Sarcopenia and vitamin D deficiency in patients with Crohn’s disease: Pathological conditions that should be linked together

Sarcopenia and vitamin D deficiency in patients with Crohn’s disease: Pathological conditions that should be linked together

Sarcopenia is a prevalent condition in patients with Crohn’s disease (CD), representing an independent predictor factor for the development of major postoperative complications.

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Introduction

Crohn’s disease (CD) is a chronic and progressive inflammatory bowel disease (IBD) that has a high impact on a patient’s quality of life. It is well known that all segments of the gastrointestinal tract can be affected by CD, mainly the terminal ileum and colon.

Inflammation is generally segmental, asymmetrical, and transmural. Although progress has been made to achieve prolonged remission, almost half of the patients over time will develop complications (i.e., strictures, fistulas, and abscesses) that require surgical treatments. The pathogenesis of CD is not yet fully understood, however, it clearly involves multiple factors, i.e., genetic susceptibility, environmental factors, and intestinal
microflora, resulting in dysregulation of multiple and overlapping immune pathways.

In the last decades, the prevalence of CD has increased continuously worldwide, especially in the developed countries, primarily due to environmental factors, such as changes in dietary patterns and alterations in body composition. Among these, the loss of muscle mass resulting in a decrease of muscle strength, a condition named sarcopenia, is an increasingly prevalent condition in patients with CD and is a strong independent predictor factor for the appearance of major postoperative complications.

Nowadays, it is widely acknowledged that vitamin D is one of the factors involved in the proliferation, differentiation, and regeneration of muscle cells. As proof of this, alterations in vitamin D levels seem to be related to sarcopenia prevalence in several pathological conditions, including CD.

Sarcopenia in Patients with CD

In the last decade, sarcopenia has emerged as a primary factor in the nutritional assessment of patients affected by chronic inflammatory diseases, including IBD. In fact, there is evidence indicating that this syndrome impacts the course of the disease, the responsiveness to specific therapies, and the outcomes of surgery..

Sarcopenia turns out to be a widespread condition in patients with IBD, in particular CD. In a recent systematic review, it is reported that up to 60% of patients with IBD present a depletion of the muscle mass when compared with healthy subjects.

It is reported that patients with CD, affected by sarcopenia, result to be overweight or obese (a condition named “sarcopenic obesity”), rather than undernourished, at the nutritional assessment tests. This extreme variability emphasizes the need for malnutrition and sarcopenia screening in all CD patients.

In addition to malabsorption and gastrointestinal surgery, other factors may contribute to the development of sarcopenia in patients with CD, such as eventual glucocorticoid treatment and hypogonadism, and a reduced physical activity [18–20]. It should be noted that the activation of inflammatory cytokines may contribute significantly to converting
the muscle protein metabolism from synthesis to degradation.

Vitamin D and Sarcopenia

Over recent years, the potential role of vitamin D on muscle function and strength has been widely debated. At a cellular level, it is known that vitamin D acts through both genomic and nongenomic pathways.

At the nuclear level, vitamin D can regulate gene expression by interacting with Vitamin D Receptor (VDR), thus forming a heterodimeric complex of liganded VDR with Retinoid-X-receptor (RXR) and up-regulating or down-regulating target genes transcription. The non-genomic effects of Vitamin D are mediated by the activation of intracellular signal pathways through signal molecules, e.g., phospholipase C and phospholipase A2, and the production of second messengers, protein kinases, and the opening of Ca2+ and Cl− channels.

Focusing on the biological mechanisms that regulate differentiation, proliferation, and regeneration of muscle cells, it has been demonstrated that vitamin D regulates several myogenic transcription factors involved in muscle cells proliferation, e.g., insulin-like growth factor 2 and follistatin, and in muscle cells differentiation, e.g., fetal myosin, the neural cell adhesion molecule, insulin-like growth factor 1, fibroblast growth factor and myogenic differentiation protein 1.

