A Sense of Loss

Trying to understand the slippery slope behind weight gain.

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A few weeks into the new year and I, like so many Americans, have already neglected my predictable resolution to eat more healthfully. This year I kept it pretty simple, endeavoring to eat more super foods like berries, nuts, and oatmeal, and fewer butter cookies and blueberry muffins. While I have eaten more of the healthy super foods, I admit I’ve also eaten more desserts, too (there were just so many left over from the holidays).

I’m left wondering how I could I have failed so quickly. Is it just laziness and bad habits that make achieving the task feel so extraordinary?

Perhaps it’s not simply laziness or habit, at least. While willpower and discipline certainly play an important role in how we eat, I have come across a growing body of research hinting at biological underpinnings that may also, silently but surely, compel food cravings.

One recent study showed how the much-feared “empty calories” in sugar might be less dangerous than the way that too much sugar sets off a kind of chain reaction that unhinges appetite and drives weight gain. Researchers at the University of Florida College of Medicine showed just how this happens by comparing two groups of rats that were identical (in terms of body weight, body fat, and blood levels of leptin, glucose, cholesterol, and insulin) and fed the same diet except for one key difference: one group was given lots of sugar (specifically fructose) while the other group received none.

After six months, the two groups still looked very much the same — there was no significant difference in weight gain. The sugar group did, however, have higher levels of triglycerides, a significant finding since elevated triglyceride levels are known to impair leptin from reaching the brain, and leptin is known to be a crucial hormone for balancing the body’s food intake with energy expenditure. If leptin doesn’t reach the brain, the brain never knows to send out a “stop eating” signal.

The researchers illustrated this occurrence by administering leptin to all the animals. They documented that the rats in the no-sugar group ate less than they had (a normal response), while the rats in the sugar group did not (an abnormal response). The impact of leptin resistance was even clearer later, when the researchers offered all of the rats a high-fat, high-calorie diet. The leptin-resistant animals, the ones initially exposed to the high-sugar diet, could not stop eating. Over time they gained significantly more weight and fat than the others.

It’s not a far leap to guess that too much sugar has the same impact in humans, although research on this has not yet been done. Whether reducing or removing fructose and other sugars from the diet can reverse leptin resistance is also unclear — the researchers are planning future studies to investigate. For sugar overloaders everwhere, let’s hope so.

Meanwhile, it’s not just sugar that messes with our biology. Other recent research has shown that too much fat is also a bad influence on appetite. Again, the problem occurs rather insidiously, by quietly unbalancing the body’s natural circadian rhythm — the biological clock that plays an important role in many of the body’s physiologic and behavioral functions, including metabolism.

Circadian rhythms are primary affected by sleep, and a lack of it is known to drive down levels of leptin while driving up levels of ghrelin, a hormone that stimulates appetite. Researchers at Hebrew University of Jerusalem found that eating too much fat can also unbalance the clock, with similar effects. They fed mice either a low- or high-fat diet, and then measured the effects on adiponectin — a hormone that is involved in maintaining proper glucose and lipid metabolism and that the researchers determined was controlled by the biological clock.

In the mice fed a low-fat diet, the adiponectin signaling pathway had normal circadian rhythmicity. The mice on the high-fat diet, however, experienced a disruption in their circadian clock that impaired their ability to metabolize fat. Related research from Northwestern University found that a high-fat diet disrupted the normal sleep-wake cycle in mice, leading to eating at inappropriate times, impaired metabolic function, and weight gain.

Again, as with the sugar findings, the implications of these findings on humans are far from conclusive. But they do hint that a fatty diet could contribute to obesity not just by calories but also by impairing the body’s normal metabolism. Perhaps calories and weight gain are not be as tightly linked as once believed. Certainly, at least, appetite is one tricky customer.

Until more is learned, the takeaway from both studies during the economic downturn might be this: At the very least, don’t give into the tug of the so-called “recession diet.” This is the diet in which people save money by cutting back on healthy fresh foods and instead eat cheaper, less healthy pre-packaged and processed foods, which tend to be high in saturated fats, refined sugars, and salt. Based on the scientific research at hand, this kind of diet could leave us carrying around the effects for longer than the recession lasts. In other words, at all costs, avoid that fast-food dollar menu. • 22 January 2009

SOURCES: Shapiro A, Mu W, Roncal C, Cheng KY, Johnson RJ, Scarpace PJ. “Fructose-induced leptin resistance exacerbates weight gain in response to subsequent high-fat feeding.” Am J Physiol Regul Integr Comp Physiol. 2008 Nov;295(5):R1370-5. Barnea M, Madar Z, Froy O. “High-Fat Diet Delays and Fasting Advances the Circadian Expression of Adiponectin Signaling Components in Mouse Liver.” Endocrinology. 2009 Jan;150(1):161-8. Kohsaka A, Laposky AD, Ramsey KM, et al. “High-fat diet disrupts behavioral and molecular circadian rhythms in mice.” Cell Metab. 2007;6:414-21.

 

Jennifer Fisher Wilson is the science reporter for Annals of Internal Medicine. Her stories are available at www.annals.org.

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