Changing dietary trends and the obesity epidemic
Last Sunday the New York Times published a color spread on the US Department of Agriculture (USDA) data on the changes in food consumption in this country between 1970 and 2006, which got me to musing.
To the uninformed, which, sadly, probably means most people working in the nutrition industry and even those employed in a nutritional capacity at the USDA, these changes (all save two) seem to be in a positive direction. The intake of dairy products has decreased; the intake of vegetables has increased; the intake of red meat has fallen; the intake of fish, chicken and skyrocketed; the intake of fruit is up; the intake of grains has increased markedly; and the intake of vegetable fats has almost doubled. The only two negatives are that sugar and sweeteners have increased and overall food consumption has gone up by about 11 percent, or an addition 1.8 pounds per person per week.
At the same time all these positive changes have been taking place, changes that all the (misinformed) people in the mainstream nutritional biz have been advocating, there has been an enormous increase in the rate of obesity. According to the Centers for Disease Control (quoted in the Times article) the rate of obesity has more than doubled since 1970, which is interesting because up until 1970 the rates of obesity hummed along at about the rate of 15 percent for decades.
What has happened since 1970 to cause this enormous societal change?
If asked, people give many answers: too much saturated fat, too much refined carbohydrate, too much food, etc.
I have my own opinions, which I will elaborate. I believe that the obesity epidemic has probably been driven by several dietary changes that have occurred since 1970. These changes are an increase in fructose and vegetable oil consumption and a decrease in saturated fat consumption. I believe that another contributing factor is the increased overall consumption of carbohydrates, which leads to an increased food consumption in general.
I want to emphasize that these are my opinions based on a pretty good knowledge of nutrition, metabolism, biochemistry, and physiology.
First, a sort of no-brainer. Since the USDA came out with the idiotic Food Pyramid we all loathe, there has been a major strategy in the food industry to move away from fats and toward carbohydrates. We have all seen this in various food consumption statistics. And we can tease it out from this Times piece if we look at which foods have increased and which have decreased in the diet. There has been a large increase in carbohydrate consumption as evidenced by the large increase in grains, vegetables, fruits and sweeteners.
Forgetting about all the metabolic events that carb intake precipitates that we all know cause obesity (i.e., increased blood sugar, increased insulin, etc.), let’s focus on simply one of the brain processes that carbs affect. The satiety center, located in the hypothalamus, is the part of the brain that tells us when we’re full. Unfortunately, it runs about 20-30 minutes behind our actual eating pattern, so we can stuff food in for a good while before our brains tell us we’ve had enough. Fortunately, it works a little more quickly (thanks to the help of cholecystokinin and some other gut hormones) when we eat primarily fat. If you eat a big steak, you feel full more quickly than if you eat a lot of carbs. Carbs tend to override the satiety center, allowing you to eat more. Let me describe a situation we’ve all experienced, and you’ll see what I mean.
You’re at a restaurant. You’re just at the end of a big meal and you’re stuffed. One of your dinner partners asks you to try a bite of his wonderful swordfish. It’s the best he’s ever tasted, he tells you. You say, I just can’t eat another bite. If I do, I’ll be sick. Then appears the waiter with the dessert tray, loaded with wonderful gooey treats. You look them over and say: I’ll take the carrot cake (or the chocolate mousse or whatever). How can you eat this calorically-laden dessert when you’ve just refused a bite of meat because you were so full? Because your brain’s satiety center is overridden by the carbs. And you haven’t even eaten the carbs yet. But experience has taught you that no matter how full you seem to be, there is always room for carbs. And fat, since most desserts are pretty high in fat as well. But it’s the carbs that do the satiety-center-blunting trick. It’s the reason dessert is always at the end of the meal. If you ate the dessert first, you would never be able to eat all the steak. And this carb overriding of the satiety center is why people don’t binge on steak, eggs and bacon. They binge on cake, chips, cookies and other high carb treats because they can stuff them without their satiety center telling them they’re full.
Since we’ve (as a nation) significantly increased our carb intake, it only makes sense that we’ve also increased the overall amount of food we eat. Carbs let us do that without even trying.
