Research
The Microscopic Colitis Foundation seeks to increase the amount of research and research funding devoted to identifying root causes and new treatments for the disease. A search of PubMed demonstrates the lack of research on this growing, but neglected Inflammatory Bowel Disease (IBD).
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High dose vitamin D3 reduces relapse rates for Crohn's disease patients
In a small double-blind, random
controlled trial, 34 Crohn's patients were recently treated with either
1,000 IU or 10,000 IU of vitamin D3 for a period of 12 months (Narula,
Cooray, Anglin, & Marshall, 2016).1 All subjects were in remission
from the clinical symptoms of Crohn's disease at the beginning of the
trial. During the 12 months, half of the original 16 low dose patients
dropped out of the trial, and one third of the original 18 high dose
patients dropped out. Apparently side effects were not the main reason
for the dropouts, since more low dose patients than high dose patients
left the trial early. It was reported that only one subject from each
group left because of side effects. The low dose dropout reported
heartburn and nausea side effects, and the high dose dropout reported
acne. No one showed any symptoms of toxicity, and the supplementation
was reported as well tolerated. According to the report, about half of
the subjects in each group were already taking a vitamin D supplement
before enrolling in the study.
The researchers found (not surprisingly) that the high dose treatment significantly increased blood levels of vitamin D. The average level increased from 29 ng/ml (73 nmol/L) to 64 ng/ml (161 nmol/L) after taking 10,000 IU daily for 12 months. By contrast, the low dose treatment only increased blood levels of vitamin D by a small amount. Average levels increased from 28 ng/ml (71 nmol/mL) to 33 ng/ml (83 nmol/L). For the subjects who remained in the study for the duration, the high dose patients experienced no relapses of clinical symptoms, whereas 3 of the remaining 8 low dose patients experienced relapses (38 %). Both groups noted significant reduction in depression symptoms.
There is a good chance that these beneficial effects were due to a reduction in intestinal permeability (leaky gut), as demonstrated by previous research (Raftery et al., 2015).2 In this earlier double-blind, randomized, placebo-controlled study, 27 Crohn's disease patients who were in remission at the beginning of the study were given either 2,000 IU of vitamin D3 per day, or a placebo.
After 3 months of treatment, the researchers found that vitamin D blood levels of the treated group were significantly higher than the controls, and intestinal permeability integrity of the treated patients was maintained. By contrast, intestinal permeability had increased in the patients who received the placebos.
It was noted that patients who had vitamin D blood levels equal to or above 30 ng/ml (75 nmol/L) had significantly lower C-reactive protein (CRP) levels, higher levels of natural antimicrobial proteins (AMPs), a significantly lower Crohn's disease activity index (CDAI), and a higher quality of life. AMPs are natural defensive proteins produced by most organisms, including the human body (Bahar, & Ren, 2013).3 They are part of the innate immune system and they serve as a first line of defense against invaders such as bacteria, viruses, and fungi.
So could high doses of vitamin D3 be used to treat microscopic colitis? Maybe. It appears that serum 25-hydroxyvitamin D [25(OH)D] levels above 40 ng/ml (100 nmol/L) might possibly be beneficial for all IBD patients, based on these research data for Crohn's disease patients. It also appears that IBD patients can safely take relatively high doses of supplemental vitamin D3 for extended periods without undue risk of an overdose condition. In the first study cited above, patients were treated with daily doses of 10,000 IU of vitamin D3 for 12 months, and the researchers reported that the treatment was well tolerated. Average blood levels of vitamin D went from 29 ng/ml (73 nmol/L) to 64 ng/ml (161 nmol/L) during the 12 months of treatment. Hopefully someone will do the research necessary to verify that this line of treatment may be beneficial for all types of inflammatory bowel disease, including MC.