Regarding muscle regeneration, it has been demonstrated that vitamin D promotes the initial increase of the cross-sectional area of skeletal muscle fibres, by arresting the cell cycle, and suppresses the expression of myostatin, a key factor implicated in muscular degeneration.

According to the current knowledge, vitamin D seems to mainly affect type IIA muscle cells, i.e., the “fast twitch oxidative” cells [71]. Indeed, by using muscle biopsy, in previous works it has been shown that vitamin D deficiency is associated with type IIA muscle cells atrophy and fibrosis and, by contrast, the supplementation of vitamin D has been shown to increase the number and the diameter of type IIA muscle cells, thus increasing
muscle strength.

Furthermore, it should be mentioned that elevated PTH may contribute to the pathogenesis of sarcopenia, given its direct effect on skeletal muscle protein metabolism and the recent demonstration that elevated PTH levels are associated with vitamin D deficiency in sarcopenia.

Probiotic Lactobacillus acidophilus shows promise for treating inflammatory bowel disease and other intestinal inflammation disorders

Probiotic strain LA1 has a therapeutic effect that both prevents and treats intestinal inflammatory disorders caused by “leaky gut,” report researchers in The American Journal of Pathology.

Intestinal epithelial tight junctions (TJs) act as a functional and structural barrier against harmful antigens that promote intestinal inflammation in inflammatory bowel disease (IBD) and other inflammatory conditions of the gut. A defective intestinal TJ barrier, sometimes known as “leaky gut,” plays an important role in exacerbating and prolonging intestinal inflammation. New research reported in The American Journal of Pathology, published by Elsevier, shows that the probiotic Lactobacillus acidophilus (L. acidophilus) strain known as LA1 can generate a rapid and sustained enhancement of this defective intestinal barrier and effectively treat intestinal inflammation by preserving and restoring the intestinal barrier.

The use of probiotics has emerged as a therapy for a number of intestinal disorders, including IBD and necrotizing enterocolitis; however, specific probiotic bacteria with true beneficial effects on intestinal disease need to be identified. In this study researchers used high-throughput screening to assess over 20 probiotic bacteria to determine their ability to increase intestinal barrier function, using both a cell culture model of the intestinal epithelial lining and live mice.

The probiotic bacterial species L. acidophilus, specifically the LA1 strain, produced a rapid and marked increase in intestinal TJ barrier; other strains within L. acidophilus had no effect. The researchers found that this particular strain interacted with intestinal cells in a unique way to activate pathways that tightened the intestinal barrier, treating intestinal inflammation. It attaches to the intestinal epithelial membrane surface by directly interacting with the toll-like receptor–2 complex, which alerts the intestine to trigger an immune response.

The researchers also performed in vivo proof-of-concept studies in live mice to investigate the effect of LA1 and another strain, LA3, in the enhancement of mouse intestinal barrier and the therapeutic efficacy of LA1 in maintaining intestinal barrier and protecting against induced colitis. They found that LA1, but not LA3, caused rapid and marked enhancement of small intestine and colonic epithelial barrier in mice.  Treatment studies after the onset of colitis found that LA1 was also effective in the healing of intestinal barrier and colitis.

“Our data indicate that LA1 is able to prevent colonic inflammation formation and promote colitis healing,” said lead investigator Thomas Ma, MD, PhD, Penn State College of Medicine, Hershey Medical Center, Hershey, PA, USA. “The implications of the present findings are that this bacterial strain can be used in a wide variety of intestinal permeability disorders, including IBD, coeliac disease, alcoholic liver disease, non-alcoholic fatty liver disease, and necrotizing enterocolitis, to treat inflammation associated with the leaky gut.”

Original source here.

Wisdom, loneliness and your intestinal multitude

It may take guts — or more precisely, a diverse gut microbiome — to achieve wisdom and fend off loneliness. Or perhaps it’s the other way around, report UC San Diego researchers.

By Scott LaFee.

