Obesity and Hunger in America and Benin

Here in Benin, I find myself thinking a lot about food, nutrition, and weight from both a biological and sociological perspective. Many people here don’t have healthy food options or are malnourished due to simple lack of food. It’s quite common to see people who are skeletally thin (marasmus), people who are bloated from lack of protein (kwashiorkor), and people who are just fat from a diet high in carbohydrates. A lot of this range is typical for developing countries. Carbohydrates play a key role as staple food items, eaten with every meal to fill the stomach. They are typically cheap and easy to prepare and gives a feeling a fullness without adding much nutritional value. Here the staples are pâte (“blanc“, “noir“, or “rouge” made with corn meal, yam skins or corn meal and tomato sauce), yam pilée (boiled and smashed yams), akassa (fermented pâte), or the remnants of colonialism: rice, spaghetti, or couscous. Of those carbohydrate staples, only couscous has any sort of real protein value, and although the unprocessed, natural staples do have some nutritional value, they are primarily used to simply fill the stomach and curb hunger. With the carb, a meal will usually include a palm oil based sauce made with tomatoes and onions, a vegetable sauce with okra, a sesame based sauce or a peanut sauce with a protein item if it is available: goat, chicken, guinea fowl, or wagasi (traditional cheese). Often times a meal is just a large pile of carbohydrates with a simple sauce when money is too tight for meat. This type of eating after a while leads to obesity and protein deficiencies in children and adults. For the most part, obese or overweight people in Benin do not follow an observable socioeconomic trend. The richer are often overweight just from overeating, the poor from a low quality diet. Mostly, though, obesity is not a nationwide health problem here, but a symptom of malnutrition in general.

Thinking about these things, I started wondering what was going on in the US. Right now in the United States, obesity has reached epidemic proportions. Over 65% of American adults and 16% of children are considered overweight or obese (having a Body Mass Index of 25 kg/m2 or higher) and it’s only getting worse with processed sugars, oils, and sugar sodas and beverages. It is estimated that by 2015, 41% of all Americans will be obese (BMI over 30 kg/m2). Clearly this is an important issue, and one that is much broader than the scope of my little blog post today, but it got me thinking about the medical science behind obesity, hunger, and satiety. So I pulled out my handy dandy pathophysiology textbook, The Pathologic Basis of Disease by Robbins and Cotran, and turned to Chapter 9: Environmental and Nutritional Diseases. I wanted to find out what makes some people fat and some people thin and how we can, as a nation and as individuals, work toward curbing the obesity epidemic and keep ourselves healthy.

First off I read about what exactly the problem with fat really is. We all know that obesity can lead to higher levels of cardiovascular disease, hypertension, and type 2 diabetes. Obesity has also been strongly correlated with rates of cancer in both men and women, as well as breathing problems and liver disease. All of these risks are increased if the fat is primarily stored in the middle of the body, around the midsection in the mesentery and around viscera in the abdominal cavity. I believe that modern medicine, and current scientific research clearly indicate that being overweight is a health risk. There are also many social pressures to be thin and the interplay between health and society with weight issues is an interesting one, but not what I want to talk about right now. Right now, I want to know what’s going on with the biochemical pathways that lead to obesity and why some people are fat and others thin.

At its most basic level, obesity is a “disease of caloric imbalance that results from an excess intake of calories above their consumption by the body” (439). A person is fat if they’ve consistently eaten more calories than they’ve burned off. It really is that simple. Of course, the pathogenesis of obesity is incredibly complex and not totally understood yet. Hunger, satiety, the urge to eat and to stop eating, metabolic pathways and mechanisms are all things that need ongoing research. It is clear that genetics, environmental signals, nutritional factors, and psychological signals all go into the triggering of the metabolic response and that it is a complex system based on many different interactions. However, obviously obesity would not occur without the intake of food.

