Tag Archives: diet

Which Diet is Best for Irritable Bowel Syndrome? A Randomized Trial

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A Rej et al. Clin Gastroenterol Hepatol 2022; 20: 2876-2887. Open Access! Efficacy and Acceptability of Dietary Therapies in Non-Constipated Irritable Bowel Syndrome: A Randomized Trial of Traditional Dietary Advice, the Low FODMAP Diet, and the Gluten-Free Diet

Methods: In patients (n=99) with Rome IV–defined non-constipated IBS, outcomes after randomization to one of three diets were compared. The “traditional dietary advice” group: “Its principles include adopting healthy, sensible eating patterns such as having regular meals, never eating too little/too much, maintaining adequate hydration, and reducing the intake of (1) alcohol/caffeine/fizzy drinks, (2) fatty/spicy/processed foods, (3) fresh fruit to a maximum of 3 per day, (4) fiber and other commonly consumed gas-producing foods (eg, beans, bread, sweeteners, etc), and (5) addressing any perceived food intolerances (eg, dairy).” (Link: National Institute for Health and Care Excellence advice on IBS mgt). The Gluten-Free diet allowed for cross-contamination. All patients had specialist dietary counseling.

Key findings:

  • All three diets resulted in improvement. The primary end point of ≥50-point reduction in IBS-SSS was met by 42% (n = 14/33) undertaking TDA, 55% (n = 18/33) for LFD, and 58% (n = 19/33) for GFD (P = .43)
  • Alterations in stool dysbiosis index were similar across the diets, with 22%–29% showing reduced dysbiosis
  • “The pragmatic study design, whereby the responsibility was left on patients to undertake the diets following appropriate education, means our findings can be generalized”

My take: All three diet approaches would be appropriate to reduce IBS symptoms, thought the TDA is the easiest for patients.

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What is An Emulsifier and Are They Safe in Our Diets?

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Two recent articles examine emulsifiers and their potential impact on the GI tract and beyond.

Levine et al provide a good overview of the topic of emulsifiers. Key points:

  • Emulsifiers allow “the mixing of water and and water-soluble agents with fats and fat-soluble agents that is they possess both hydrophilic and lipophilic properties”
  • The FDA “has been responsible for approving the use of all direct food additives” (n=~3000) and “for regulatory purposes, [the FDA excluded] some substances that were generally regarded as safe (GRAS) (n=~450)…Precisely how some emulsifiers gained GRAS status is unclear.
  • “Lecithin” is derived from the Greek name for egg yolk (lekithos). “Over the years the use of the term “lecithin” has been taken to include various mixtures of different phospholipids” (not just phosphatidylcholine).
  • Lecithin can provide the substrate “for the production of trimethylamine N-oxide (TMAO)…linked to cardiac events and cardiovascular inflammation.”
  • “The list of emulsifiers that are widely used, but not considered GRAS, most notably include polysorbate 80 (p80), carboxymethylcellulose (CMC) and carrageenan…these emulsifiers have been linked to the disruption of the microbiota and gut mucosal lining…In addition, low-grade inflammation [has been] associated with consumption of emulsifying agents such as CMC and p80” [in mouse models].
  • The International Organization for the Study of Inflammatory Bowel Disease (IOIBD) has recommended that IBD patients “limit consumption of certain commonly encountered synthetic emulsifiers, specifically carboxymethylcellulose (E466/cellulose gum) and polysorbate 80 (E433) [which] are present in many processed foods, such as ice cream. The group also recommends a decrease in foods containing carrageenan”

In the second study by Chassaing et al with 16 healthy adults, the authors studied the effects of CMC in those with an emulsifier-free diet (n=9) or an identical diet enriched with CMC (n=7).

Key findings:

  • Relative to control subjects, CMC consumption modestly increased postprandial abdominal discomfort and perturbed gut microbiota composition in a way that reduced its diversity
  • CMC-fed subjects exhibited changes in the fecal metabolome, particularly reductions in short-chain fatty acids and free amino acids
  • 2 subjects consuming CMC who exhibited increased microbiota encroachment into the normally sterile inner mucus layer, a central feature of gut inflammation, as well as stark alterations in microbiota composition

My take: The dramatic increase in the prevalence of IBD over the past 50 years indicates a strong influence of environment factors, particularly diet. Determining which of these factors are most important will be challenging. These articles indicate that some emulsifiers could be contributing to GI tract inflammation and non-GI tract inflammation as well.

The challenges with identifying dietary factors relate to difficulties with using randomized controlled trials (especially eliminating delicious foods) to assess the impact over a long period of follow-up.

