Neither the mutually beneficial relationship between some microorganisms and their mammal hosts nor the correlation between host disease and disturbance of such harmony is novel. Recent advances in genetics, however, have provided scientists with new tools that shed a brighter light on the different functions of groups of bacteria and their interaction with each other and the host. Researchers are now excitedly hopeful about better understanding of related disease states and even the introduction of new therapies.

Neither the mutually beneficial relationship between some microorganisms and their mammal hosts nor the correlation between host disease and disturbance of such harmony is novel. Recent advances in genetics, however, have provided scientists with new tools that shed a brighter light on the different functions of groups of bacteria and their interaction with each other and the host. Researchers are now excitedly hopeful about better understanding of related disease states and even the introduction of new therapies.

Microbiota refers to microorganisms (mostly bacteria and some fungi and viruses) that live in our gut. Your body has 30 trillion human cells, yet over 100 trillion bacteria reside in your gut, mostly in the colon: 800 different bacterial species with over 7,000 strains. The human body (the host) and the microbiota have a symbiotic relationship. We provide food and shelter and they provide protective, metabolic, and nutritional services. These “good” bacteria compete for space and food with pathogens (bad microbes) and crowd them out. Microbiota also help in the production of essential vitamins and amino acids. Moreover, the continuous exposure to endless types of gut microbes trains the immune system to both avoid excessive inflammatory responses to harmless antigens and still fight pathogens.

Although diet is the main player affecting gut microbiota, age, stress, medications, and even climate are also involved. Antibiotic therapy, alcohol consumption, low-fiber diet, and many diseases are linked with alterations in the gut microbial balance, which may lead to inflammatory bowel disease, obesity, metabolic syndrome, alcoholic and non-alcoholic liver disease. Lack of diversity in microbiota and diet—literally, not eating enough different vegetables and fruits—is the major cause of microbial imbalance (dysbiosys) in the gut, which consequently leads to disease, mainly inflammation and/or metabolic disorders.

Research suggests that microbial imbalance in the gut allows disease-causing bacteria to flourish and encourages neutral ones to turn pathogenic. It seems to alter the immune cells responsible for prevention of invasion by bacteria; disrupts the gut epithelial barrier (alters the permeability of the gut lining), and causes these so-called pathobionts or their toxins to leak into the blood stream leading to systemic inflammatory responses seen in diabetes and obesity.

Scientists have identified LPS (lipopolysaccharide), for example, as endotoxins that trigger inflammation, which leads to insulin resistance; causes the body to store more fat; and slows down metabolism. Some suggest that gut bacteria can also manipulate behavior through the endocrine, immune, and nervous systems, creating cravings for foods that are favorable to them or ones that are harmful to their competition.

The key concept here seems to be diversity or worse, lack thereof. People with less diverse microbiota communities tend to be more obese and more prone to inflammation and metabolic disease. Healthy adults have higher concentrations of Bacteroides (involved in the biosynthesis pathway for biotins and riboflavin), Prevotella (which synthesizes thiamin and folate), and Ruminococcus (very important in the digestion of cellulose plant cell walls). Obese people, on the other hand, have more Firmicutes and Staphylococcus aureus but less Bifidobacterium and Lactobacillus.

The common wisdom so far is this. High-plant diet—fruits and vegetables, especially cruciferous vegetables (cauliflower, cabbage, broccoli)—supports a healthy microbiome as opposed to a high-fat diet, which seems to accompany high serum LPS levels. NM504 (designed by Mark Heiman, PhD and team) is the first in a new class of therapies known as GI (gastrointestinal) microbiome modulators. With ingredients extracted from food, the drug is presently helping patients with diabetes. It will be sometime, though, before we know exactly how diet affects our microbiome.

Don’t get me wrong, I love to read. I find science fascinating, I admire its innovations, and I learn much along the way. Yet, sometimes after an exhausting journey of research, it is somewhat disappointing to discover that the moral of such a long story is nothing but an old cliché: eat your blooming vegetables!

Susan Cohen © 2014

Lexicon

Antigens are protein markers present on all living cells and function as identification cards/thumbprints. These markers enable human immune cells to differentiate between friendly cells (body cells, for example) and other pathogens.

Microbiome is the collective genomes (entire genetic makeup) of these microorganisms.

Microbiota, in this article, refers to microorganisms (mostly bacteria and fungi) that reside in the gut and have a symbiotic relationship with the human host. In this article, the words microorganisms, bacteria, flora, or microbes are synonymous.

Pathobionts are gut bacteria that turn bad (pathogenic) under certain circumstances.

Pathogens are harmful microorganisms.

Permeability (what can and cannot go through a certain membrane) in this article, refers to the permeability of the gut wall. Under healthy conditions, neither microorganisms nor their toxins can penetrate/seep through the gut wall into the blood stream. Scientists believe that disturbances in the microbiome cause microbes or their toxins to penetrate the gut wall into the blood stream.