1. P-064 Impact of high dose vitamin D3 supplementation in treatment of Crohn's disease in remission: A randomized double-blind controlled study
Narula, N., Cooray, M., Anglin, R., & Marshall, J. (2016). . Inflammatory Bowel Diseases, 22(P-064), Retrieved from http://journals.lww.com/ibdjournal/Abstract/2016/03001/P_064_Impact_of_High_Dose_Vitamin_D3.89.aspx
2. Effects of vitamin D supplementation on intestinal permeability, cathelicidin and disease markers in Crohn’s disease: Results from a randomised double-blind placebo-controlled study
Raftery, T., Martineau, A. R., Greiller, C. L., Ghosh, S., McNamara, D., Bennett, K., . . . O’Sullivan, M. (2015). United European Gastroenterology Journal, 3(3), 294–302. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC440538/
3. Antimicrobial Peptides
Bahar, A. A., & Ren, D. (2013). Pharmaceuticals (Basel), 6(12), 1543–1575. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3873676/
The researchers found (not surprisingly) that the high dose treatment significantly increased blood levels of vitamin D. The average level increased from 29 ng/ml (73 nmol/L) to 64 ng/ml (161 nmol/L) after taking 10,000 IU daily for 12 months. By contrast, the low dose treatment only increased blood levels of vitamin D by a small amount. Average levels increased from 28 ng/ml (71 nmol/mL) to 33 ng/ml (83 nmol/L). For the subjects who remained in the study for the duration, the high dose patients experienced no relapses of clinical symptoms, whereas 3 of the remaining 8 low dose patients experienced relapses (38 %). Both groups noted significant reduction in depression symptoms.
There is a good chance that these beneficial effects were due to a reduction in intestinal permeability (leaky gut), as demonstrated by previous research (Raftery et al., 2015).2 In this earlier double-blind, randomized, placebo-controlled study, 27 Crohn's disease patients who were in remission at the beginning of the study were given either 2,000 IU of vitamin D3 per day, or a placebo.
After 3 months of treatment, the researchers found that vitamin D blood levels of the treated group were significantly higher than the controls, and intestinal permeability integrity of the treated patients was maintained. By contrast, intestinal permeability had increased in the patients who received the placebos.
It was noted that patients who had vitamin D blood levels equal to or above 30 ng/ml (75 nmol/L) had significantly lower C-reactive protein (CRP) levels, higher levels of natural antimicrobial proteins (AMPs), a significantly lower Crohn's disease activity index (CDAI), and a higher quality of life. AMPs are natural defensive proteins produced by most organisms, including the human body (Bahar, & Ren, 2013).3 They are part of the innate immune system and they serve as a first line of defense against invaders such as bacteria, viruses, and fungi.
So could high doses of vitamin D3 be used to treat microscopic colitis? Maybe. It appears that serum 25-hydroxyvitamin D [25(OH)D] levels above 40 ng/ml (100 nmol/L) might possibly be beneficial for all IBD patients, based on these research data for Crohn's disease patients. It also appears that IBD patients can safely take relatively high doses of supplemental vitamin D3 for extended periods without undue risk of an overdose condition. In the first study cited above, patients were treated with daily doses of 10,000 IU of vitamin D3 for 12 months, and the researchers reported that the treatment was well tolerated. Average blood levels of vitamin D went from 29 ng/ml (73 nmol/L) to 64 ng/ml (161 nmol/L) during the 12 months of treatment. Hopefully someone will do the research necessary to verify that this line of treatment may be beneficial for all types of inflammatory bowel disease, including MC.
1. P-064 Impact of high dose vitamin D3 supplementation in treatment of Crohn's disease in remission: A randomized double-blind controlled study
Narula, N., Cooray, M., Anglin, R., & Marshall, J. (2016). . Inflammatory Bowel Diseases, 22(P-064), Retrieved from http://journals.lww.com/ibdjournal/Abstract/2016/03001/P_064_Impact_of_High_Dose_Vitamin_D3.89.aspx
2. Effects of vitamin D supplementation on intestinal permeability, cathelicidin and disease markers in Crohn’s disease: Results from a randomised double-blind placebo-controlled study
Raftery, T., Martineau, A. R., Greiller, C. L., Ghosh, S., McNamara, D., Bennett, K., . . . O’Sullivan, M. (2015). United European Gastroenterology Journal, 3(3), 294–302. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC440538/
3. Antimicrobial Peptides
Bahar, A. A., & Ren, D. (2013). Pharmaceuticals (Basel), 6(12), 1543–1575. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3873676/
Research verification that IBDs can be successfully treated by diet changes
A new day has dawned in the treatment of IBDs. On
December 27, 2016, the Journal of Clinical Gastroenterology published
an article about a treatment trial that was based on the use of the
specific carbohydrate diet (SCD) to bring remission in pediatric Crohn's
and ulcerative colitis (UC) patients. Out of 12 pediatric patients who
agreed to participate in the study for a period of 12 weeks, 2 dropped
out because they were unable to stick with the diet, 2 saw no benefits
from the treatment, and the other 8 showed sufficient improvement in
both clinical symptoms and laboratory markers to be considered to be in
remission at the end of the trial (Suskind et al., 2016).1 At the end
of the 12-week period their mean C reactive protein level was
significantly reduced, and their gut bacteria profile showed definite
improvement.