The evolving science of wisdom rests on the idea that wisdom’s defined traits correspond to distinct regions of the brain, and that greater wisdom translates into greater happiness and life satisfaction while being less wise results in opposite, negative consequences.

Scientists have found in multiple studies that persons deemed to be wiser are less prone to feel lonely while those who are lonelier also tend to be less wise. In a new study, published in the March 25, 2021 issue of the journal Frontiers in Psychiatry, researchers at University of California San Diego School of Medicine take the connection between wisdom, loneliness and biology further, reporting that wisdom and loneliness appear to influence — and/or be influenced by — microbial diversity of the gut.

The human gut microbiota is comprised of trillions of microbes — bacteria, viruses, fungi — that reside within the digestive tract. Researchers have known for a while about the “gut-brain axis,” which is a complex network that links intestinal function to the emotional and cognitive centers of the brain.

This two-way communication system is regulated by neural activity, hormones and the immune system; alterations can result in disruptions to stress response and behaviors, said the authors, from emotional arousal to higher-order cognitive abilities, such as decision-making.

Past studies have associated gut microbiota with mental health disorders including depression, bipolar disorder and schizophrenia, as well as personality and psychological traits regarded as key, biologically based components of wisdom. Recent research has connected the gut microbiome to social behavior, including findings that people with larger social networks tend to have more diverse gut microbiotas.

The new Frontiers in Psychiatry study involved 187 participants, ages 28 to 97, who completed validated self-report-based measures of loneliness, wisdom, compassion, social support and social engagement. The gut microbiota was analyzed using fecal samples. Microbial gut diversity was measured in two ways: alpha-diversity, referring to the ecological richness of microbial species within each individual and beta-diversity, referring to the differences in the microbial community composition between individuals.

“We found that lower levels of loneliness and higher levels of wisdom, compassion, social support and engagement were associated with greater phylogenetic richness and diversity of the gut microbiome,” said first author Tanya T. Nguyen, PhD, assistant professor of psychiatry at UC San Diego School of Medicine.

The authors said that the mechanisms that may link loneliness, compassion and wisdom with gut microbial diversity are not known, but observed that reduced microbial diversity typically represents worse physical and mental health, and is associated with a variety of diseases, including obesity, inflammatory bowel disease and major depressive disorder.

A more diverse gut microbiota may be less susceptible to invasion by outside pathogens, which could contribute to and help promote better resilience and stability of the community.

“It is possible that loneliness may result in decreased stability of the gut microbiome and, consequently, reduced resistance and resilience to stress-related disruptions, leading to downstream physiological effects, such as systemic inflammation,” the authors wrote.

“Bacterial communities with low alpha-diversity may not manifest overt disease, but they may be less than optimal for preventing disease. Thus, lonely people may be more susceptible to developing different diseases.”

The relationship between loneliness and microbial diversity was particularly strong in older adults, suggesting that older adults may be especially vulnerable to health-related consequences of loneliness, which is consistent with prior research.

Conversely, the researchers said that social support, compassion and wisdom might confer protection against loneliness-related instability of the gut microbiome. Healthy, diverse gut microflora may buffer the negative effects of chronic stress or help shape social behaviors that promote either wisdom or loneliness. They noted that animal studies suggest that gut microbiota may influence social behaviors and interactions, though the hypothesis has not been tested in humans.

The complexity of the topic and study limitations, such as the absence of data about individuals’ social networks, diet and degree of objective social isolation versus subjective reports of loneliness, argue for larger, longer studies, wrote the authors.

“Loneliness may lead to changes in the gut microbiome or, reciprocally, alterations of the gut milieu may predispose an individual to become lonely,” said Dilip V. Jeste, MD, Distinguished Professor of Psychiatry and Neurosciences at UC San Diego School of Medicine and senior author of the paper. “We need to investigate much more thoroughly to better understand the phenomenon of the gut-brain axis.”

Original source here.

