What is it?

Irritable Bowel Syndrome (IBS) or Spastic Colitis is a chronic disorder of the gastrointestinal tract and is associated with reduced quality of life and productivity at work. Data from 2015 show that SLE prevails in 7 to 21% of the general population and usually in people under 50 years old.

In fact, it seems that SLE occurs more often in women, but is not associated with increased death rates.

It is a disorder that is due to a number of causes (multifactorial) among which are:

• gastrointestinal motility disorder,
• visceral hypersensitivity, changes in the microbial flora of the intestine,
• food intolerances,
• intestinal or non-intestinal infections,
• various antibiotics,
• genetic factors

but also various psychosocial factors. In particular, it has been shown that in 40-60% of patients coexist psychological disorders and mainly depression and anxiety.

Therefore, it is not clear whether psychosocial factors are a cause or a consequence of SLE. Typical symptoms of the disease include flatulence, abdominal pain, abdominal distention, and a change in bowel habits (diarrhea or constipation, or alternating between the two).

Finally, there are factors that can trigger the onset of SLE symptoms, in addition to psychological disorders. These factors include: stress, alcohol and substance abuse, various drugs, infection and inflammation, various components of the diet (will be analyzed below), hormones e.g. menstrual cycle and the alternations of the seasons.

The diagnosis of SLE is made in the presence of specific symptoms in the absence of organic disease. Initially, the possibility of celiac disease and lactose and fructose intolerance should be ruled out.

The ROME IV (2016) criteria are then applied, according to which SLE is categorized as a functional bowel disorder characterized by abdominal pain, which is associated with two or more of the following:

• improvement of bowel movements,
• changes in the composition of the bowel movements and
• changes in the frequency of bowel movements.
• The criteria should be met at least once a month for the last 3 months, with the onset of symptoms at least 6 months before diagnosis.

At the same time, 4 types of TEU have been described:

• IBS-C with the predominant symptom of constipation,
• IBS-D with the predominant symptom of diarrhea,

the mixed type, IBS-M and the not defined type by the usual symptoms, IBS-U.

Although the association of osteoporosis and other gastrointestinal disorders, such as celiac disease (gluten intolerance), ulcerative colitis, and Crohn’s disease, has been extensively studied and has been shown to increase the risk of both osteoporosis and fractures, with the SLE there is still insufficient research data.

First, it should be noted that osteoporosis is the condition, which is characterized by loss of bone mass, disruption of the micro-architecture of bone and skeletal fragility, resulting in an increased risk of fractures.

Today it is characterized as a multifactorial systemic disease that is influenced by genetic, hormonal, environmental and nutritional factors and is diagnosed by measuring bone density.

Existing research data reveal that in SLE the risk of osteoporosis, but also fractures, is higher compared to the healthy population, but lower than other intestinal diseases.

More specifically, the highest risk is observed in women aged 40-59 years, followed by men aged 40-60 years. In people under the age of 40, it seems that women still have a higher risk of osteoporosis than men. Therefore, it is understood that SLE is a risk factor for osteoporosis.

But why is this happening?

Modifications of various inflammatory cells have been shown to cause changes in the intestinal mucosa, resulting in reduced nutrient absorption and, in this case, calcium, which is a component of bone and vitamin D.

Decreased vitamin D leads to an increase in parathyroid hormone (PTH), which in turn causes osteolysis and removal of calcium from the bones into the circulation and ultimately, osteoporosis and the risk of fractures.

An additional mechanism that has been described concerns estrogen, which protects bones from lysis, induces their formation and increases their lifespan. However, during menopause, this mechanism stops working, which explains why osteoporosis occurs more often in women with SLE than in men.

Finally, it is worth mentioning that many patients experience an exacerbation of symptoms after consuming dairy and lactose in general. As a result, they exclude such products from their diet, which, however, are the main sources of calcium.

In this way they do not absorb sufficient amounts of this essential nutrient for the bones and thus, the risk of osteoporosis increases.

The role of diet in SLE is not fully understood and diet alone is not an effective solution for all patients. Many foods have been implicated in inducing the symptoms of SLE. However, different foods can cause symptoms in each patient.

That is why it is necessary for everyone to keep a diary in which they will record the food they consume and the symptoms that appear.

In general, it is best to avoid

•  alcohol,
• caffeine,
• carbonated soft drinks,
• fatty foods,
• lactose,
• sorbitol,
• mannitol and
• xylitol (sugar substitutes – found e.g. in chewing gum),

while among the foods followed by flare-ups are the following:

• haricot beans,
• chickpeas,
• lentils,
• cabbage,
• cauliflower,
• broccoli,
• onions,
• garlic,
• turnips,
• brussels sprouts,
• corn,
• peas,
• celery,
• carrots,
• raisins,
• bananas,
• apples,
• plums,
• apricots,
• potatoes,
• wheat products and pastries, as well as high amounts of fructose in fruits such as pear and watermelon.

Finally, foods that can be consumed without fear are the following:

• meat,
• poultry,
• fishes,
• rice and soy substitutes,
• fruits and vegetables that are well tolerated by the body.

We must not forget that each organization is unique and that the diagnosis and treatment of SLE should be done in collaboration with the doctor and the dietitian!

Advises Ms. Tsitsou Sofia, Dietitian – Nutritionist, Graduate of Harokopio University of Athens, MSc Diabetes and Obesity, Athens Medical School