Now this was obviously a very small trial, and it only covered a period of 12 weeks. But it's an important first step in establishing the legitimacy of dietary treatments for IBDs. The truth is, complimentary and alternative medicine (CAM) treatment methods for IBDs have been in common use for some time, especially in the case of pediatric patients, but the official side of mainstream medicine has continued to try to ignore the trend. Some sources claim that in some locations as many as 70 % of pediatric IBD patients are routinely treated by CAM methods(Wong et al., 2009).2 While CAM treatments don't always involve diet changes, in many cases they do. Wong et al, (2009) noted that:
In the Markowitz et al study, patients were included based on census data from the 2000 US Census identifying the total number of children living in the surveyed area (16). They estimated that the prevalence of CAM was 50.8% within the previous 12 months. The most common types of CAM used were identified as nutritional supplements, followed by special diets (milk-/dairy-free, low carbohydrates, gluten-free), and only a small percentage used herbal remedies (5.1%).
The SCD is very similar to the diet that the Microscopic Colitis Foundation has suggested for treating microscopic colitis. The primary difference is that the classic SCD allows yogurt, a fermented dairy product. Experience shows (and IgA-based antibody stool tests verify) that most microscopic colitis (MC) patients produce antibodies to casein (the primary protein in all dairy products). Some authors writing articles that interpret the research published by Suskind et al., (2016) have assumed that all dairy products were excluded during the study, but it's unclear whether that's actually true, based on the abstract of the original research report. If it's true, then the researchers used a modified SCD during the trial and this would have been the most effective way to use the diet to bring remission.
While the publishing of this report is definitely good news for the future of treatment options for IBD patients, there's a disturbing issue with the premise upon which the suggested mechanism for the success of the treatment is reported. The researchers assumed that the diet helps to bring remission by altering the gut microbiome of the subjects. Not one word is mentioned in the report about food sensitivities and the fact that the foods omitted by the SCD are highly inflammatory and can be shown (by IgA-based stool testing) to cause the production of antibodies that result in the perpetuation of inflammation in most IBD patients. Instead, full credit for the improvement is theorized as being due to the improvement in gut bacteria balances (with no explanation for why that should be the case).
While it's certainly true that any significant diet change will also change gut bacteria balances, just changing gut bacteria population balances will not automatically bring remission for IBD patients. Remission will only occur if all of the foods that promote the production of antibodies are eliminated from the diet (which can be done by a modified SCD).
Sadly, the researchers completely failed to recognize the significance of food intolerances and the inflammation they cause, as even a possibility. Instead, they conveniently assumed that because there was a change in the gut microbiome, that change must be responsible for the improvement seen in the treatment trial. In doing so, they ignored the equally prominent change in the C reactive protein level of the subjects. That dramatic reduction in C reactive protein levels clearly indicates a major drop in inflammation levels, implying that the immune system was almost certainly involved. But despite that indiscretion, which in no way affects the outcome of the research trial, the publishing of this information will hopefully go a long way toward encouraging further research that will eventually result in a correct interpretation of the reason for the success of an anti-inflammatory diet for treating IBDs.