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New and Improved Biomarker Blood Test for Crohn’s Disease?

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A recent study (G D’Haens, O Kelly, R Battat et al. Gastroenterol 2020; 158: 515-26,editorial 463) describes the development and validation of a blood test panel to assess Crohn’s disease (CD) endoscopic activity level.  The authors evaluated a blood test which measured 13 proteins in the blood using samples from 278 patients.  Then there were two validation cohorts:

  • 116 biologic-naive CD patients -cohort 1
  • 195 biologic-exposed CD patients -cohort 2

The blood tests were used to develop an endoscopic healing index (EHI) score (0-100). Higher scores indicate greater disease activity.

Key findings:

  • EHI values below 20 identified remission with a sensitivity of 97.1%  and 83.2% in cohorts 1 & 2 respectively; specificity was 69% and 37% respectively.
  • EHI values below 50 points identified patients with highest specificity of 100% and 88% in cohorts 1 and 2 respectively.
  • EHI AUROC (area under the receiver operating characteristic curve) did not differ significantly from that of fecal calprotectin and were higher than measurement of serum CRP (in cohort 1 but not cohort 2).

The editorial notes that the EHI performed much better in younger, biologically-naive patients and that the EHI could potentially be incorporated into a treat-to-target strategy which would potentially entail followup endoscopy in those with EHI >50.

My take: While the stool calprotectin has some logistical barriers in many patients, the EHI is likely a much more expensive test and needs further validation.  For now, the combination of CRP and calprotectin are the best noninvasive biomarkers to assess CD activity.

Briefly noted: Vedolizumab-Induced Pulmonary Toxicity -Case report of a patient with ulcerative colitis who developed interstitial lung disease (Gastroenterol 2020; 158: 478-9).

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Good Food and Bad Food for Crohn’s Disease -No Agreement

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As noted in a previous blog (IBD Briefs August 2019), there have been numerous diets proposed to help with Crohn’s disease.   The chart below illustrates the lack of any consensus.

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Bad Diets –>High Mortality

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A recent article in Lancet (“Health effects of dietary risks in 195 countries, 1990–2017:
a systematic analysis for the Global Burden of Disease Study 2017″ -open access) estimated that bad diets lead to 11 million deaths per year. Thanks to Ana Ramirez for sending me this article. “High intake of sodium, low intake of whole grains, and low intake of fruits were the leading dietary risk factors for deaths and DALYs globally and in many countries.”

A summary of this study was reported on NPR: Bad Diets Are Responsible For More Deaths Than Smoking, Global Study Finds

An excerpt:

About 11 million deaths a year are linked to poor diet around the globe…

As part of a new study published in The Lancet, researchers analyzed the diets of people in 195 countries using survey data, as well as sales data and household expenditure data. Then they estimated the impact of poor diets on the risk of death from diseases including heart disease, certain cancers and diabetes. (They also calculated the number of deaths related to other risk factors, such as smoking and drug use, at the global level.)…

“Generally, the countries that have a diet close to the Mediterranean diet, which has higher intake of fruits, vegetables, nuts and healthy oils [including olive oil and omega-3 fatty acids from fish] are the countries where we see the lowest number of [diet-related] deaths,” …

What would happen if everyone around the globe began to eat a healthy diet, filling three-fourths of their plates with fruits, vegetables and whole grains? We’d run out…

Improving diets won’t be easy: A range of initiatives may be needed, including nutrition education and increased access to healthy foods, as well as rethinking agricultural production.

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Big Data for Personalized Diets

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A recent commentary in the NY Times discusses the future of personalized diets.  Along the way, the commentary notes how little we know about the best diet and how difficult nutrition research is to complete.

The A.I. Diet by Eric Topol who is the author of the forthcoming “Deep Medicine,” from which this essay is adapted

An excerpt:

It turns out, despite decades of diet fads and government-issued food pyramids, we know surprisingly little about the science of nutrition. It is very hard to do high-quality randomized trials: They require people to adhere to a diet for years before there can be any assessment of significant health outcomes…

Meanwhile, the field has been undermined by the food industry, which tries to exert influence over the research it funds.

Now the central flaw in the whole premise is becoming clear: the idea that there is one optimal diet for all people…

Only recently, with the ability to analyze large data sets using artificial intelligence, have we learned how simplistic and naïve the assumption of a universal diet is. It is both biologically and physiologically implausible: It contradicts the remarkable heterogeneity of human metabolism, microbiome and environment, to name just a few of the dimensions that make each of us unique. A good diet, it turns out, has to be individualized.

