Digestive Wellness: Strengthen the Immune System and Prevent Disease Through Healthy Digestion, Fourth Edition (145 page)

Low-grade inflammation

Subsequent leaky gut

Elevated levels of lipopolysaccharides (LPS) and endocannabinoids

If obesity is left unchecked it can lead to metabolic syndrome, type II diabetes, high serum lipids, and cardiovascular disease.

The gut microbiome is responsible for maintaining our metabolism and determining how much fat we store. People who are obese have a different balance of gut microorganisms than thin people do. This much is known, yet we don’t really know yet exactly which bacteria are involved.

Eighty to 90 percent of the bacteria in our gut are from two main families or phyla: Bacteroidetes and Firmicutes. Original work by Dr. R. E. Ley and colleagues demonstrated that fat mice had more than half as many Bacteroidetes and twice as many Firmicutes bacteria than lean mice. They observed the same thing in 12 people. These people then followed either a low-fat or low-carbohydrate diet for a year, which nearly normalized their balance of Bacteroidetes and Firmicutes bacteria. However, the plot thickens because other researches did not find these differences. Dr. S. H. Duncan and colleagues found no differences in the amount of Bacteroidetes in stool of people who were obese, and levels didn’t change when people dieted. Firmicutes levels went down when people dieted, which is the opposite finding from Ley’s group.

It appears that research looking at specific species of bacteria will yield better results than just looking at humungous phyla. To that point, there seems to be more of an agreement among researchers about the roles of Bifidobacterium species and Streptococcus aureus in obesity. P. D. Cani and Delzenne found in obese rats that there were reduced amounts of bifidobacteria in both species and number. Kalliomaki and colleagues found a higher number of bifidobacteria in children who were lean at age seven than in children who were overweight. Drs. Marko Kalliomaki, Erika Isolauri, and colleagues also found higher amounts of Staphylococcus aureus in children who became overweight and propose that staph may trigger low-grade inflammation. Other research indicates that increasing B. bifidum and B. breve while decreasing B. catenulatum and S. aureus can also make us leaner.

It seems well established that there is a low-grade inflammatory process occurring in people who are obese. This is mediated by our gut microbiome. Patrice Cani, Nathalie Delzenne, and colleagues have a large body of work that looks at the inflammatory pathways in obesity. Mice given antibiotics to simulate imbalances in the microbiota had increased inflammation and toxic by-products in the gut and in stools. The changes in the gut bacteria lessened the mice’s ability to handle glucose and provoked increases in body fat, weight gain, inflammation, and oxidative stress, which led to increased intestinal permeability. Cani and Delzenne have also demonstrated that lipopolysaccharides (LPS), components of gram negative bacteria, trigger early, low-grade, chronic inflammation. LPS levels are increased with high-fat
diet. High-fat diets also increased gut permeability and lowered bifidobacteria levels.

Did you ever get the munchies from smoking pot? Well, marijuana is an external cannabinoid, but we also make our own internal cannabinoids in our brain, muscles, liver, digestive system, and fat cells. When turned on, food tastes amazing. Endo-cannabinoids help to regulate appetite, regulate our perception of pain, affect our mood, protect our nervous system and neurons, control certain phases of memory processing, act as a feedback loop that signals our neurons to stop secreting neurotransmitters, help regulate heart rate, blood pressure, and bronchial function, and has effects on our fat cells, liver, muscles, and pancreas.

This system, called the endocannabinoid system (eCS), is comprised of lipids (fats) and receptors (CB1 and CB2). Along with the hypothalamus, it stimulates production of ghrelin and we feel hungry. It also regulates energy balance. In people who have central adiposity (are apple shaped) the eCS is overactivated and levels are high.

The endocannabinoids slow gastric emptying, slow intestinal transit, and make food taste great. The eCS also aids in nutrient transport and storage of fat. When we eat more calories than we need at any given time, our body converts those extra calories into fat. When we have eaten enough, cholecystokinin is secreted in our duodenum and leptin is secreted, which lowers our appetite and turns off the eCS. Levels of endocannabinoids drop as leptin is secreted. We no longer feel hungry.

In obese people, levels of endocannabinoids stay chronically high. If we keep the eCS activated continually, it leads to high triglyceride levels, which in turn can lower our protective HDL cholesterol, increase LDL cholesterol, and lead to atherosclerosis (plaque buildup in our arteries). High levels of eCS also decrease adiponectin, which in turn decreases insulin sensitivity. This leads to increased weight gain and ultimately can lead to metabolic syndrome and/or type 2 diabetes.

This constant inflammation contributes to increased gut permeability. The increased permeability leads to more inflammation and food sensitivities. If the inner lining of our duodenum is inflamed, we may not release cholecystokinin and our eCS stays activated. When active, eCS stimulates our liver to make fatty acids.

What is not known is how high endocannabinoid levels are in lean people and what the mechanism is that keeps them lean despite it.

For a long time clinicians working with food sensitivities have noticed that when people deal directly with their food sensitivities, they begin to lose weight. Although there is little research to support this, it makes sense. Food can be inflammatory and obesity is an inflammatory condition, so going on an anti-inflammatory diet can help lower inflammation and help normalize function. Cell Science Systems, maker of the ALCAT food sensitivity testing process, has sponsored a couple of studies that verify that by avoiding foods you are sensitive to, you can facilitate weight loss. In clinical practice, when working with someone who is obese, I often begin by putting someone on an elimination diet. I’m not the only person who finds this useful: Elson Haas, M.D., wrote a book called
The False Fat Diet
(Ballantine Books, 2001), which utilizes an elimination diet for weight loss, and Mark Hyman, M.D., wrote
The Ultra Simple Diet
(Pocket Books, 2007) to express how an elimination diet plus detoxification could jump-start weight loss as well.

Food sensitivities are tightly linked with leaky gut. So, it makes sense that if leaky gut is associated with obesity, food sensitivities will follow. By avoiding inflammatory foods and following the information in
Chapter 4
, you may find that it’s easier to lose weight.

Metabolic syndrome affects about 47 million Americans. If you have more than three of these factors, you may be diagnosed with metabolic syndrome: large waist size, triglyceride levels higher than 150 mg/dl, low HDL cholesterol levels, high blood pressure, and fasting blood sugar levels of over 100 mg/dl. It’s characterized by insulin resistance and difficulty in handling glucose. Most people with metabolic syndrome are overweight and often apple-shaped, but this also occurs in people who are thin. If left unchecked, metabolic syndrome often leads to type 2 diabetes and increased risk for cardiovascular disease.

Comprehensive digestive stool testing:
This test will give an indication of microbial balance and probiotic levels.

Hemaglobin A1C:
This test gives a three-month average of glucose levels and is a better indicator of pre-diabetes than fasting glucose levels.

Frucosamine:
Frucosamine is similar to Hemaglobin A1C but gives about a two-week average of glucose levels.

Food sensitivity testing:
Delayed food sensitivities can predispose to obesity.