We have definitely increased our intake of fructose since 1970. I used the figures in the Times article to make my own calculations. Considering that table sugar is one half fructose and high-fructose corn syrup is 55 percent fructose (the most commonly used variety; some go as high as 90 percent fructose), I calculated that we ate about 50 grams of fructose per capita per day in 1970. By 2006 that figure had increased to 75 grams, a 50 percent increase. And we’ve got to bear in mind that these are average figures. I eat maybe 3 grams of fructose per day, and MD eats the same. That means that two other people out there are eating their 75 grams plus our extra 72 to make the averages come out as they do. I would suspect that most of the people reading this blog eat very little fructose, leaving a lot of other people to consume their share to keep the averages up.
But even 75 grams of fructose is a helluva lot. A little fructose – the amount you might find in a piece of fruit, for example – actually helps with glucose metabolism. It more or less primes the pump so that less insulin is required to reduce blood glucose. Large amounts of fructose are a different story, however. Fructose bypasses the enzyme phosphofructokinase, which is the rate-limiting enzyme in the glucose metabolism pathway. Consequently, large amounts of fructose are shunted past the sugar-regulating pathways and into the fat-formation pathway instead. The liver converts this fructose to fat, much of which, unfortunately, remains in the liver. ( Here is a nice paper on fructose metabolism. Ignore the idiotic conclusion, which is just another ad hoc attempt to make the data fit a preconceived notion acceptable to all academics.)
With continued consumption of large amounts of fructose, fat tends to accumulate in the liver leading to a condition called non-alcoholic fatty liver disorder (NAFLD). At this point, not only are we in an obesity and a diabetes epidemic, we are in an epidemic of NAFLD. Studies on ‘normal’ adults have shown that a little more than a third have significant fat accumulations in their livers. Even worse, 15-20 percent of children show the same thing.
NAFLD is the same disease people get who chronically over consume alcohol. Under the microscope NAFLD looks exactly the same; pathologically it acts the same. The only way to differentiate is by history of alcohol consumption: if there is fat in the liver and no history of chronic alcohol abuse, then NAFLD it is.
NAFLD has the same progression as the alcoholic variety. First, an accumulation of fat that becomes inflamed leading to a condition called non-alcoholic steatohepatitis (NASH), which means a non-alcoholic inflammation of fat in the liver. This condition can then progress to liver fibrosis, then to cirrhosis, then, ultimately, to liver cancer. Not all NAFLD follows this complete progression just as not all alcoholics get cirrhosis, but enough follow it to not make you want to get NAFLD if you can help it.
And one of the big ways not to get it is to avoid fructose.
By increasing fat in the liver, fructose also increases circulating insulin levels, which can lead to hyperinsulinemia and insulin resistance. How? Because a liver full of fat doesn’t work as well as a non-fatty liver. One of the jobs of the liver is to metabolize hormones and clear them from the circulation when their work is done. When you consume carbs or protein you stimulate the release of insulin to deal with them. Once insulin has done its job, the liver breaks it down to its amino acid components and puts them back in the circulating amino-acid pool. If the liver is filled with fat, it can’t do this as well. Insulin stays elevated (and in a diabolical twist even stimulates more fat synthesis in the liver) and tends to downregulate the insulin receptors, making them less responsive. The entire process can lead to insulin resistance, hyperinsulinemia and ultimately to obesity.
Below is a nice chart showing how the increase in obesity has paralleled the rapid increase in sugar consumption. Remember that table sugar is half fructose. Also remember that correlation is not causation. But in this case we do have the biochemistry of why worked out.
From Johnson RJ et al, AJCN 2007; 86:899-906
What about saturated fat? How does a decrease in saturated fat cause obesity. First, the decrease in saturated fat has tracked with the increase in vegetable oils, which are typically rich in omega-6 fats. Omega-6 fats have been shown in numerous studies to be proinflammatory. They have also been shown to worsen alcoholic fatty liver disease, and, one would assume, NAFLD as well. I haven’t seen any studies showing a worsening of NAFLD with increased consumption of vegetable oil – it hasn’t been studied as far as I know. (Maybe one of you readers can dig up a paper.) But it has been shown repeatedly with alcoholic liver disease, and since NAFLD is basically the same disorder, it makes sense that vegetable oil would worsen NAFLD as well. And if vegetable oil indeed does worsen NAFLD, then it promotes obesity by the mechanism described above.