1. Clinical and Fecal Microbial Changes With Diet Therapy in Active Inflammatory Bowel Disease
Suskind, D. L., Cohen, S. A., Brittnacher, M. J., Wahbeh, G., Lee, D., Shaffer, M. L., . . . Miller, S. I. (2016). Journal of Clinical Gastroenterology, 00(00), 1–9. Retrieved from http://journals.lww.com/jcge/Abstract/publishahead/Clinical_and_Fecal_Microbial_Changes_With_Diet.98120.aspx
2. Use of Complementary Medicine in Pediatric Patients With Inflammatory Bowel Disease: Results From a Multicenter Survey
Wong, A. P., Clark, A. L., Garnett, E. A., Acree, M., Cohen, S. A., Ferry, G. D. & Heyman, M. B. (2009). The Journal of Pediatric Gastroenterology and Nutrition, 48(1), 55–60. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3250599/
Now this was obviously a very small trial, and it only covered a period of 12 weeks. But it's an important first step in establishing the legitimacy of dietary treatments for IBDs. The truth is, complimentary and alternative medicine (CAM) treatment methods for IBDs have been in common use for some time, especially in the case of pediatric patients, but the official side of mainstream medicine has continued to try to ignore the trend. Some sources claim that in some locations as many as 70 % of pediatric IBD patients are routinely treated by CAM methods(Wong et al., 2009).2 While CAM treatments don't always involve diet changes, in many cases they do. Wong et al, (2009) noted that:
In the Markowitz et al study, patients were included based on census data from the 2000 US Census identifying the total number of children living in the surveyed area (16). They estimated that the prevalence of CAM was 50.8% within the previous 12 months. The most common types of CAM used were identified as nutritional supplements, followed by special diets (milk-/dairy-free, low carbohydrates, gluten-free), and only a small percentage used herbal remedies (5.1%).
The SCD is very similar to the diet that the Microscopic Colitis Foundation has suggested for treating microscopic colitis. The primary difference is that the classic SCD allows yogurt, a fermented dairy product. Experience shows (and IgA-based antibody stool tests verify) that most microscopic colitis (MC) patients produce antibodies to casein (the primary protein in all dairy products). Some authors writing articles that interpret the research published by Suskind et al., (2016) have assumed that all dairy products were excluded during the study, but it's unclear whether that's actually true, based on the abstract of the original research report. If it's true, then the researchers used a modified SCD during the trial and this would have been the most effective way to use the diet to bring remission.
While the publishing of this report is definitely good news for the future of treatment options for IBD patients, there's a disturbing issue with the premise upon which the suggested mechanism for the success of the treatment is reported. The researchers assumed that the diet helps to bring remission by altering the gut microbiome of the subjects. Not one word is mentioned in the report about food sensitivities and the fact that the foods omitted by the SCD are highly inflammatory and can be shown (by IgA-based stool testing) to cause the production of antibodies that result in the perpetuation of inflammation in most IBD patients. Instead, full credit for the improvement is theorized as being due to the improvement in gut bacteria balances (with no explanation for why that should be the case).
While it's certainly true that any significant diet change will also change gut bacteria balances, just changing gut bacteria population balances will not automatically bring remission for IBD patients. Remission will only occur if all of the foods that promote the production of antibodies are eliminated from the diet (which can be done by a modified SCD).
Sadly, the researchers completely failed to recognize the significance of food intolerances and the inflammation they cause, as even a possibility. Instead, they conveniently assumed that because there was a change in the gut microbiome, that change must be responsible for the improvement seen in the treatment trial. In doing so, they ignored the equally prominent change in the C reactive protein level of the subjects. That dramatic reduction in C reactive protein levels clearly indicates a major drop in inflammation levels, implying that the immune system was almost certainly involved. But despite that indiscretion, which in no way affects the outcome of the research trial, the publishing of this information will hopefully go a long way toward encouraging further research that will eventually result in a correct interpretation of the reason for the success of an anti-inflammatory diet for treating IBDs.
