We have, it seems, moved on from acknowledging it takes a village to raise a human being. We are well into the realm of realization that it takes a village just to be one. More and more studies are demonstrating the importance of the germs that outnumber our cells by an order of magnitude at least, to virtually every aspect of physiology. But while epiphanies of this sort are redolent with promise, they can be dizzying as well, and pose a threat of disequilibrium and distraction. If we can miss the forest for the trees, there is, I think, a comparable risk of missing the importance of lifestyle for the Lactobacilli. My motivation here is the hope that we will not.
While I can no longer readily recall what life was like before email, I certainly do recall medical practice before the widespread popularity of probiotics. Only very recently did the use of ingestible bacteria transition from the realm of far-fetched to all-but-standard, and from “you must be kidding!” to “where to do I get mine?” Not all that long ago, the only good germ was a dead germ.
Progress since the initial uptake of the probiotic concept has been astounding. The now well-established potential to prevent and treat C. difficile colitis, a dire complication of antibiotic therapy, with probiotics is a considerable advance all by itself.
The more we’ve learned about the importance of our resident microbes, the more we’ve learned about the need and opportunity to learn more. The process may be likened to climbing a hill, and then gaining a view of the higher hills and mountains beyond. There is a lot of climbing left to do.
One peak now within view involves the important relationships among our immune system, cohabiting bacteria, and other organisms. In An Epidemic of Absence, Moises Velaszquez-Manoff makes a thorough and compelling case for the unintended consequences of sanitizing our environments and the eradication of parasites. How best to apply such lessons to the management of allergy and autoimmune disease is a work in progress, but that it’s vitally important work now seems abundantly clear.
The other peak before us is the one that worries me a bit. It beckons with tantalizing new findings related to weight control.
We have known for quite some time that commensal microbes play a vital role in digestion. In fact, we surmised this about bacteria living in our guts before we knew much else about them; after all, what else would they be doing there? More recently, we have come to learn that bacterial colony counts influence our energy efficiency and the number of calories we can extract from food. Differences in the microbiome can make it harder or easier to lose weight, and may account for more flagrant cases of weight loss resistance. In some instances, when all else fails, the wholesale transplantation of gut microbes may allow for weight control.
This provocative tale is further embellished by a cluster of recent papers in preeminent scientific journals. An article published in Nature Reviews in early August explores the causal pathway from intestinal microbes to obesity risk. A study published in late August in Nature compared the microbiota in 123 lean and 169 obese Danish adults. The authors report greater genetic variety among gut microbes in lean individuals than obese. A brief report of an intervention in the same issue of the journal reported an increase in the genetic richness of gut microbes when obese and overweight individuals were put on a weight-reducing diet. And even more of Nature’s rarefied real estate has been allocated to this topic to accommodate commentaries and editorials.
And a report in Science indicated that the gut microbes from obese adult twins could make germ-free mice get fat, while the gut microbes from their lean siblings had the opposite effect.
Why does this all worry me?
I fully acknowledge the almost certain importance of our microbial diversity to energy balance and weight regulation. I accept that indelible links are being forged among genes, germs, and resultant girth.
But we are all too easily distracted from the accessible means of both losing weight and finding health, by new and exotic theories. Excessive preoccupation with the microbiome could lead us into our next great boondoggle.
Consider that behaviors we control directly, as opposed to microbial colonies we may not, explain 80 percent of the variation in the risk for all major chronic diseases. Consider that overwhelmingly, when people eat well and exercise, they lose weight — and if the behaviors persist, so does the weight loss. Consider that obesity was rather uncommon a half century ago in the days before drive-through fast-food restaurants, a vast proliferation of junk foods, and a comparable proliferation of labor-saving technologies.
In other words, while scrutiny of our microbes may help account for enigmatic cases of weight gain, they are, for most of us, the trees that may cause us to overlook the forest. The fixable causes of obesity and chronic disease are on prominent display, all around us. Most of us will gain weight when we take in too many calories, even if from wholesome sources. Most of us will lose weight if we restrict calories enough, even if those calories come from Twinkies. Energy balance does not seem to require a bacterial referendum.
For the most part, people who exercise diligently and eat very well are both leaner and healthier than others who don’t. What a remarkable coincidence it would be if those who best attended to calories in and calories out just happened to be those with the genes and germs conducive to trim guts.
This does not mean the germs and genes in our guts are not germane to weight and health; they clearly are. But the available evidence suggests they are at least as much effects as causes.
In other words, the same adverse exposures that tend to make us sick and fat appear to do much the same to our resident bugs. It doesn’t much change the relevance of junky diets and physical inactivity to poor health and weight gain to note that along with all of the other adverse effects of such behaviors, they disrupt and distort the microbiome. All this really means as that we, and our germs, are in this together — we flourish, or founder, together.
For a quick analogy, imagine if we had just discovered atherosclerosis and reached the conclusion that it is the “real” cause of heart disease. That would be true, but it would be a serious mistake to toss out what we knew about tobacco, physical activity, and diet as a result. Those factors influence atherosclerosis, which in turn influences the likelihood of heart attack. Similarly, shifts in our bacterial colonies may be part of the pathway by which behaviors translate into changes in both weight, and health. This is in no way an invitation to jettison anything we already knew about the importance of those behaviors.
There may well be some opportunities to address the microbiome directly, from probiotics to fecal transplant. There are, analogously, ways to address atherosclerotic plaque directly with angioplasty and coronary bypass surgery. But just as lifestyle can keep arteries healthy in the first place, or even restore them to health, so too, it seems, can the very same lifestyle practices that protect our health do the same for our inner menagerie.
Over the years, we have heard about many “obesity genes.” But these genes were around long before obesity was a salient public health concern. Genes that haven’t changed recently can’t really account for recent changes in epidemiology. Similarly, while our understanding of our intimate codependence on gut microbes is fairly recent, the codependence is not. The bugs were there all along. If they have suddenly become complicit in epidemic obesity, it might be tempting to pass the buck to the bugs, but it begs the question: What changed them?
This, in turn, offers the silver lining of insight within the dark clouds of potential diversion. One of the prevailing mistakes about obesity is to pin it all on personal responsibility. There is, clearly, a case for personal responsibility; but the choices we make are in turn governed by the choices we have. It never made sense to presume that the current generation of 7-year-olds was less endowed with personal responsibility than every prior generation of 7-year-olds; but they sure are fatter! It makes even less sense to ascribe less personal responsibility to the current generation of Saccharomyces.
Of course, the “fault” lies not in our Saccharomyces! The explanations for what is awry within us are all around us; the very factors of lifestyle, environment and culture that have changed us have changed our resident flora as well. The behaviors that lead to better health and healthier weight may do so in part by moderating the expression of genes, and favorably shifting the populations of gut microbes.
It takes a healthy village within, it seems, to be a healthy human being. It still takes healthy choices by that human being to tend the village.
David L. Katz is the founding director, Yale-Griffin Prevention Research Center. He is the author of Disease-Proof: The Remarkable Truth About What Makes Us Well.