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Glasser family

Glasser family

Mental Health Strategy

For roughly one in every hundred people, food containing even the smallest amounts of gluten can deliver a gutful of hurt and pose severe risks to their health.

While a domino effect of immunological reactions can be traced back to their genetic roots, a number of contributing factors are also involved, making it difficult to map the precise chain of events that causes celiac disease.

Using transgenic mice, an international team led by scientists from McMaster University in Canada has identified a crucial role played by the very cells making up the gut’s lining, describing a major stepping stone that could lead to new therapies.

Celiac disease is a lifelong autoimmune disorder triggered by the presence of a group of structural proteins known as gluten in the intestines.

Eating virtually anything made with wheat, barley, or rye – meaning most baked goods, breads, and pastas – puts people with the condition at risk of transient symptoms like bloating, pain, diarrhea, constipation, and sometimes reflux and vomiting.

Related: Gluten Intolerance vs Celiac Disease: Experts Reveal The Key Differences

Currently the only way to avoid the symptoms is to avoid the foods that trigger them. Over the longer term, immune attacks triggered by gluten can damage the small intestine’s villi. These tiny structures increase the internal surface area of the intestinal walls, which aids absorption of nutrients from food.

People with celiac disease – particularly if it’s untreated – face serious health risks, such as being more likely to develop colorectal cancer and cardiovascular disease. The disease is associated with a myriad of conditions, with just some examples including anemia, osteoporosis, growth delays, reproductive issues, and neurological disorders.

“The only way we can treat celiac disease today is by fully eliminating gluten from the diet,” says McMasters gastroenterologist Elena Verdu.

“This is difficult to do, and experts agree that a gluten-free diet is insufficient.”

Around 90 percent of people diagnosed with the condition carry a pair of genes that encode for a protein called HLA-DQ2.5. Of the remaining 10 percent, most have a similar protein called HLA-DQ8.

Like other kinds of ‘HLA’ (or human leukocyte antigen) proteins, the proteins hold pieces of fallen invaders aloft like macabre trophies on a class of immune cells, warning other defensive tissues to be on the lookout.

In the specific case of HLA-DQ2.5 and HLA-DQ8, the proteins are shaped to hold chunks of gluten peptide that are resistant to digestion, instructing murderous T cells to go on the hunt.

Unfortunately, these instructions aren’t the clearest at distinguishing between a threat and similar-looking materials in our body, meaning those with the genes are at risk of a variety of autoimmune conditions.

Not everybody who expresses either HLA-DQ2.5 or HLA-DQ8 will develop an immune disorder like celiac disease, however.

For that to happen, those torn-up pieces of gluten first need to be carried across the gut wall by a transporting enzyme that binds with the peptide and alters it in ways to make it even more recognizable.

Cells in the intestinal wall are responsible for releasing this transporting enzyme into the gut, so they clearly have a critical role in the early stages of the disease.

They are also known to express the family of proteins to which HLA-DQ2.5 and HLA-DQ8 belong, which are typically regulated by inflammatory responses in the gut.

What hasn’t been clear is how this staging ground for people with celiac disease actually functions within the pathology itself.

To focus on this important link in the chain, the research team double-checked the expression of the major immune complex in the cells lining the intestines of people with treated and untreated celiac disease, and in mice with the human genes for HLA-DQ2.5.

They then created functional living models of the gut, called an organoid, using the mouse intestinal cells, to study the expression of their immune proteins up close, subjecting them to inflammatory triggers as well as predigested and intact gluten.

“This allowed us to narrow down the specific cause and effect and prove exactly whether and how the reaction takes place,” says McMasters biomedical engineer Tohid Didar.

From this it became evident the cells lining the gut weren’t just passive bystanders suffering collateral damage in a misguided effort to rid the body of gluten – they were key agents, presenting a mash-up of gluten fragments broken down by gut bacteria and transporting enzymes to gluten-specific immune cells firsthand.

Knowing the types of tissue involved and their enhancement by the presence of inflammatory microbes gives researchers a new list of targets for future treatments, potentially allowing millions of people worldwide to enjoy a gluten-filled pastry or two without the risk of discomfort.

This research was published in Gastroenterology.

An earlier version of this article was published in August 2024.

Background/Significance

The human microbiome, consisting of approximately three trillion bacteria and other microorganisms, is critical in regulating physiological processes, including immune responses and chemotherapy efficacy. Given the potential influence of microbiome composition on therapeutic outcomes, this pilot study investigated microbiome variations in breast tissue, skin, and stool samples and their associations with pathological complete response (pCR) in breast cancer patients undergoing neoadjuvant chemotherapy.

Materials and Methods

Eleven breast cancer patients receiving neoadjuvant chemotherapy were included in this single-institution study. Treatment regimens were docetaxel, carboplatin, trastuzumab, and pertuzumab (n = 5); pembrolizumab-based immunotherapy (n = 5); and doxorubicin, cyclophosphamide, and paclitaxel (n = 1). Following therapy, breast tissue, skin, and stool samples were collected for microbiome analysis. Breast tissue 16S rRNA sequencing data were cross-referenced with skin microbiome data to exclude potential contaminants, removing taxa with >0.01% average skin abundance and ≥10% positivity. Whole-genome shotgun analysis excluded 295 taxonomic members, and microbial profiles were re-normalized to calculate the mean relative abundance.

