Obesity and Bacteria
By Dr. Rizwana Rahim
Chicago, IL

We could easily be the least physically active generation ever.
Being more productive today than ever before in history is little more than an acknowledgment of numerous labor-saving, time-consuming devices developed over the years.
If it wasn’t the TV ‘remote control’ that turned us into a nation of couch-potatoes, it must be the calorie-dense, low-cost fast-food and the ‘junk food’, besides the very stress of being competitively more productive, that added a few pounds we find so difficult to lose on the treadmill in our basement or in a growing number of inspirational, 24-hour health and fitness clubs in our neighborhoods.
The latest statistics indicate about 64% of the adult Americans (i.e., close to 130 million, and roughly similar number in both genders) are overweight to obese. Over the past 40-plus years, the upward trend has been unmistakably clear. Obesity is now indeed an epidemic, a testimony to ‘la dolce vita’.
What is considered overweight and obese is not, thank heavens, defined by professional models. One simple way is to use Body-Mass-Index (BMI), as follows: Body weight (in lbs), divided by the square of height (in inches), and that multiplied by 704.5.
American Obesity Association (AOA) considers a BMI of 30 or more as ‘obese’, and between 25 to 29.9 as ‘overweight’. Both AOA and Centers for Disease Control and Prevention consider the 85th percentile of BMI (25) as ‘overweight’ ; AOA takes the 95th percentile of BMI (30) as ‘obese’.
Available statistics for the young children are appalling, to say the least. From 1971 to 2000, among different age-groups under 20, there has been a 2-4 fold increase in obesity in both sexes (to roughly 15% of their current population). Among black and Hispanic teenagers, roughly 20+% are considered obese, which is about 2x higher than in Whites (non-Hispanic), and about 36-44% overweight among older Black and Hispanic teenagers, as opposed to about 26% in the same age-group non-Hispanic Whites.
Based on BMI, about 62% women and 67% men would be overweight. If a person is highly muscular, or pregnant or lactating, these BMI figures would need some adjustment. Being obese is not just morbidly overweight, but it (obesity) is a chronic disease with a familial component and, according to AOA, obesity is the second cause of unnecessary deaths (adding about 300,00 excess deaths in the US).
Obesity contributes to the risk of having high blood pressure, Type 2 (adult-onset) diabetes, cardiovascular disease, stroke, and cancer of the breast, prostate and colon. A 10% reduction in weight would have significant health benefits, as most physicians would advise us. Unfortunately however, US National Institutes of Health, the premier health research organization of the world, spends less than 1% of its annual budget on obesity-related research.
Lack of physical activity, the amount and quality of consumed food and the stress of our daily life are, individually and in combination, significant contributing factors to obesity. In addition and surprisingly, some bacterial population (micro-flora, micro-biota) in our gastro-intestinal (GI) tract may also have a major role in obesity, according to some ground-breaking research by researchers in Washington University School of Medicine (St. Louis, MO) led by Jeffrey I. Gordon (also the Director of its Human Genome Sciences Center) published in the British journal, ‘Nature’. This research, along with commentaries on it, came out (Nature: 444, pages 1009, 1022, 1027, Dec. 21, 2006), coincidentally, in the midst of the Holiday season.
NOT all bacteria are necessarily harmful or pathogenic. Both pathogenic and benign (not harmful) exist in our body. For instance, our gastrointestinal tract (GI) is home to trillions of bacteria (~ 10x more than the cells in the human body), some of these species help us digest the food that would otherwise have been difficult to process.
Two groups (phyla) of beneficial bacteria – the Bacteroidetes and the Firmicutes – are dominant in our GI microflora. Firmicutes, the largest bacterial phylum (with 250 genera), have considerable variety and include both that require absolutely anoxic conditions, i.e., obligate anaerobes, like Clostridium sp., and others (e.g., Bacilus sp., and Streptococcus pyogenes that causes ‘Strep throat’) that need aerobic conditions. Bacteroidetes -- obligate anaerobes, mostly benign (but could be ‘opportunistic pathogens’ under some circumstances) -- have about 20 genera, and are found in the GI system of many warm-blooded organisms, including human GI system where B. thetaiotaomicron is the most abundant microbe of this group. While human GI contains fewer than 100 carbohydrate-metabolizing/digesting enzymes, B. thetaiotaomicron has two-and-a-half times more (about 240) such enzymes, derived from 550 different bacterial species residing in the human GI.
This research was first conducted on mice. In the genetically obese mice (ob/ob), they found that the Bacteroidetes population was about half of what's present in the lean mice (+/+), and correspondingly more Firmicutes in the obese than in their lean siblings.
Their earlier research showed that mice with injections of Betathetaiotaomicron (B. theta) were able to digest food better than mice with no such bacterial injections, and that mice inoculated with a combination of B. theta and an archaean bacteria, Methanobrevibacter smithii (M. smithii), extracted much more calories from the same amount of food, and this additional energy was stored as excess fat.
The microbes in the obese mice seem to be able to extract calories during digestion more effectively than those in the lean (+/+) mice. When the GI micro-culture from the obese mice was transferred to a germ-free strain of mice, the latter which had remained thin no matter what they ate, now grew fat. Mice with GI bacteria ate less (29%) but had more body fat (42%). However, when the germ-free mice were given GI bacteria, they got fat within two weeks, reaching the same weight as the other mice.
This research in mice was followed up in human-volunteers (12 obese people) for one year. They were randomly assigned to either (i) a fat-restricted (Fat-R) or (ii) a carbohydrate-restricted (Carb-R) low-calorie group. Their GI microbial ecology was monitored during the course of the experiment, along with sequencing 16s ribosomal (r) RNA genes for their stool samples. An increase in Bacteroidetes correlated well with the % loss in bodyweight, but not with changes in diet calories over time. As volunteers lost weight, the number of GI Firmicutes decreased, with an increase in the Bacteroidetes population. This correlation was held best after a person had lost at least 6% of his bodyweight on the Fat-R diet, and at least 2% on the Carb-R diet.
These researchers had earlier isolated a gene (‘obese gene’) that produced a hormone, leptin. Mice that have this gene are obese, and those that lack it are lean. Both in mice and humans, leptin deficiency leads to unrestrained caloric intake with a low expenditure of it, resulting in weight gain. Even a slight excess of caloric intake (say 1%) over its expenditure would lead to fat and weight accumulation over a period of time.
The health store market already has some pre-biotic items that increase the relative abundance of certain microbes and probiotics like yogurts that have live bacteria.
If this research on human GI microbial ecology is confirmed, it may also present new therapeutic opportunities for obesity: by adjusting or manipulating, with the help of diet or medication (antibiotics), a favorable microflora composition in the GI.


Editor: Akhtar M. Faruqui
2004 . All Rights Reserved.