Showing posts with label hyperphagia. Show all posts
Showing posts with label hyperphagia. Show all posts

Tuesday, 7 May 2013

Princess Health and The Neurobiology of the Obesity Epidemic. Princessiccia

Princess Health and The Neurobiology of the Obesity Epidemic. Princessiccia

I recently read an interesting review paper by Dr. Edmund T. Rolls titled "Taste, olfactory and food texture reward processing in the brain and the control of appetite" that I'll discuss in this post (1). Dr. Rolls is a prolific neuroscience researcher at Oxford who focuses on "the brain mechanisms of perception, memory, emotion and feeding, and thus of perceptual, memory, emotional and appetite disorders." His website is here.

The first half of the paper is technical and discusses some of Dr. Rolls' findings on how specific brain areas process sensory and reward information, and how individual neurons can integrate multiple sensory signals during this process. I recommend reading it if you have the background and interest, but I'm not going to cover it here. The second half of the paper is an attempt to explain the obesity epidemic based on what he knows about the brain and other aspects of human biology.

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Sunday, 28 April 2013

Princess Health and Food Variety, Calorie Intake, and Weight Gain. Princessiccia

Princess Health and Food Variety, Calorie Intake, and Weight Gain. Princessiccia

Let's kick off this post with a quote from a 2001 review paper (1):
Increased variety in the food supply may contribute to the development and maintenance of obesity. Thirty-nine studies examining dietary variety, energy intake, and body composition are reviewed. Animal and human studies show that food consumption increases when there is more variety in a meal or diet and that greater dietary variety is associated with increased body weight and fat.
This may seem counterintuitive, since variety in the diet is generally seen as a good thing. In some ways, it is a good thing, however in this post we'll see that it can have a downside.
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Sunday, 24 March 2013

Princess Health and Neuronal Control of Appetite, Metabolism and Weight. Princessiccia

Princess Health and Neuronal Control of Appetite, Metabolism and Weight. Princessiccia

Last week, I attended a Keystone conference, "Neuronal Control of Appetite, Metabolism and Weight", in Banff. Keystone conferences are small, focused meetings that tend to attract high quality science. This particular conference centered around my own professional research interests, and it was incredibly informative. This post is a summary of some of the most salient points.

Rapid Pace of Scientific Progress

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Sunday, 10 August 2008

 Princess Health and Rats on Junk Food.Princessiccia

Princess Health and Rats on Junk Food.Princessiccia

If diet composition causes hyperphagia, we should be able to see it in animals. I just came across a great study from the lab of Dr. Neil Stickland that explored this in rats. They took two groups of pregnant rats and fed them two different diets ad libitum, meaning the rats could eat as much as they wanted. Here's what the diets looked like:
The animals were fed two types of diet throughout the study. They were fed either RM3 rodent chow alone ad libitum (SDS Ltd, Betchworth, Surrey, UK) or with a junk food diet, also known as cafeteria diet, which consisted of eight different types of palatable foods, purchased from a British supermarket. The palatable food included biscuits, marshmallows, cheese, jam doughnuts, chocolate chip muffins, butter flapjacks, potato crisps and caramel/chocolate bars.
It's important to note that the junk food-fed rats had access to rat chow as well. Now here's where it gets interesting. Rats with access to junk food in addition to rat chow ate 56% more calories than the chow-only group! Here's what they had to say about it:
These results clearly show that pregnant rats, given ad libitum access to junk food, exhibited hyperphagia characterised by a marked preference for foods rich in fat, sucrose and salt at the expense of protein-rich foods, when compared with rats that only had access to rodent chow. Although the body mass of dams was comparable among all groups at the start of the experiment, the increased energy intake in the junk food group throughout gestation was accompanied by an increase in body mass at G20 [gestational day 20] with the junk food-fed dams being 13 % heavier than those fed chow alone.
Hmm, this is remarkably reminiscent of what's happening to a certain group of humans in North America right now: give them access to food made mostly of refined grains, sugar, and industrially processed vegetable oil. They will prefer it to healthier food, to the point of overeating. The junk food then drives hyperphagia by interfering with the body's feedback loops that normally keep feeding behaviors and body fat within the optimal range. These data support the hypothesis that metabolic damage is the cause of, not the result of, "super-sized" food portions and other similar cultural phenomena.

The rest of the paper is interesting as well. Pups born to mothers who ate junk food while pregnant and lactating had a greater tendency to eat junk than pups born to mothers who ate rat chow during the same period. This underscores the idea that poor nutrition can set a child up for a lifetime of problems.

Saturday, 9 August 2008

 Princess Health and Hyperphagia.Princessiccia

Princess Health and Hyperphagia.Princessiccia

One of the things I didn't mention in the last post is that Americans are eating more calories than ever before. According to Centers for Disease Control NHANES data, in 2000, men ate about 160 more calories per day, and women ate about 340 more than in 1971. That's a change of 7% and 22%, respectively. The extra calories come almost exclusively from refined grains, with the largest single contribution coming from white wheat flour (correction: the largest single contribution comes from corn sweeteners, followed by white wheat flour).

Some people will see those data and decide the increase in calories is the explanation for the expanding American waistline. I don't think that's incorrect, but I do think it misses the point. The relevant question is "why are we eating more calories now than we were in 1971?"

