{"id":7555,"date":"2024-12-10T09:37:44","date_gmt":"2024-12-10T08:37:44","guid":{"rendered":"https:\/\/kompetenz-statt-demenz.dsgip.de\/prevention-treatment\/nutrition\/gluten-als-risikofaktor-fuer-demenz\/"},"modified":"2024-12-10T09:42:23","modified_gmt":"2024-12-10T08:42:23","slug":"gluten-als-risikofaktor-fuer-demenz","status":"publish","type":"page","link":"https:\/\/kompetenz-statt-demenz.dsgip.de\/en\/prevention-treatment\/nutrition\/gluten-als-risikofaktor-fuer-demenz\/","title":{"rendered":"Gluten as a risk factor for dementia"},"content":{"rendered":"

 <\/p>\n\n

Gluten, also known as gluten protein, owes its name to its two main components: <\/span>gliadin<\/span><\/b> and <\/span>glutenin<\/span><\/b>. Gliadine sind gro\u00dfe Proteinmolek\u00fcle, die reich an den Aminos\u00e4uren Glutamin und Prolin sind. Sie k\u00f6nnen wiederum in Subgruppen unterteilt werden, alpha-Gliadine, beta-Gliadine, Gamma-Gliadine und Omega-Gliadine. Von Letzteren wird insbesondere das Omega-5-Gliadin mit Nahrungsmittelunvertr\u00e4glichkeiten in Verbindung gebracht. <\/span><\/p>\n

Gliadins ensure the elasticity and binding of the dough during production. Glutenins, on the other hand, are responsible for elasticity and viscosity [19]. Together they make up around 80-85% of the total protein in wheat. <\/span><\/p>\n

The history of wheat goes back to the beginnings of agriculture. Original varieties such as einkorn and emmer were developed through breeding into higher-yielding, more disease-resistant and more bakeable varieties. <\/span>However, different types of wheat (einkorn, emmer, spelt, durum and soft wheat) show large differences in the composition of their proteins. Wheat (common and durum wheat) contains the highest amounts of potentially allergenic proteins, including omega-5 gliadin. <\/span>Spelt and emmer have slightly reduced amounts, about half as much as common wheat. Einkorn contains the lowest amounts, with a reduction of around 5.4 times that of common wheat [1]. <\/span><\/p>\n

This could explain why the increased consumption of wheat products has led to an increase in gluten-related diseases. A meta-analysis shows that the number of coeliac disease diagnoses has risen by around 7.5% annually in recent decades [5]. In Germany, around 1% of the population – i.e. one in 100 people – is affected. Recent research findings indicate that gluten-related diseases, in particular coeliac disease, not only affect the gut but can also cause neurological symptoms. These include brain fog, memory loss, disorientation and confusion. It is striking that these symptoms are similar to those of neurodegenerative diseases such as Alzheimer’s. There is evidence that celiac disease and gluten sensitivity may be indirectly related to various forms of dementia such as Alzheimer’s disease, frontotemporal dementia and vascular dementia [8,10,11]. These symptoms may occur due to communication between the gut and the brain. <\/span><\/p>\n

Communication between the gut and the brain<\/span><\/h3>\n

Communication between the gut and brain is crucial for the exchange of chemical and physical substances, which ensures the smooth functioning of both organs. This exchange takes place via various systems, such as the gut-brain axis and via the bloodstream through the blood-brain barrier. <\/span><\/p>\n

The gut-brain axis<\/span><\/i><\/h4>\n
\"The

Image 2<\/p><\/div>\n

The gut-brain axis is a highly complex communication system that facilitates the exchange between the gut and the brain. Around 90 % of the signals flow from the gut to the brain, only 10 % in the opposite direction. This exchange takes place via nerve connections, immune reactions as well as messenger substances and metabolic products produced by the intestinal microbiome [2,11,16,17]<\/span>.<\/span><\/p>\n

The blood-brain barrier<\/span><\/i><\/h4>\n

Substances can be transported from the intestine to the brain via the bloodstream. The blood-brain barrier<\/a> is a protective barrier that protects the brain from harmful substances in the blood. It ensures that only important nutrients and waste products reach the brain. At the same time, it prevents large molecules and toxic substances from entering the brain [12]. <\/span><\/p>\n

How does gluten lead to dementia?<\/span><\/b><\/h3>\n

Although the exact mechanisms are not yet known, there are some theories that are still in the early stages of research.<\/span><\/p>\n

