’t it be convenient to stave off critical diseases just modifying your food habits — doing away with the need for expensive drugs or diagnostic tests'