We weren't exactly starving in 1971. And average energy expenditure, if anything, has actually increased. So why are we eating more? I believe that our increased food intake, or hyperphagia, is the result of metabolic disturbances, rather than the cause of them.

Humans, like all animals, have a sophisticated system of hormones and brain regions whose function is to maintain a proper energy balance. Part of the system's job is to keep fat mass at an appropriate level. With a properly functioning system, feedback loops inhibit hunger once fat mass has reached a certain level, and also increase resting metabolic rate to burn excess calories. If the system is working properly, it's very difficult to gain weight. There have been a number of overfeeding studies in which subjects have consumed huge amounts of excess calories. Some people gain weight, many don't.

The fact that fat mass is hormonally regulated can be easily seen in other mammals. When was the last time you saw a fat squirrel in the springtime? When was the last time you saw a thin squirrel in the fall? These events are regulated by hormones. A squirrel in captivity will put on weight in the fall, even if its daily food intake is not changed.

A key hormone in this process is leptin. Leptin levels are proportional to fat mass, and serve to inhibit hunger and eating behaviors. Under normal conditions, the more fat tissue a person has, the more leptin they will produce, and the less they will eat until the fat mass has reached the body's preferred 'set-point'. The problem is that overweight Westerners are almost invariably leptin-resistant, meaning their body doesn't respond to the signal to stop eating!

Leptin resistance leads to hyperphagia, overweight and the metabolic syndrome (a common cluster of symptoms that implies profound metabolic disturbance). It typically precedes insulin resistance during the downward slide towards metabolic syndrome.

I suspect that wheat, sugar and perhaps other processed foods cause hyperphagia. I believe hyperphagia is at least partially secondary to a disturbed metabolism. There's something about industrial foods that reached a critical mass in the mid-70s. The shift in diet sent us into a tailspin of excessive eating and unprecedented weight gain.

Wednesday, 9 July 2008

 Princess Health and Another China Tidbit.Princessiccia

Princess Health and Another China Tidbit.Princessiccia

A final note about the Chinese study in the previous post: the overweight vegetable-eaters (read: wheat eaters) exercised more than their non-vegetable-eating, thin neighbors. So although their average calorie intake was a bit higher, their expenditure was as well. 

Although I speculated in the last post that affluent people might be eating more wheat and fresh vegetables, the data don't support that. Participants with the highest income level actually adhered to the wheat and vegetable-rich pattern the least, while low-income participants were most likely to eat this way.

Interestingly, education showed a (weaker) trend in the opposite direction. More educated participants were more likely to eat the wheat-vegetable pattern, while the opposite was true of less educated participants. Thus, it looks like wheat makes people more educated. Just kidding, that's exactly the logic we have to avoid when interpreting this type of study!

Tuesday, 8 July 2008

 Princess Health and Wheat in China.Princessiccia

Princess Health and Wheat in China.Princessiccia

Dr. Michael Eades linked to an interesting study yesterday on his Health and Nutrition blog. It's entitled "Vegetable-Rich Food Pattern is Related to Obesity in China."

It's one of these epidemiological studies where they try to divide subjects into different categories of eating patterns and see how health problems associate with each one. They identified four patterns: the 'macho' diet high in meat and alcohol; the 'traditional' diet high in rice and vegetables; the 'sweet tooth' pattern high in cake, dairy and various drinks; and the 'vegetable rich' diet high in wheat, vegetables, fruit and tofu. The only pattern that associated with obesity was the vegetable-rich diet. The 25% of people eating closest to the vegetable-rich pattern were more than twice as likely to be obese as the 25% adhering the least.

The authors of the paper try to blame the increased obesity on a higher intake of vegetable oil from stir-frying the vegetables, but that explanation is misleading. A cursory glance at table 3 reveals that the vegetable-eaters weren't eating any more fat than their thinner neighbors. Dr. Eades suggests that their higher carbohydrate intake (+10%) was partially responsible for the weight gain, but I wasn't satisfied with that explanation so I took a closer look.  Dr. Eades also pointed to their higher calorie intake (+120 kcal/day), which makes sense to me.

One of the most striking elements of the 'vegetable-rich' food pattern is its replacement of rice with wheat flour. The 25% of the study population that adhered the least to the vegetable-rich food pattern ate 7.3 times more rice than wheat, whereas the 25% sticking most closely to the vegetable-rich pattern ate 1.2 times more wheat than rice! In other words, wheat flour rather than rice was their single largest source of calories. This association was much stronger than the increase in vegetable consumption itself!

All of a sudden, the data make more sense. Wheat seems to associate with health problems in many contexts. Perhaps the reason we don't see the same type of association in American epidemiological studies is that everyone eats wheat. Only in a culture that has a true diversity of diet can you find a robust association like this. The replacement of rice with wheat may have caused the increase in calorie intake as well. Clinical trials of low-carbohydrate diets as well as 'paleolithic diets' have shown good metabolic outcomes from wheat avoidance, although one can't be sure what role wheat plays from those data.

I don't think the vegetables had anything to do with the weight gain, they were just incidentally associated with wheat consumption. But I do think these data are difficult to reconcile with the idea that vegetables protect against overweight.