My take: Dr. Topol makes some important observations and he is right that there is not a simple diet solution for everyone.  Nevertheless, in the near future, personalized medicine is not coming to our dinner tables and we have to rely on what we know right now –don’t eat too much sugar, do eat more fruits and vegetables, and don’t eat too much.

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Low Free Sugar Diet for Nonalcoholic Fatty Liver Disease in Adolescent Boys

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A recent randomized study (Jeffrey B. Schwimmer, MD1,2; Patricia Ugalde-Nicalo, MD1; Jean A. Welsh, PhD, MPH, RN3,4,5; et al JAMA. 2019;321(3):256-265. doi:10.1001/jama.2018.20579) examined the beneficial effects of a low free sugar diet for Nonalcoholic Fatty Liver Disease (NAFLD) in adolescent boys.  Congratulations to the authors, particularly to Miriam Vos (my Emory colleague & corresponding author) and Jeffrey Schwimmer (whose training overlapped with mine in Cincinnati).

Key finding:

“In this randomized clinical trial that included 40 adolescent boys aged 11 to 16 years with nonalcoholic fatty liver disease followed up for 8 weeks, provision of a diet low in free sugars compared with usual diet resulted in a greater reduction in hepatic steatosis [based on MRI] from 25% to 17% in the low free sugar diet group and from 21% to 20% in the usual diet group, a statistically significant difference of −6.23% when adjusted for baseline.”

Summary of this study in NY Times: To Fight Fatty Liver, Avoid Sugary Foods and Drinks

An excerpt from NY Times:

To make the diet easier and more practical for the children in the limited-sugar group to follow, the researchers asked their families to follow it as well. They tailored the diet to the needs of each household by examining the foods they consumed in a typical week and then swapping in lower sugar alternatives. If a family routinely ate yogurts, sauces, salad dressings and breads that contained added sugar, for example, then the researchers provided them with versions of those foods that did not have sugar added to them.

Fruit juices, soft drinks and other sweet drinks were forbidden. They were replaced with unsweetened iced teas, milk, water and other nonsugary beverages. Dietitians prepared and delivered meals to the families twice a week, which helped them stick to their programs.

Full abstract:

Importance  Pediatric guidelines for the management of nonalcoholic fatty liver disease (NAFLD) recommend a healthy diet as treatment. Reduction of sugary foods and beverages is a plausible but unproven treatment.

Objective  To determine the effects of a diet low in free sugars (those sugars added to foods and beverages and occurring naturally in fruit juices) in adolescent boys with NAFLD.

Design, Setting, and Participants  An open-label, 8-week randomized clinical trial of adolescent boys aged 11 to 16 years with histologically diagnosed NAFLD and evidence of active disease (hepatic steatosis >10% and alanine aminotransferase level ≥45 U/L) randomized 1:1 to an intervention diet group or usual diet group at 2 US academic clinical research centers from August 2015 to July 2017; final date of follow-up was September 2017.

Interventions  The intervention diet consisted of individualized menu planning and provision of study meals for the entire household to restrict free sugar intake to less than 3% of daily calories for 8 weeks. Twice-weekly telephone calls assessed diet adherence. Usual diet participants consumed their regular diet.

Main Outcomes and Measures  The primary outcome was change in hepatic steatosis estimated by magnetic resonance imaging proton density fat fraction measurement between baseline and 8 weeks. The minimal clinically important difference was assumed to be 4%. There were 12 secondary outcomes, including change in alanine aminotransferase level and diet adherence.

Results  Forty adolescent boys were randomly assigned to either the intervention diet group or the usual diet group (20 per group; mean [SD] age, 13.0 [1.9] years; most were Hispanic [95%]) and all completed the trial. The mean decrease in hepatic steatosis from baseline to week 8 was significantly greater for the intervention diet group (25% to 17%) vs the usual diet group (21% to 20%) and the adjusted week 8 mean difference was −6.23% (95% CI, −9.45% to −3.02%; P < .001). Of the 12 prespecified secondary outcomes, 7 were null and 5 were statistically significant including alanine aminotransferase level and diet adherence. The geometric mean decrease in alanine aminotransferase level from baseline to 8 weeks was significantly greater for the intervention diet group (103 U/L to 61 U/L) vs the usual diet group (82 U/L to 75 U/L) and the adjusted ratio of the geometric means at week 8 was 0.65 U/L (95% CI, 0.53 to 0.81 U/L; P < .001). Adherence to the diet was high in the intervention diet group (18 of 20 reported intake of <3% of calories from free sugar during the intervention). There were no adverse events related to participation in the study.