1. Clinical and Fecal Microbial Changes With Diet Therapy in Active Inflammatory Bowel Disease
Suskind, D. L., Cohen, S. A., Brittnacher, M. J., Wahbeh, G., Lee, D., Shaffer, M. L., . . . Miller, S. I. (2016). Journal of Clinical Gastroenterology, 00(00), 1–9. Retrieved from http://journals.lww.com/jcge/Abstract/publishahead/Clinical_and_Fecal_Microbial_Changes_With_Diet.98120.aspx
2. Use of Complementary Medicine in Pediatric Patients With Inflammatory Bowel Disease: Results From a Multicenter Survey
Wong, A. P., Clark, A. L., Garnett, E. A., Acree, M., Cohen, S. A., Ferry, G. D. & Heyman, M. B. (2009). The Journal of Pediatric Gastroenterology and Nutrition, 48(1), 55–60. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3250599/
Physician Burnout — A Serious Problem with the Current Health Care System
Are we heading toward a disastrous shortage of
practicing medical professionals? The current trend certainly suggests
that we may be unless something is done soon to turn the situation
around. An article published in the Mayo Clinic Proceedings in December,
2015, which was based on survey results from 2011 through 2014, stated
this conclusion:
Conclusion
Burnout and satisfaction with work-life balance in US physicians worsened from 2011 to 2014. More than half of US physicians are now experiencing professional burnout.
And according to the latest survey for 2016, burnout rates today are even worse. During the last 3 years, burnout rates reported on surveys by female and male physicians have increased from 45 % and 37 % respectively in 2013, to 55 % and 46 % respectively in 2016. That's roughly a 23 % increase in self-reported burnout rates in only 3 years. And note that female physicians consistently report higher burnout rates than their male colleagues. This suggests that the current system is even less friendly toward female physicians than it is toward male physicians. It's impossible to determine whether this is just a continuation of the prior atmosphere of gender bias in medicine, or if part of the blame rests with new policies recently implemented. Needless to say, if this trend continues, this country will surely be facing a severe shortage of physicians at some point in the relatively near future.
Obviously this is bound to be having an adverse effect on patient care. The most disturbing part of this trend appears to be defined in the top 7 reasons listed for the causes of burnout, namely:
While interpretations of these data will surely vary depending on one's viewpoint, all of these issues appear to be a direct result of the changes in the health care system that have been imposed by what some would probably describe as unnecessarily heavy-handed implementation of the Affordable Care Act. But just in time, before the bureaucratic juggernaut brings the health care system to it's knees, hope can be seen on the horizon. Some of the biggest problems have been associated with implementation of electronic health record systems and Medicare's so-called "meaningful use incentive program" connected with it. The Centers for Medicare & Medicaid Services (CMS) has finally decided to tackle the job of reworking the widely despised program to make it much more physician-friendly. And there are rumors that the electronic health records system will be revised so that it will be more focused on the actual needs of individual medical practices, rather than the needs of the government. That will be a huge improvement, if it becomes reality.
And apparently the current protocol for how Medicare pays physicians will also be drastically changed. So despite the problem of forcing physicians to go through a steep learning curve once again, at least there will be some incentive for doing so. The current program seems to focus on rewarding physicians for using the electronic health records system. The revised version will supposedly focus on rewarding physicians for improved patient outcomes. Clearly that will be another giant step in the right direction.
One of the frustrations that many clinicians previously expressed was that the meaningful-use program forced them to choose between complying with the overly-burdensome record keeping system or spending more time with their patients. The general consensus seems to be that the way in which the program is currently administrated adds nothing to a clinicians ability to properly care for her or his patients. Instead it arguably interferes with optimal patient care. So it's no wonder that physician burnout rates have been steadily rising. Let's hope that these promised changes will reverse the trend.
Of course all of the details still have to be worked out and then implemented. So if all of this isn't done in a timely manner it could just add to the frustration. No one is expecting all of these changes to be made with lightening speed. But there is reason to hope that progress can be made soon enough to begin turning around current physician burnout rates so that the next survey will show much more optimistic results.
Additional detailed information can be found online in the Medscape article at the first link below, and in the abstract of an article published in the Mayo Clinic Proceedings at the second link below:
Bias and Burnout
Changes in Burnout and Satisfaction With Work-Life Balance in Physicians and the General US Working Population Between 2011 and 2014
Conclusion
Burnout and satisfaction with work-life balance in US physicians worsened from 2011 to 2014. More than half of US physicians are now experiencing professional burnout.