Saturated fat is a healthful food. Read this article by Mary Enig that describes in detail the health benefits that come from eating saturated fat. I’ll address a couple of different issues.
Saturated fat is, well, saturated. That means that every carbon in the fatty acid chain has a full complement of hydrogens attached to it. There are no double bonds. In the picture below you can see a saturated fatty acid on top and a monounsaturated (one double carbon-carbon bond) fatty acid on the bottom.
Double bonds make fats unstable. These double bonds are the places that free radicals strike to convert unsaturated fats into peroxides, or oxidized fats. The more carbon-carbon double bonds a fatty acid has, the more susceptible it is to oxidation. Oxidized fats don’t function as well as non-oxidized fats. They make faulty cell membranes and less than optimal membranes for all the organelles within the cell. Oxidized fats can themselves become free radicals attacking adjacent fats and damaging them, or worse, starting an entire free-radical-fat-damaging cascade. All these forces work even more effectively at higher temperatures, so unsaturated fats shouldn’t be used for cooking. Unless, of course, your goal is to eat oxidized fats.
Saturated fats have no double bonds. They are immune to free radical attack. They are immune to heat damage. You can cook with them, you can hit them with a hammer, you can throw them on the floor and jump up and down on them. And they stay the same. Saturated fats are stable fats.
Most people don’t realize this, but the body has the ability to convert saturated fats to unsaturated fats. But the body doesn’t have the ability to convert unsaturated fats to saturated ones. The body can make saturated fats (palmitic acid, a 16-carbon-chain fatty acid) from excess carb consumption, but it can’t make a saturated fat out of an unsaturated one. If nature hadn’t wanted us to have saturated fat, why did she make us so that we make our own if we eat too many carbs. Could it be that during our evolutionary past the only time we might over consume carbs would have been when there was no meat available…and we needed the saturated fat? Sounds reasonable to me.
We have enzymes called desaturases that desaturate, i.e., add carbon-carbon double bonds, fats. We can take unsaturated fats and make them more unsaturated. And we can take saturated fats and make them unsaturated. But we can’t go the other way. In order to have saturated fats that provide the necessary structural stability that only saturated fats can provide is to get them in the diet, which we can do by eating saturated fats or by eating a whole lot of carbs. Since over consuming carbs comes with its own set of problems that we would rather avoid, that leaves eating saturated fats.
So how does avoiding saturated fats lead to obesity. In my opinion in a couple of ways. First, indirectly, by having them replaced by vegetable oil, particularly hydrogentated vegetable oil, i.e., trans fat. Due to their stability, saturated fats have cooking properties that no other natural fats have. Food chemists have created trans fats to have the same cooking properties – and in some situations even better cooking properties – as saturated fats. But the addition of trans fats to the diet creates a host of other problems. The medical literature is crawling with studies showing that trans fats drive the development of obesity.
The other reason is that saturated fats compose the lion’s share of normal membranous fats and of the brain. When membranes don’t work as well, especially mitochondrial membranes, our energy storage and regulation system doesn’t work as well. Anything that impairs membrane functioning impairs signaling function. If signaling function falls off, then various hormones, neurotransmitters, etc. lose function. As insulin loses function, more insulin is required, more insulin leads to more downregulation of receptors, all of which ultimately leads to obesity.
Even overeating carbs doesn’t help even though saturated fats are produced as a result. Carbs stimulate the production of palmitic acid, a 16-carbon chain fat. For proper membrane function and signaling we need shorter-chain saturated fats as well. These we can’t make – we get them from diet only. We can make shorter fats longer with elongase enzymes, but we can’t make longer fats shorter. We’ve got to get them via mouth.
Since this is speculation on my part – educated speculation, but speculation nevertheless – we may ultimately find that there are other reasons for the obesity epidemic instead of these or in addition to these. In fact, I can think of a few other minor causes, which I’ll save for a later post.) But I’ll bet that when all the work is done – which may not be for a hundred years given the academic climate of today – I’ll bet these ideas will be close to the mark.