Conclusions and Relevance  In this study of adolescent boys with NAFLD, 8 weeks of provision of a diet low in free sugar content compared with usual diet resulted in significant improvement in hepatic steatosis. However, these findings should be considered preliminary and further research is required to assess long-term and clinical outcomes.

 

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Better Diet -Less Fatty Liver

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A recent study (J Ma et al. Gastroenterol 2018; 155: 107-17) shows that a “better diet” was associated with less liver fat.

Among the 1521 participants form a Framingham Heart Study cohort (Mean age 51 years at start of study), the authors assessed diet with a 125-item Harvard food frequency questionnaire and liver fat using liver-phantom ratio (LPR) on CT images between 2002-2005 and then again 2008-2011.  They specifically looked at 2 diet scores:

  • Mediterranean-style diet score (MDS)
  • Alternative Healthy Eating Index (AHEI)

Key findings:

  • For each 1 standard deviation increase in MDS, the LPR increased (less liver fat) by 0.57 and the odds for incident fatty liver decreased by 26% (P=.002)
  • Similarly, for each 1 standard deviation increase in AHEI, LPR increased by 0.56 and the odds for incident fatty liver decreased by 21% (P=.02)

My take: This study shows that Improved diet quality over 6 years was associated with reduced liver fat accumulation

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Dietary Patterns in First Year of Life May Increase Risk of Celiac Autoimmunity

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M Barroso et al. Gastroenterol 2018; 154: 2087-96.

Background: “Western-like diets –mainly characterized by high intake of red and processed meats, refined grains, simple sugars, and saturated fats and low intake of fruits, vegetables, and whole grains– have been associated with low-grade chronic inflammation, which is involved in the etiology of inflammatory conditions.” Ref: Br J Nutr 2015; 114: 999-1012.

To examine how diet may influence the development of celiac autoimmunity, defined by TG2A positivity, the authors examined a subset of patients (n=1997) from the prospective Generation R study (Netherlands); 27 in this cohort developed celiac autoimmunity (1.4%).

Key finding:

  • Higher adherence to a “prudent” diet which had a higher intake of vegetables, vegetable oils, pasta, and grains and low consumption of refined cereals and sweet beverages at 1 year of age was associated with a lower odds of celiac autoimmunity at 6 years of age with an odds ratio of 0.67.

This study is limited by the relatively low number who had celiac autoimmunity and by its use of a food questionnaire.

My take: This study indicates that diet plays a role in the development of celiac along with other disease, but this likely involves a complex mix of components rather than a single toxic agent.

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Diet and Stress in Pediatric Eosinophilic Esophagitis

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When it comes to eosinophilic esophagitis (EoE), I sometimes worry that some treatments are worse than the disease, depending on the severity of the EoE. A recent study (C Case et al. JPGN 2017; 65: 281-84) indicates that dietary therapy is often stressful for families.

This study examined children ages 2-18 during an annual American Partnership for Eosinophilic Diseases (APFED.org) patient education conference. What I found most interesting was Table 3. “Stress associated with eosinophilc esophagitis.”

Some of the data:

  • In response to ‘how stressful do you find the following since your child’s diagnosis of EoE?’ Family structure at mealtimes: Not stressful 13.5%, somewhat stressful 21.6%, moderate stressful 16.2%, significant stressful 32.4%, and severe stressful 16.2%
  • In response to ‘how stressful do you find the following since your child’s diagnosis of EoE? Buying and cooking separate foods/meals for your child: Not stressful 2.6%, somewhat stressful 21.1%, moderate stressful 21.1%, significant stressful 31.6%, and severe stressful 23.7%
  • In response to ‘how stressful do you find the following since your child’s diagnosis of EoE? Financial strain due to cost of food: Not stressful 10.5%, somewhat stressful 21.1%, moderate stressful 18.4%, significant stressful 23.7%, and severe stressful 36.3%
  • What is your current stress level in response to your child’s EoE? Not stressful 2.6%, somewhat stressful 15.8%, moderate stressful 36.8%, significant stressful 42.1%, and severe stressful 2.6%
  • 62% of respondents indicated that child’s EoE has affected marital relationship.

In addition, the study documented that “half of youth were affected by worry, anger, and sadness related to specialized diets.”  As this study relied on participants at an APFED meeting, this could skew the EoE population to be more severely affected.

My take: This study shows the emotional burden that dietary treatment of EoE places on families.

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