Diet, Weight and Health Round Up

Nikhil Swaminathan, The Skinny of Fat: You’re Not Always What You Eat
Serotonin and the regulation of energy metabolism. See Laura’s nice psychology take here.

Science Daily, Psychological Stress Linked to Overeating, Monkey Study Shows
Stressed out monkeys like calorie-rich foods

Science Daily, Hunger Hormone Increases During Stress, May Have Antidepressant Effect
Ghrelin, being hungry, and not getting anxious about what you’ve got to do (at least in mice)

Jonah Lehrer, Caloric Rewards (Or Why Diet Soda Isn’t Good for Diets)
Sweet soda without calories confuses energy tracking; but real sugar can also make dopamine spike

Dr. X, Sugar and ADHD
Is sugar getting a bad wrap for getting kids wired? Plus the power of belief

Continue reading “Diet, Weight and Health Round Up”

Live healthy, turn on your genes

For all those out there who still think that ‘it’s all in the genes,’ here’s a recent news story on the way that changes in lifestyle can affect genetic activity. Will Dunham at ABC News brings us, Healthy Lifestyle Triggers Genetic Changes: Study (I also pulled it off the Reuters feed). The study was small, and I doubt that it was nearly as rigorous as really necessary, but the findings are interesting.

In a small study, the researchers tracked 30 men with low-risk prostate cancer who decided against conventional medical treatment such as surgery and radiation or hormone therapy.

The men underwent three months of major lifestyle changes, including eating a diet rich in fruits, vegetables, whole grains, legumes and soy products, moderate exercise such as walking for half an hour a day, and an hour of daily stress management methods such as meditation.

As expected, they lost weight, lowered their blood pressure and saw other health improvements. But the researchers found more profound changes when they compared prostate biopsies taken before and after the lifestyle changes.

After the three months, the men had changes in activity in about 500 genes — including 48 that were turned on and 453 genes that were turned off.

Continue reading “Live healthy, turn on your genes”

Comfort Food and Social Stress

Comfort Food, for Monkeys is John Tierney’s article today, reporting on recent research by Mark Wilson and colleagues at Yerkes Primate Center about rhesus monkeys, sweet tooths, social stress and inequality. Familiar themes, all of them.

Normally, low-status monkeys eat roughly the same amount of bland monkey chow as dominant individuals. But add sweet banana-flavored pellets to the mix, and suddenly the equation changed: “While the dominant monkeys dabbled in the sweet, fatty pellets just during the daytime, the subordinate monkeys kept scarfing them down after dark.”

Tierney goes on to outline reasons why this scarfing vs. dabbling dynamic might emerge in socially complex species like rhesus monkeys. As Wilson et al. note in their paper, “this ethologically relevant model may help understand how psychosocial stress changes food preferences and consumption leading to obesity.”

Tierney describes research by Dallman et al., who have proposed that people can directly impact stress hormones through eating, largely by mediating anxiety: “[P]eople eat comfort food in an attempt to reduce the activity in the chronic stress-response network with its attendant anxiety.” So individuals with greater stress reactivity and negative mood tend to eat more in their stressed vs. control experimental paradigm.

As Tierney notes with a quip about a “stressed-out wage slave who has polished off a quart of Häagen-Dazs at midnight while contemplating the day’s humiliations,” inequality can bring on stress reactivity and negative mood (for more on that, see previous stress and inequality posts on Sapolsky and Blakey). In turn, inequality feeds into the obesity epidemic through both social and cultural dynamics.

But Tierney also knows that seeking food, not simply reactive eating, is key to overall weight gain. Continue reading “Comfort Food and Social Stress”

Fat Cells Die?

Gina Kolata, whose book Rethinking Thin prompted a series of posts on obesity earlier, had a recent article, Study Finds That Fat Cells Die and Are Replaced. Every year ten percent of your fat cells die; every year they are replaced. This research reinforces the emerging conclusion that “losing or gaining weight affects only the amount of fat stored in the cells, not the number of cells.” It also leads to more questions:

“What determines how many fat cells are in a person’s body? When is that number determined? Is there a way to intervene so people end up with fewer fat cells when they reach adulthood? And could obesity be treated by making fat cells die faster than they are born?”