Targeted opioid that hones in on inflamed tissues stops colitis pain without side effects

Study in mice points to promising treatment for pain in inflammatory bowel disease.

A targeted opioid that only treats diseased tissues and spares healthy tissues relieves pain from inflammatory bowel disease without causing side effects, according to new research published in the journal Gut.

The study, led by researchers at New York University College of Dentistry and Queen’s University in Ontario, was conducted in mice with colitis, an inflammatory bowel disease marked by inflammation of the large intestine.

Opioids, which are used to treat chronic pain in people with inflammatory bowel disease, relieve pain by targeting opioid receptors, including the mu opioid receptor. When opioids activate the mu opioid receptor in healthy tissues, however, they can cause severe and life-threatening side effects, including difficulty breathing, constipation, sedation, and addiction.

“We wanted to understand whether it is possible to activate this receptor only in diseased tissues and not in normal tissues,” said senior study author Nigel Bunnett, PhD, professor and chair of the Department of Molecular Pathobiology at NYU College of Dentistry. “Essentially, can you control pain without triggering these devastating side effects?”

The answer may lie in a novel opioid called NFEPP, discovered by Christoph Stein, MD, of Charité-Universitätsmedizin Berlin, a collaborator on the Gut study. NFEPP is a reengineered form of the opioid fentanyl; an added fluorine atom helps the drug to only bind to the mu opioid receptor in an acidic environment. This steers NFEPP to diseased tissues—sites of inflammation or injury—which become acidic due to changes in the tissues’ metabolism.

The researchers investigated the use of NFEPP and fentanyl in mice with colitis, which caused their gut tissue to be mildly acidic. Both NFEPP and fentanyl inhibited colon pain in mice with colitis. However, in sharp contrast to fentanyl, NFEPP did not cause side effects such as constipation, suppressed breathing, and altered movement. In healthy mice without inflammatory bowel disease, NFEPP did not alter pain activity or cause side effects.

“The preference of NFEPP for activating opioid receptors in acidic tissues accounts for its ability to selectivity relieve pain in the inflamed but not healthy colon,” said Bunnett. “By sparing healthy tissues, we avoided the detrimental side effects seen with fentanyl use.”

The researchers are now collecting tissue samples from people with inflammatory bowel disease to determine whether their colons, like those in mice, are also acidic environments. If so, they plan to test NFEPP’s ability to inhibit pain in the human gut and ultimately conduct clinical trials.  

“Treatments designed to preferentially engage opioid receptors in diseased tissues could offer the potential for effective pain relief without the side effects. These drugs would represent a major advance in the treatment of painful diseases, including inflammatory bowel disease and cancer,” said Bunnett. “More broadly, engineering drugs beyond pain treatments that target only diseased tissues could open the door to more effective and precise therapies for a wide range of disorders.”

Original source here.

Defects in a specific cell type may cause ulcerative colitis

There are many variants of “goblet cells” in the intestines and they seem to have different functions, according to a new study from the University of Gothenburg.

The entire inside of our intestines is covered by a thin layer of mucus that protects the fragile mucous membrane (mucosa) from bacteria and other microorganisms. If the microorganisms repeatedly come into contact with the intestinal mucosa, inflammation and even cell changes may result. These increase the risk of intestinal cancer. In a healthy colon, the mucus layer is up to a millimeter thick. This layer, which undergoes complete renewal hourly, is formed from cells of a special type, known as goblet cells.

Many different goblet cells

In the present study, now published in the journal Science, the scientists separated goblet cells from other cells and investigated which proteins each individual goblet cell expresses. There proved to be many different subtypes of these cells, and goblet cells’ functions turned out to vary more than researchers have previously realized.

“We believe this is important knowledge that may enable us to influence the protective function of the gut in the future. The system that maintains the protective intestinal mucus layer seems to be able to change its functions, and we could utilize this capacity by reprogramming the layer with various signals, for example by using new drugs”, says Malin Johansson, Associate Professor at Sahlgrenska Academy, University of Gothenburg, who led the research behind the present study.