The mechanisms that regulate energy balance can be separated into three parts: the peripheral or afferent system, the arcuate nucleus in the hypothalamus, and the efferent system. The afferent system generates signals from various site such as LEPTIN and ADIPONECTIN produced from fat cells, GHRELIN by the stomach, PEPTIDE YY (PYY) from the intestines, and INSULIN from the pancreas. The hypothalamus processes and integrates these signals and generates efferent signals. The efferent system carries the signals from the hypothalamus to control food intake and energy expenditure.

I want to talk about a few of the afferent components that regulate appetite and satiety: leptin, adiponectin, and gut hormones. Stick with me, this is cool stuff.

LEPTIN. The name leptin comes from the Greek word “leptos”, meaning “thin.” It is a hormone synthesized by fat calls and is a product of the ob gene. The leptin receptor is the product of the diabetes gene and belongs to the same family of receptors as IL-2 and other cytokine receptors. Mice deficient in either leptin (ob/ob mice) or leptin receptors (db/db mice) overeat and gain weight because they don’t sense their fat stores and behave as if they were starving (439). Leptin levels are regulated by multiple post-transcriptional mechanisms. In the hypothalamus, leptin causes the secretion of anorexigenic neuropeptides and inhibits neurons that cause feeding-inducing (orexigenic) neuropeptides. Basically leptin makes you feel full. In people with stable weight, these factors are all in balance. In someone with inadequate stores of body fat, however, leptin secretion is diminished and food intake increases.

Loss of function mutations in the leptin pathway in people are extremely rare. Some individuals (5% of massively obese people) could have problems with the receptors that sense the anorexigenic signals (the sense of feeling full) and would continue to overeat as if undernourished. These conditions are rare, but it’s been proposed that problems with the pathway could be associated with more common forms of obesity such as leptin resistance, rather than deficiency. Another way leptin works is to stimulate physical activity, heat production, and energy expenditure (440).

ADIPONECTIN. This hormone is produced by adipocytes and directs fatty acids to muscle for oxidation. It causes an increase in insulin sensitivity and has most receptors in skeletal muscle. Adiponectin has been called a “fat-burning molecule” and the “guardian angel against obesity” and when injected into mice, it causes a significant decrease in fat mass.

The total number of adipocytes is established during childhood and adolescence and cannot be changed in adulthood. Fat people have more fat calls than lean people. People can gain and lose weight by increasing or decreasing the size of existing adipocytes, but the number is predetermined. Trying to keep weight off is difficult because of a lack of a decrease in the number of adipocytes as well as an enhanced appetite caused by leptin deficiency.

GUT HORMONES. There are several hormones produced in the stomach, intestines, and pancreas. One of the most interesting is ghrelin. It is the only known gut hormone that increases food intake (orexigenic effect). If injected into mice, they eat voraciously, causing weight gain through increased caloric intake and reduced energy expenditure. Ghrelin levels rise before meals and fall 1 to 2 hours after eating. Interesting to note is that in obese and overweight people, the postprandial suppression of ghrelin is weakened which maintains the obesity through continued eating.

PYY is secreted from endocrine cells in the ileum and colon and levels of this hormone are low during fasting and increase after food intake. PYY levels increase after gastric bypass surgery and if injected, energy intake decreases. There is research going on now to use PYY as a treatment for obesity. Amylin, a peptide secreted from the pancreas with insulin that reduces food intake and weight gain, is also being evaluated as a drug for obesity. Both of these hormones act by triggering the hypothalamus to reduce food intake.

All of these factors work together to control hunger and satiety. Knowing what we know now, what can we do to prevent obesity and the risks that come with it? To a certain extent, how much lectin, how much adiponectin, and all those other hormones are predetermined by your diet as a child and genetics. You can keep your weight low, but if you have a lot of adipocytes and are naturally heavier, it’s going to be more difficult to regulate your weight. I’m pretty sure I fall into this category, and maintaining my weight in a healthy range is very important to me for both health and societal reasons.

Diabetes, cancer, hypertension, atherosclerosis, and cardiovascular disease all run in my family and there is indeed a correlation with high body fat content. Knowing how to eat and how much to eat is necessary for both my weight and credibility as a future physician. Eating a healthy diet of high fiber and low animal fat can help prevent colon cancer. Avoiding nitrosamines and nitrosamides from preservatives in meats can protect from gastric carcinomas, and just generally eating a healthy diet rich in veggies, whole grains, fruits, complex carbohydrates, healthy oils, and low in salt can help protect against cancers and heart disease.