As the lead researcher Kirsty Spalding puts it, “The million-dollar question now is, What regulates this process? And where can we intervene?”

Not all scientists are so sanguine. Lester Salans, an old-timer in this area, answers, “I suspect that the body’s regulation of weight is so complex that if you intervene at this site, something else is going to happen to neutralize this intervention.”

And the real interventions, the ones that happen everyday? High-calorie processed foods; fast food restaurants on street corners; an increasingly sedentary lifestyle? Well, there’s a reason I stuck that image of David up.

Dopamine and Eating

In an earlier post The Sugar Made Me Do It, I covered recent research by de Araujo, Oliveira-Maia et al. on how food, specifically sucrose, can reinforce eating by activating mid-brain dopamine circuitry, even in the absence of taste. In the accompanying editorial essay by Andrews and Horvath, this great graphic appeared, representing what is known about how eating can act on the hypothalamus and on the mesolimbic dopamine system (ventral tegmental area, nucleus accumbens, and prefrontal cortex).

Here is a much more convincing link to how eating can become appetite-driven, which previous posts on Genetics and Obesity and On the Causes of Obesity had raised as an important issue in the obesity problem.

Just one more note on the graphic: in terms of how taste can affect dopamine function, see some thoughts in the post on the neuropeptide orexin.

Figure 1. Schematic Illustration Depicting Some of the Major Findings of de Araujo and Oliveira-Maia et al

Taste alone (noncaloric sweetener), taste with caloric value (sucrose solution), or caloric value only (in the absence of taste receptors) can all equally activate the midbrain reward circuitry. To date, major emphasis has been placed on the hypothalamus and its various circuits, including orexin (ORX/Hcrt)- and melanin concentrating hormone (MCH)-producing neurons in the lateral hypothalamus as well as neuropeptide Y (NPY)/agouti-related protein (AgRP)- and -melanocyte-stimulating hormone (-MSH)-producing neurons in the arcuate nucleus, as a homeostatic center for feeding, responding to various peripheral metabolic hormones and fuels. The mesencephalic dopamine system is also targeted by peripheral hormones that affect and alter behavioral (and potentially endocrine) components of energy homeostasis. The results by de Araujo and Oliveira-Maia et al. highlight, however, that without classical hedonic signaling associated with reward-seeking behavior, the midbrain dopamine system can be entrained by caloric value arising from the periphery. While the precise signaling modality that mediates caloric value on dopamine neuronal activity remains to be deciphered, overall it is reasonable to suggest that distinction between hedonic and homeostatic regulation of feeding is redundant. DA, dopamine; GABA, γ-aminobutyric acid; Glut, glutamate.

Red meat, Neandertals were meant to eat it

The Meat and Livestock Association (MLA) of Australia has these great television commercials featuring actor Sam Neill (and by ‘great,’ I don’t mean ‘scientifically accurate’). They’re all about how we humans were ‘meant’ to eat red meat. They’re obviously meant to counteract growing concern about red meat in our diet, in the environmental impact of livestock, and other issues, and they use evolutionary arguments to try to get Australians to ‘beef up’ the amount of red meat in their diet, because of course, Australians don’t eat enough meat (trust me if you’re not in Australia — that’s probably not the biggest health issue here, ‘lack’ of red meat in the Aussie diet). For more information on the campaign, check out the MLA’s webpage, ‘Red Meat. We were meant to eat it.’ (You can download the video of the ads from that site if, like me, you want to incorporate it into your lecture on human evolution and diet.)

Especially interesting is the third ad in the campaign, ‘Evolution.’ The text of that ad is:

‘Evolution’ set the scene for the story of red meat and its role in human evolution. It also highlights the bundle of nutrients in red meat making it a foundation food essential for brain development and function. Red meat. We were meant to eat it.

But an article by M. P. Richards and colleagues soon to appear in the Journal of Human Evolution suggests that the evolutionary prize for red meat-eating should have gone, not to Homo sapiens sapiens but to Homo sapiens neanderthalensis (or H. neanderthalensis). Richards and the research team examined carbon and nitrogen ratios in Neandertal bone collagen to figure out what the Neandertals were eating.

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