Connected with ulcerative colitis

The most impermeable part of the mucus layer is formed by glands in the gut. In particular, the research team studied one of the specific types of goblet cells, found on the outermost surface of the mucosa. These goblet cells provide another type of mucus, which contributes to the protection of the gut but allows certain nutrients to pass through.

“If the function of these specific cells is impaired, we see that unprotected cell surfaces arise. These lead to inflammation, both in studies on mice and in samples from patients with ulcerative colitis,” Johansson says.

Appear to cause damage to mucosal protection

In the study, these specific goblet cells seemed to be repelled by the mucosa earlier than normal in patients with ulcerative colitis. Accordingly, the cells became fewer.

“To our surprise, we were able to observe this both in patients with active ulcerative colitis and in those who were temporarily asymptomatic. This indicates that premature rejection of the particular goblet cells we’ve been studying damages the mucus protection and that this is a contributing cause of inflammatory bowel disease. It could also be a partial explanation for these patients’ elevated cancer risk,” Johansson says.

Original source here.

A T-cell stimulatory protein and interleukin-10 synergize to prevent gut inflammation


Researchers have found an unexpected synergy between a T-cell stimulatory protein — the ICOS ligand — and interleukin-10, an immunoregulatory cytokine, to prevent inflammatory bowel disease in mice.

The study will aid the understanding of, and future research into, this immune disorder, which includes Crohn’s disease and ulcerative colitis.

Interleukin-10, or IL-10, was already known as a major player to prevent gut inflammation by establishing and maintaining immune homeostasis in the gut, where it is vital for the host to have a peaceful coexistence with normal intestinal microbes, while the immune system still stands guard against pathogens. IL-10 is produced by CD4+ T-regulatory cells in the gut.

ICOS ligand, or ICOSL, is expressed on B cells and dendritic cells of the immune system, and it helps to control T-cell activation and differentiation, two steps of the host immune response to microbes and microbial pathogens. Both IL-10 and ICOSL were known risk alleles for inflammatory bowel disease, but their synergistic interaction was not known.

The research, published in the Proceedings of the National Academies of Science, was led by Craig Maynard, Ph.D., assistant professor in the University of Alabama at Birmingham Department of Pathology.  

“Collectively, our data identify a synergy between two inflammatory bowel disease-related pathways — T-cell-derived IL-10 and ICOSL-dependent anti-commensal antibodies — that promotes mutualism with the gut microbiota,” Maynard said. “Furthermore, we identify ICOSL deficiency as an effective platform for exploring the functions of anti-commensal antibodies in host–microbiota mutualism.”

In humans, complete deficiency of ICOSL or the ICOS receptor that ICOSL bind to causes a combined immunodeficiency with repeated bacterial and viral infections. In contrast, mice with ICOSL or ICOS receptor deficiencies maintain a healthy gut homeostasis under specific pathogen-free conditions. 

In the current study, the UAB researchers found that ICOSL-deficient mice — like the ICOS receptor-deficient mice Maynard’s group has previously studied — harbored increased frequencies and numbers of IL-10-producing CD4+ T cells, particularly in the proximal colon. 

When researchers transiently depleted the IL-10-producing cells in the ICOSL-deficient mice, they saw a striking change — rapid onset of severe inflammation in the proximal colon.

While the number of IL-10-producing CD4+ T cells was increased in the ICOSL-deficient mice, the numbers of colon-associated T-follicular helper cells and the plasma cells that produce immunoglobulin A and immunoglobulin G, or IgA and IgG respectively, were decreased.  

The mice also had dramatic reductions in antibodies against normal gut microbes, which included a limited recognition of antigens implicated in the progression of inflammatory bowel disease. These included flagellin antigens derived from several members of the family Lachnospiraceae. These bacteria are known to enrich in the mucus-associated communities of the gut, and Crohn’s disease patients have antibodies against two of the Lachnospiraceae flagellin antigens. The mice also had reduced IgA and IgG antibodies that targeted antigens from multiple species of anaerobic bacteria known to be associated with active inflammatory bowel disease.