Theory 1: Leaky-good leads to leaky-brain<\/span><\/h4>\n

Gluten ingested with food reaches the small intestine via the mouth and stomach. In the stomach and small intestine, digestive enzymes break down the gluten into glutenin and gliadin, whereby gliadin cannot be completely broken down into its individual amino acids. The undigested gliadin reaches the intestine, where it can trigger so-called leaky gut, particularly in gluten-sensitive people. This clinical picture is characterized by damage to the intestinal wall, which can lead to the destruction of its barrier function. This can trigger a permanent activation of the intestine-associated immune system and thus contribute to chronic inflammation. This can spread to the central nervous system and thus to the brain. The intestinal colonization, the intestinal microbiome, can also be adversely affected by gluten. Both mechanisms are described in detail below. <\/span><\/p>\n

Destruction of the intestinal wall<\/span><\/i><\/h5>\n
\"Zonulin

Image 3<\/p><\/div>\n

U<\/span>digested gluten proteins, especially gliadin, bind to the intestinal cells (epithelial cells) that form the intestinal wall via various receptors. In particular, binding to the receptor CXCR3 triggers a signaling cascade that leads to increased production and release of a protein called zonulin. Zonulin then binds to special receptors on the epithelial cells, which loosens the junctions between the epithelial cells, the so-called tight junctions. This literally creates “gaps” between the epithelial cells, making the intestinal wall more permeable [3,4,7]. <\/span><\/p>\n

Through a permeable intestinal barrier, undigested food components such as gliadins, toxic metabolic products and surface proteins of intestinal bacteria such as LPS (lipopolysaccharides), microorganisms or cytokines can enter the bloodstream directly. The penetration of these substances activates the immune system and leads to the release of pro-inflammatory cytokines such as IL-6, IL-1\u03b2 and TNF-\u03b1. Via the bloodstream, these cytokines finally reach the blood-brain barrier, which also becomes more permeable as a result of these inflammatory processes, which can lead to the so-called “leaky brain”. <\/span><\/p>\n

Due to the “leaky gut”, undigested food components, pathogens and metabolic products of the microbiome can increasingly enter the bloodstream. Through the “leaky brain”, these substances also increasingly enter the brain. There they lead to increased neuroinflammation and oxidative stress or, in the case of LPS (lipopolysaccharides), even to the increased formation of plaques, which increases the risk of neurological diseases such as dementia [12]. <\/span><\/p>\n

Changes in the gut microbiome<\/span><\/i><\/h5>\n

In people with coeliac disease, the gut microbiome (all bacteria in the gut) can be altered by a gluten-containing diet or gluten-induced inflammation, resulting in an imbalance between the physiological and pathogenic bacteria in the gut (dysbiosis) [12,15]. <\/span><\/p>\n

Our physiological gut bacteria produce important metabolic products such as short-chain fatty acids (SCFA) or neurotransmitters (e.g. the happiness hormone serotonin or GABA). An imbalance in our microbiome in favor of pathogenic germs can lead to increased production of lipopolysaccharides (LPS), which can trigger inflammation and thus also impair the blood-brain barrier. Toxic metabolic products of these pathogenic bacteria can also enter the bloodstream via the intestine and potentially also the brain. In addition, dysbiosis leads to a reduced number of acid-forming flora and thus to a reduced synthesis of short-chain fatty acids (SCFAs), which have an anti-inflammatory effect [17]. Furthermore, the production of neurotransmitters such as GABA and serotonin can also be impaired. Reduced production of these neurotransmitters can have a negative impact on cognitive function and mood regulation [12]. <\/span><\/p>\n

An altered gut microbiome and changes in metabolic products have also been demonstrated in Alzheimer’s patients [6,17]. These findings come mainly from animal and in vitro studies, and more research is needed to better understand the exact relationships. <\/span><\/p>\n

Theory 2: molecular mimicry and cross-reactivity <\/span><\/h4>\n

In patients suffering from coeliac disease or gluten sensitivity, the immune system falsely recognizes gluten peptides such as gliadin as harmful. In response, the immune system in the intestine, which acts as an essential immunological barrier for the body, forms special antibodies against the gluten proteins. Studies show that gluten proteins have similarities in their amino acid sequence to certain proteins in the brain. This similarity can lead to the gluten antibodies also attacking brain proteins – this is known as cross-reactivity. Such attacks can lead to inflammatory reactions or functional disorders in the brain. <\/span><\/p>\n

However, the mechanism of these cross-reactions has not yet been fully proven and remains largely hypothetical. Further research is needed to better understand the exact relationships and effects. The following brain proteins are thought to be affected by this cross-reactivity: <\/span><\/p>\n