Another thought is the idea of calorie restriction. It has been shown convincingly that caloric restriction decreases the incidence of many diseases and increases the lifespan in experimental animals. The particulars are not completely understood but it is thought to be related to lowering of insulin and IGF-1 levels and increased activation of sirtuins, proteins that promote metabolic activity and longevity (also associated with red wine, yay!). With a calorie restricted diet, animals live longer due to less oxidation and thus telomere breakdown and have a greater resistance to carcinogenesis and lower cholesterol levels. Most obviously, a restricted diet leads to weight loss and thus protection against many risk factors associated with obesity.

After doing all this research, I’ve decided that one of the best ways to stay healthy is to maintain a weight between BMI 18 kg/m2 and 24 kg/m2. I know BMI is not a perfect measurement, but for now, it’s the best we’ve got. Of course you can still be unhealthy within that range, and of course there are some people who can maintain health outside of that range, but in general, it’s a good indication of an appropriate weight to decrease risk factors associated with obesity and being overweight. In addition to maintaining a healthy weight, a low calorie diet with healthy foods seems to be a good option. Lots of fiber, healthy proteins, complex carbohydrates (limited pâte or yam pilée!), and lots of fruits and vegetables is a good solution. And as always, exercise. Several times a week for at least half an hour, up to 60 minutes when possible, your heart rate should be significantly elevated. This is such a simple thing that so many Americans, both obese and normal range weight, just don’t do enough. Exercise increases endorphins, makes you feel good, keeps your weight low and your figure slim, keeps your heart healthy, and helps stimulates the metabolic pathways. It’s win-win. Eat less, eat healthier, exercise more, and maintain a healthy weight range. Check.

Addressing the national problem is a question that countless physicians are working on. I think public service announcements, frank conversations with primary care doctors and pediatricians, and nutritional guidelines and information are all good starts. The obesity epidemic is complex, so close to issues of race and socioeconomic status, connected to ideals of beauty and worth, value in society and mental health. It’s going to take a lot of effort to really effectively stem the trends and there are a lot of political aspects to the changes that should be proposed. One thing we can all do for posterity is to help make sure our kids have healthy options and to really think about childhood obesity as a major sociological problem. Issues like sugar soda in schools, healthy lunches, sedentary lifestyle changes, and videogames all go into it. We know now that the number of fat cells is determined in childhood and adolescence, and we also know from personal experience and anecdotal evidence that it’s hard to lose weight as an adult if you were fat as a kid. So let’s keep our children within healthy weight ranges by making sure their diets are rich with nutrients and they’re staying active. That way when they grow up they’ll have an easier time staying healthy and avoiding all those risks associated with being overweight or obese.

Like America, Benin has a lot of work to do in curbing both obesity and malnutrition in general. With more and more outside influences like sugar soda, candy, and other processed sugars and starches, developing countries are becoming increasingly at risk for obesity. As a health worker here, I am often talking to people about diet, especially about the importance of eating vegetables and lean protein. Fish is popular here and cheaper than red meat which helps make my job a little easier. It’s tough, though. A lot of the reasoning behind the unhealthy diets here is money, just like it is in the US. I think it’s easy to forget that sometimes, especially when thinking about the United States. But it’s true. To facilitate behavior change, we have to address the problem in a local, community based way. I’m learning that every day here and I know that understanding will be crucial to me as a physician later. It might not be easy, but change starts now. It starts with us. I know I don’t always eat as healthy as I should, especially when I’m in America (Taco Bell anyone?), but I think I’m beginning to see the importance of diet in long term health a little more clearly now that I have all this free time to think about food.

This has been a nerd alert, shared from me to you. So go out there, and use your nerdiness to do some good in the world!

Thanks for listening 🙂

-E

PS. My app has been verified! Yay! Now I just have to wait for secondaries!

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