Simultaneous ablation of both pathways, ICOSL and IL-10, in newborn mice caused severe colitis with evidence of disease as early as four weeks, if the mice were fostered with ICOSL-deficient dams. However, this early onset intestinal inflammation was delayed when the newborn mice were fostered by ICOSL-sufficient dams, showing a protective role for maternal antibodies.

Maynard says the overall results suggest that induction of ICOSL-dependent antibodies and T-cell-derived IL-10 may be simultaneous host adaptations to microbial occupation of a niche near the epithelium in the gut. “Future exploration of the specific microbes that drive these responses,” he said, “could potentially identify novel antigen-specific approaches to bolster mucosal immune defenses.”

Original source here.

A T-cell stimulatory protein and interleukin-10 synergize to prevent gut inflammation


Researchers have found an unexpected synergy between a T-cell stimulatory protein — the ICOS ligand — and interleukin-10, an immunoregulatory cytokine, to prevent inflammatory bowel disease in mice.

The study will aid the understanding of, and future research into, this immune disorder, which includes Crohn’s disease and ulcerative colitis.

Interleukin-10, or IL-10, was already known as a major player to prevent gut inflammation by establishing and maintaining immune homeostasis in the gut, where it is vital for the host to have a peaceful coexistence with normal intestinal microbes, while the immune system still stands guard against pathogens. IL-10 is produced by CD4+ T-regulatory cells in the gut.

ICOS ligand, or ICOSL, is expressed on B cells and dendritic cells of the immune system, and it helps to control T-cell activation and differentiation, two steps of the host immune response to microbes and microbial pathogens. Both IL-10 and ICOSL were known risk alleles for inflammatory bowel disease, but their synergistic interaction was not known.

The research, published in the Proceedings of the National Academies of Science, was led by Craig Maynard, Ph.D., assistant professor in the University of Alabama at Birmingham Department of Pathology.  

“Collectively, our data identify a synergy between two inflammatory bowel disease-related pathways — T-cell-derived IL-10 and ICOSL-dependent anti-commensal antibodies — that promotes mutualism with the gut microbiota,” Maynard said. “Furthermore, we identify ICOSL deficiency as an effective platform for exploring the functions of anti-commensal antibodies in host–microbiota mutualism.”

In humans, complete deficiency of ICOSL or the ICOS receptor that ICOSL bind to causes a combined immunodeficiency with repeated bacterial and viral infections. In contrast, mice with ICOSL or ICOS receptor deficiencies maintain a healthy gut homeostasis under specific pathogen-free conditions. 

In the current study, the UAB researchers found that ICOSL-deficient mice — like the ICOS receptor-deficient mice Maynard’s group has previously studied — harbored increased frequencies and numbers of IL-10-producing CD4+ T cells, particularly in the proximal colon. 

When researchers transiently depleted the IL-10-producing cells in the ICOSL-deficient mice, they saw a striking change — rapid onset of severe inflammation in the proximal colon.

While the number of IL-10-producing CD4+ T cells was increased in the ICOSL-deficient mice, the numbers of colon-associated T-follicular helper cells and the plasma cells that produce immunoglobulin A and immunoglobulin G, or IgA and IgG respectively, were decreased.  

The mice also had dramatic reductions in antibodies against normal gut microbes, which included a limited recognition of antigens implicated in the progression of inflammatory bowel disease. These included flagellin antigens derived from several members of the family Lachnospiraceae. These bacteria are known to enrich in the mucus-associated communities of the gut, and Crohn’s disease patients have antibodies against two of the Lachnospiraceae flagellin antigens. The mice also had reduced IgA and IgG antibodies that targeted antigens from multiple species of anaerobic bacteria known to be associated with active inflammatory bowel disease.

