Functional gastrointestinal problems are common. In fact, about 1 in 4 people in the US are forced to limit their daily activities as a result of uncomfortable and embarrassing GI troubles. Chronic constipation, irritable bowel syndrome, delayed stomach emptying and gallbladder sludge can be symptoms of motility problems that are commonly seen in thyroid patients. The conditions account for almost half of the GI problems seen by doctors.
Functional problems can also involve the gut’s ability to secrete digestive enzymes that allow nutrient breakdown and absorption. Bloating, gas, smelly stools and bacterial overgrowth can be symptoms of these problems. Functional problems can also involve a condition called “leaky gut.” This is increased permeability of the intestinal lining, which can set off body-wide inflammation and increase the risk for autoimmune disorders, including Hashimoto’s thyroiditis. Thyroid hormones help maintain tight junctures between the cells lining the intestines and have been shown to protect gut mucosal lining from stress-induced ulcers.
Another important function (and increasingly understood role) of the gut is to host 70% of the immune tissue in the body. This portion of the immune system is collectively referred to as GALT, or gut-associated lymphoid tissue. The GALT comprises several types of lymphoid tissues that store immune cells, such as T&B lymphocytes, that carry out attacks and produce antibodies against antigens, molecules recognized by the immune system as potential threats. It is also a warehouse to living microbiota and organisms that are crucial to immune health.
Problems occur when these protective functions of the gut are compromised. When the intestinal barrier becomes permeable (i.e. “leaky gut syndrome”), large protein molecules escape into the bloodstream. Since these proteins don’t belong outside of the gut, the body mounts an immune response and attacks them. We also know that thyroid hormones strongly influence the tight junctions in the stomach and small intestine. These tight junctions are closely associated areas of two cells whose membranes join together to form the impermeable barrier of the gut. T3 and T4 have been shown to protect gut mucosal lining from stress induced ulcer formation.
Inflammation in the gut also reduces T3 by raising cortisol. Cortisol is a steroidal hormone that is released by the adrenal gland in response to everyday events such as waking up in the morning and exercising, but also during acute and chronic stress situations. Excessive cortisol load informs blood sugar regulation, immune function, weight management, proper digestion and nutrient absorption. Women who secrete high levels of cortisol when they are under stress tend to eat more at those times than women who secrete less cortisol. Additionally, since T3 is the ‘available’ or active form of thyroid hormone, thyroid activity further decreases as a result of how the gut is functioning.
Each cell in your body requires thyroid hormones to function properly. Because of this it’s no surprise that low thyroid activity–and the resulting low metabolism–can cause gastrointestinal trouble. A lot of that trouble is “functional.” That is, it has to do with the way the gut functions in real life and is not some structural abnormality that will show up on endoscopy, x-rays or blood tests. These functional problems are likely to involve GI tract motility–the coordinated movement of food from top to bottom, not to mention acid reflux and GERD.