Results

Six patients (55%) achieved pCR following neoadjuvant chemotherapy. Breast tissue microbiome analysis revealed no significant differences between patients with and without pCR. However, stool microbiome composition differed between these groups. Patients without pCR exhibited elevated levels of Eubacterium (0.85 vs 0.39; P <.01), Bilophila wadsworthia (0.19 vs 0.05; P = .01), Alistipes shahii (1.65 vs 0.37; P = .01), and Dorea (0.42 vs 0.21; P = .02) compared with those with pCR. Conversely, patients achieving pCR had higher levels of Clostridiales (0.84 vs 1.83; P = .02), suggesting a potential correlation between the presence of specific bacterial taxa and therapeutic response.

Conclusion

This study highlights significant associations between stool microbiome composition and pCR in breast cancer patients undergoing neoadjuvant chemotherapy. Clostridiales, in particular, may enhance chemotherapy effectiveness through immune modulation and production of lithocholic acid, an antitumor metabolite. While limited by sample size, these findings suggest the need for larger studies to explore how gut microbiota influence treatment outcomes, potentially offering new strategies to optimize therapy.

Hand strength measurement with the Rotterdam Intrinsic Hand Myometer (RIHM). In this measurement, the strength of the muscles involved palmar abduction of the thumb are measured Credit: https://commons.wikimedia.org/wiki/File:Rotterdam_Intrinsic_Hand_Myom

Hazard ratios of developing low HSG (A) and average number of years required to develop low HGS based on cystatin-c/total cholesterol ratio (B), difficulty climbing stairs, depression, age, and gender (C), and various comorbidities and poor quality of lif

Scientists demonstrate how a weak handgrip can accurately correlate with numerous diseases and poor performance of daily chores among older adults

SHARJAH, EMIRATE OF SHARJAH, UNITED ARAB EMIRATES, July 7, 2025 /EINPresswire.com/ — Researchers have provided robust scientific evidence that ailments like depression, high blood pressure, diabetes mellitus, Alzheimer’s disease, osteoarthritis, and difficulties performing daily activities are associated with a frail handgrip, particularly among older adults.

The team, led by scientists from the University of Sharjah, says their study is the first large-scale investigation to present the prognostic efficacy of probable sarcopenia, the progressive loss of muscle strength among individuals over 50.

The scientists present their findings, which they claim accurately predict the correlation between several diseases and a frail grip, in the journal Aging Clinical and Experimental Research. (https://doi.org/10.1007/s40520-025-03007-6)

The data for the study is collected from the Survey of Health, Aging, and Retirement in Europe (SHARE), a large-scale European research project that studies individuals aged 50 and above. 17,960 community-dwelling geriatric adults aged 50 and over took part in the study and were monitored between 2025 and 2022.

The analysis of the data, they write, “exhibited significant prognostic accuracy for low HGS (Handgrip Strength) among men and women aged 60–79, irrespective of the quality of life, degree of depression, difficulties performing daily activities, and the presence of comorbidities, including depression, high blood pressure, diabetes mellitus, Alzheimer’s disease, and osteoarthritis.”

Doctors use handgrip strength tests to measure the strength or weakness of a person’s ability to squeeze or grip with their hands. It is a valuable tool to examine a person’s health conditions, particularly those of older adults. Medical professionals carry out these tests to predict potential health problems.

The authors acknowledge that previous studies present the predictive accuracy of the link between a poor handgrip and the development of several diseases, as well as conditions of daily life for older adults. However, they maintain that the findings in the plethora of available literature are drawn from “small subsets of hospitalized patients and were not replicated in community-dwelling older adults.”

The authors’ analysis is more comprehensive, covering a large community-dwelling population in residential settings, making it relevant to a variety of age-related lifestyle factors and comorbidities.

The authors’ investigation is not confined to health problems and diseases that can be associated with a weak handgrip. They also investigate their quality of life, several comorbidities, and difficulties performing daily chores.

They write, “We observed significant correlations between the CT ratio and handgrip strength in both men and women, regardless of BMI. This supports the general applicability of our findings across different segments of the population. The correlations were more robust in men than women of all age groups.”

BMI, or Body Mass Index, is a tool by which medical professionals measure body fat using height and weight as guidelines to determine whether an individual’s weight poses any health risks.

The authors add, “We report significant efficacy of CT ratio for probable sarcopenia in 17,960 community-dwelling older adults from 12 European countries. Specifically, the increasing CT ratio was associated with a higher risk and earlier onset of low HGS in the study population.”

The scientists demonstrate with “significant prognostic accuracy” that advancing age, male gender, higher than normal BMI, the presence of depression, and Alzheimer’s disease increase the risk of weakening an individual’s handgrip strength.

The researchers report statistically significant predictive accuracy between a low handgrip and the performance of everyday tasks and chores such as climbing stairs, getting dressed, and rising from a chair.

Men, more than women, according to the authors, develop a steeper decline in handgrip strength when reaching the age of 60 and above, coupled with a higher relevant risk threshold for mortality.

The authors’ study makes a valuable contribution to the literature, with several major strengths, namely their large representative sample drawn from 12 European countries.

Their longitudinal design, they wire, “significantly bolsters our confidence in the predictive efficacy of the CT ratio for low HGS. The standardized SHARE questionnaire, administered consistently across multiple European settings, ensured data harmonization and enhanced the study’s reliability.”

Their findings, the authors maintain, have clinical and policy implications that can help medical professionals to timely and accurately identify geriatric adults at risk of developing low handgrip strength.

They note, “Our findings have clinical and policy implications, potentially aiding healthcare providers and policymakers in identifying older adults with muscle weakness.”

LEON BARKHO
University Of Sharjah
+971 50 165 4376
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