I’m always on the lookout for new ways to improve my health, whether it be through diet, exercise or — the all-too-often neglected third member of the U.S. Army’s Performance Triad — sleep. And while some health trends border the edge of insanity (Tapeworms, anyone?), others have a fair share of scientific literature backing up their claims.
One such trend that has slowly but surely began to establish its niche in pop culture is intermittent fasting (IF). If it sounds familiar, you may have seen this video circulating on your Facebook newsfeed. While there are a handful of IF variations that exist (and you can read all about those here), they are all usually adapted to serve one common purpose — to encourage weight-loss by moderately decreasing our calorie intake by 500-1000 calories per day.
Sounds crazy, right?
Well, maybe not.
The National Institute of Health (that’s the largest biomedical research institution in the world!) concluded that low-calorie diets can lower total body weight by an average of 8% in the short term (3-12 months), and that these low-calorie diets maintain significant weight loss over a 5-year period (1) (and that’s important, because “yo-yo dieting”, or the failure to maintain weight-loss, correlates with increased body fat (2)).
But the effects of caloric restriction, at least in mice, seem to extend far beyond weight loss to include more subtle health-promoting advantages. First suggested 82 years ago by C.M. McCay (3), a research team headed by J.D. Han recently found that mice following a low-calorie diet (defined as 30% less calories than usual) were healthier and lived 20-25% longer than mice following a “normal”-calorie diet. Not only that, but these mice exhibited the lowest and most stable body weight and fat content, as well as the best metabolism (4).
Despite these exciting findings, researchers couldn't figure out why low-calorie diets increased overall health — until 2013, when Liping Zhao and his research group studied the gut bacteria in mice that followed a low-calorie diet their entire lives. Zhao and his colleagues demonstrated that calorie restriction selected for certain gut bacteria, such as Lactobacillus, whose presence in our gut correlates with longer lifespan, while also reducing the amount of gut bacteria that are associated with decreased lifespan (5). In other words, it seems that reducing our daily calorie intake promotes the growth of “good” bacteria that prevent aging, while at the same time inhibiting the growth of “bad” bacteria that makes us age quicker.
But how can gut bacteria influence our lifespan? While the answer to this question isn’t obvious, we still have a pretty good idea of what is likely happening, and it involves the process of inflammation. We’ve all seen inflammation in action — when you get a paper cut, you’ll notice your skin becoming red, warm and painful. This is the result of immune cells (and blood) rushing to the site of the cut to kill the bacteria that are trying to enter your body. This kind of inflammation doesn’t last long (a few hours to a few days), and the bacteria are promptly killed (that’s a good thing!).
Here’s the problem: something different — and more destructive — can happen inside our bodies. Our gut is littered with bacteria, and while most of them aren’t recognized by our immune system, some of them are, and this kind of inflammation can last an abnormally long time. That’s dangerous: long-term (or “chronic”) inflammation is known to speed-up the deterioration of the cardiovascular system (6), as well as increase the incidence of stroke and cognitive loss at younger ages (7). In other words, chronic inflammation shortens our lifespan.
And guess what — meals high in calories have been associated with increases in chronic, lifespan-crippling inflammation (8).
That’s why eating less calories seems to increase lifespan in mice. Zhao found that a low-calorie diet encouraged the growth of anti-inflammatory gut bacteria while simultaneously inhibiting the growth of pro-inflammatory bacteria (5). That means that by eating less (~500 fewer calories per day), we can potentially decrease chronic inflammation, thereby living longer, healthier lives.
1. Strychar, I. 2006. Diet in the management of weight loss. CMAJ 174: 56-63.
2. Mackie, G. M., D. Samocha-Bonet, and C. S. Tam. 2017. Does weight cycling promote obesity and metabolic risk factors? Obes. Res. Clin. Pract. 11: 131-139.
3. McCay, C. M., M. F. Crowell, and L. A. Maynard. 1989. The effect of retarded growth upon the length of life span and upon the ultimate body size. 1935. Nutrition 5: 155-171; discussion 172.
4. Zhou, B., L. Yang, S. Li, J. Huang, H. Chen, L. Hou, J. Wang, C. D. Green, Z. Yan, X. Huang, M. Kaeberlein, L. Zhu, H. Xiao, Y. Liu, and J. D. Han. 2012. Midlife gene expressions identify modulators of aging through dietary interventions. Proc. Natl. Acad. Sci. U. S. A. 109: E1201-1209.
5. Zhang, C., S. Li, L. Yang, P. Huang, W. Li, S. Wang, G. Zhao, M. Zhang, X. Pang, Z. Yan, Y. Liu, and L. Zhao. 2013. Structural modulation of gut microbiota in life-long calorie-restricted mice. Nature communications 4: 2163.
6. Danesh, J., P. Whincup, M. Walker, L. Lennon, A. Thomson, P. Appleby, J. R. Gallimore, and M. B. Pepys. 2000. Low grade inflammation and coronary heart disease: prospective study and updated meta-analyses. BMJ 321: 199-204.
7. Wilson, C. J., C. E. Finch, and H. J. Cohen. 2002. Cytokines and cognition--the case for a head-to-toe inflammatory paradigm. J. Am. Geriatr. Soc. 50: 2041-2056.
8. Blackburn, P., M. Cote, B. Lamarche, C. Couillard, A. Pascot, A. Tremblay, J. Bergeron, I. Lemieux, and J. P. Despres. 2003. Impact of postprandial variation in triglyceridemia on low-density lipoprotein particle size. Metabolism 52: 1379-1386.