Simultaneous ablation of both pathways, ICOSL and IL-10, in newborn mice caused severe colitis with evidence of disease as early as four weeks, if the mice were fostered with ICOSL-deficient dams. However, this early onset intestinal inflammation was delayed when the newborn mice were fostered by ICOSL-sufficient dams, showing a protective role for maternal antibodies.

Maynard says the overall results suggest that induction of ICOSL-dependent antibodies and T-cell-derived IL-10 may be simultaneous host adaptations to microbial occupation of a niche near the epithelium in the gut. “Future exploration of the specific microbes that drive these responses,” he said, “could potentially identify novel antigen-specific approaches to bolster mucosal immune defenses.”

Original source here.

Gluten intake not linked with IBD risk


Researchers have found an unexpected synergy between a T-cell stimulatory protein — the ICOS ligand — and interleukin-10, an immunoregulatory cytokine, to prevent inflammatory bowel disease in mice.

By Alex Young

Hamed Khalili, MD, MPH, from Massachusetts General Hospital, and colleagues wrote that patients with inflammatory bowel often report improvements in symptoms after restricting their gluten intake.

“This may be due to undiagnosed celiac disease, which constitutes a substantial portion of celiac cases, or an effect of gluten on IBD activity,” they wrote. “Evidence for the role of gluten in gut inflammation, independent of celiac disease, is scant.”

Researchers conducted a prospective cohort study of 208,280 individuals from the Nurses’ Health Study (NHS), NHSII and Health Professionals Follow-up study to determine the relationship between gluten intake and risk for IBD. All patients did not have IBD or celiac disease at baseline and completed semi-quantitative food frequency questionnaires.

Investigators used that data to estimate the risk for IBD based on quintiles of average-adjusted dietary gluten intake over the course of follow-up.

Khalili and colleagues identified 337 cases of Crohn’s disease and 447 cases of UC over 5,115,265 person-years of follow-up.

Compared with individuals in the lowest quintile of gluten intake, individuals in the highest quintile were not at increased risk for CD (adjusted HR = 1.16; 95% CI, 0.82-1.64) or UC (aHR = 1.04; 95% CI, 0.75-1.44). Khalili and colleagues wrote that their findings did not change after adjusting for primary sources of gluten intake.

“Long-term intake of gluten did not confer an increased risk of developing IBD in adults [in the U.S.], even among high-risk participants with a family history of IBD,” they wrote. “Our findings do not support the theory that gluten contributes to IBD development. This is important because of the established health benefits of a diet rich in whole grains.

“Gluten should not be empirically avoided in persons without celiac disease for the purpose of preventing IBD.”

Original source here.

Ingredients

  • 1 sweet potato (sliced into thin rounds)
  • 1 tsp coconut oil
  • 7 eggs
  • 3 garlic cloves (minced)
  • 8 stalks spring onion (chopped)
  • 120 baby spinach (chopped)
  • 1 tomato (diced)
  • Sea salt & black pepper (to taste)

Method

  1. Preheat the oven to 220ºC (425ºF). Grease a glass pie plate with a bit of coconut oil. Cover the base and sides of the plate with the sweet potato rounds. Layer the rounds until no glass is showing. Bake in the oven for 15 minutes.
  2. Meanwhile, crack eggs into a mixing bowl and whisk well. Set aside.
  3. Heat coconut oil in a skillet over medium heat. Add in minced garlic and spring onions. Sautee for three to five minutes. Add in chopped spinach and sautee just until wilted. Remove from heat.
  4. Add spinach mix and diced tomatoes into the egg mix. Season with salt and pepper. Stir well.
  5. Remove sweet potato crust from the oven. Pour egg mixture over top of the crust. Reduce the temperature of the oven to 190ºC (375ºF). Place quiche in the oven and bake for 30 to 40 minutes or until the top is golden brown.
  6. Remove from the oven and cut into slices. Enjoy!

Cooking time

30-40 mins