Humanity’s obesity epidemic threatens to become a pandemic.
GLOBAL OBESITY RATES
|2005||400 million (9 percent)|
|2015 (projected)||700 million (14 percent)|
|2030 (projected)||Over 1 billion (20+ percent)|
The crisis has caught the attention of the science research community and has led to amazing discoveries that not only offer hope of cures for obesity but also provide new evidence for supernatural design of the human body.
Modern, sedentary lifestyles and easy access to cheap, energy-dense foods rank as key factors in excessive body fat accumulation. Recent studies, however, demonstrate that some individuals are more susceptible to obesity than others, which suggests an important inherited component. While several studies reveal about fifty genomic features associated with obesity, a team of over forty researchers from western Europe and China has determined that the collective genome of microorganisms inhabiting the human digestive tract plays a much more important role in obesity pathology. Specifically, the team conducted experiments that showed “variation in the gut microbiome at gene and species levels defines subsets of individuals in the adult population who are at increased risk of obesity-related metabolic disorders.”1
The team first noted a previous study2 that showed only a weak correlation, at a level of only a few percent, between body mass index (BMI––mass in kilograms divided by the square of the individual’s height in meters) and apparent genetic markers for obesity. In other words, human genetic markers alone could not accurately predict obesity. The team then referenced emerging evidence that variations in the diversity of microorganisms inhabiting the human body are associated with the pathology of obesity.3 This evidence motivated the team of researchers to analyze the gut microbial composition in a sample of 292 Danish adults: 96 who were lean with a BMI less than 25, 27 who were overweight but not obese with a BMI between 25 and 30, and 169 who were obese with a BMI greater than 30. All 292 individuals in the sample were nondiabetic with no known gastrointestinal disease, no previous bariatric surgery, and they took no antibiotics or medications known to affect the immune system.
More Gut Bacteria, Less Obesity
Results showed that nonobese people predominantly possess a high gene count (HGC) in their gut bacteria while obese individuals fall into two categories: those with a low gene count (LGC) in their gut bacteria and those with an HGC. For the obese individuals the difference between the LGC and HGC groups was pronounced. The two groups had, on average, 380,000 and 640,000 genes, respectively, reflecting a substantial difference in the abundance levels of 58 bacterial species. The greatest observed contrast found that HGC individuals were richly endowed with anti-inflammatory bacterial species whereas the LGC individuals were plagued by proinflammatory bacterial species.
In addition, the LGC people manifested increased serum leptin, decreased serum adiponectin, insulin resistance, hyperinsulinaemia, increased triglyceride and fatty acids levels, increased LDL cholesterol, decreased HDL cholesterol, more marked inflammatory phenotype, and higher white blood cell counts. These markers translate into much higher risks of pre-diabetes, type 2 diabetes, and cardiovascular and inflammatory disorders.
The team further noted a strong correlation between bacterial gut gene levels and changes in BMI over a nine-year period for their sample group. Lean HGC individuals had an average BMI decrease of 0.3 while the (less common) lean LGC individuals experienced an average BMI decrease of 1.1. Meanwhile, for obese HGC persons their BMI increased by an average of 1.6 whereas obese LGC people saw their BMI increase by an average of 2.9. Thus, for all individuals, HGC works to stabilize the BMI. However, this stabilization is much more important for the obese than for the lean.
Of all the bacterial species that inhabit the human gut, the researchers found that just eight factored into significant weight gain or loss of people in their sample. Individuals with the lowest or undetectable levels of these eight species gained more weight than their counterparts with the highest levels of these species, causing the team to conclude, “These species may therefore protect against weight gain.”4 Their conclusion suggests new approaches that may finally yield effective treatment and prevention of the multitude of ailments associated with obesity.
At the very least the team has identified an effective diagnostic tool. “The obesity-associated signal in the human gut microbiome may be much stronger than that presently known in the human genome,”5 the researchers said. They end the first of the two papers on their findings with the strong recommendation that further research by the scientific community on the human microbiome at a deep metagenomic level “may spearhead development of stratified approaches for treatment and prevention of widespread chronic disorders.”6
Better Diet Helps Gut Bacteria Count
In a second paper, published in the same journal issue and including many of the same researchers, another team describes their research on the impact of dietary intervention on the richness of the human microbiome.7 This team recruited 38 obese and 11 overweight French individuals and put them on a six-week, energy-restricted, highprotein diet followed by another six weeks of a weight-maintenance diet. Of these 49 people, 18 were found to be in the LGC category and 27 in the HGC category.
Prior to the 12-week regimen, the team noted that the dietary habits of the LGC subjects included fewer fruits, vegetables, and fish products than their HGC subjects. This observation led them to conclude that long-term dietary habits may impact the gene count of gut bacteria in humans.
For the LGC group the dietary experiment demonstrated that gut bacterial gene richness increased substantially after the energy restricted diet and remained throughout the stabilization phase. It did not, however, change in any significant way for the HGC group. Nevertheless, even after the 12-week regimen was completed a measurable difference in gut bacterial gene richness between the HGC and LGC groups remained. The dietary research team concluded, therefore, that either dietary intervention offers only a partial cure for low gut bacterial gene richness or that dietary intervention needs to be extended over a longer time period or target particular diet components. The paper ends with a call for more extensive research, but at least one conclusion seems appropriate: given that humans depend on gut bacteria for metabolism that allows for all human activities, it would be prudent to use a measure of control over the ideal microbiome by maintaining healthy diets.
No other species of life comes anywhere close to a human being in its designed capacity to live a long, highly capable, highly active life. However, as wonderfully designed as the human body is, it also takes exquisite design of the human microbiome to enable it to function as capably, actively, and as long as God intends. That is, the human microbiome provides one more piece of evidence of the Creator’s supernatural, super-intelligent provision to enable humans to perform the purposes for which He created them. The research described above underscores, too, the trustworthiness and value of the Old Testament health and diet passages––biblical advice on how to best care for our physical well-being that includes doing the best to ensure that our microbiome can optimally sustain our health and longevity.