And according to the latest survey for 2016, burnout rates today are even worse. During the last 3 years, burnout rates reported on surveys by female and male physicians have increased from 45 % and 37 % respectively in 2013, to 55 % and 46 % respectively in 2016. That's roughly a 23 % increase in self-reported burnout rates in only 3 years. And note that female physicians consistently report higher burnout rates than their male colleagues. This suggests that the current system is even less friendly toward female physicians than it is toward male physicians. It's impossible to determine whether this is just a continuation of the prior atmosphere of gender bias in medicine, or if part of the blame rests with new policies recently implemented. Needless to say, if this trend continues, this country will surely be facing a severe shortage of physicians at some point in the relatively near future.
Obviously this is bound to be having an adverse effect on patient care. The most disturbing part of this trend appears to be defined in the top 7 reasons listed for the causes of burnout, namely:
- Too many bureaucratic tasks
- Spending too many hours at work
- Increasing computerization of practice
- Income not high enough
- Feeling like just a cog in a wheel
- Maintenance of certification requirements
- Impact of the Affordable Care Act
While interpretations of these data will surely vary depending on one's viewpoint, all of these issues appear to be a direct result of the changes in the health care system that have been imposed by what some would probably describe as unnecessarily heavy-handed implementation of the Affordable Care Act. But just in time, before the bureaucratic juggernaut brings the health care system to it's knees, hope can be seen on the horizon. Some of the biggest problems have been associated with implementation of electronic health record systems and Medicare's so-called "meaningful use incentive program" connected with it. The Centers for Medicare & Medicaid Services (CMS) has finally decided to tackle the job of reworking the widely despised program to make it much more physician-friendly. And there are rumors that the electronic health records system will be revised so that it will be more focused on the actual needs of individual medical practices, rather than the needs of the government. That will be a huge improvement, if it becomes reality.
And apparently the current protocol for how Medicare pays physicians will also be drastically changed. So despite the problem of forcing physicians to go through a steep learning curve once again, at least there will be some incentive for doing so. The current program seems to focus on rewarding physicians for using the electronic health records system. The revised version will supposedly focus on rewarding physicians for improved patient outcomes. Clearly that will be another giant step in the right direction.
One of the frustrations that many clinicians previously expressed was that the meaningful-use program forced them to choose between complying with the overly-burdensome record keeping system or spending more time with their patients. The general consensus seems to be that the way in which the program is currently administrated adds nothing to a clinicians ability to properly care for her or his patients. Instead it arguably interferes with optimal patient care. So it's no wonder that physician burnout rates have been steadily rising. Let's hope that these promised changes will reverse the trend.
Of course all of the details still have to be worked out and then implemented. So if all of this isn't done in a timely manner it could just add to the frustration. No one is expecting all of these changes to be made with lightening speed. But there is reason to hope that progress can be made soon enough to begin turning around current physician burnout rates so that the next survey will show much more optimistic results.
Additional detailed information can be found online in the Medscape article at the first link below, and in the abstract of an article published in the Mayo Clinic Proceedings at the second link below:
Bias and Burnout
Changes in Burnout and Satisfaction With Work-Life Balance in Physicians and the General US Working Population Between 2011 and 2014
Chronic constipation in younger patients is shown to be associated with more serious GI issues in a significant percentage of cases
Currently, the guidelines endorsed by most major
gastroenerology societies do not recommend diagnostic screening for
patients under the age of 50 who present with chronic constipation
unless they also have certain colorectal cancer markers such as
unexplained weight loss, anemia, or gastrointestinal bleeding. A
recently published study suggests that there is sufficient evidence to
warrant diagnostic screening of younger patients who have chronic
constipation as their only symptom
Although the main focus of the research article was colorectal cancer (CRC) risk, an increased risk of other adverse gastrointestinal events was also found. In addition to a significantly higher risk of CRC for patients presenting with only chronic constipation, increased risks for ischemic colitis, diverticulitis, and inflammatory bowel disease were also found. The study showed that chronic constipation patients had approximately 6 times the risk of having CRC, approximately 8 times the risk of having ischemic colitis, approximately a 5 times the risk of having diverticulitis, and approximately 1.5 times the risk of having an inflammatory bowel disease, compared with controls.
It should be noted however, that while the relative risks associated with this group of patients were significantly higher than the respective risks associated with a control group, the absolute risks of developing the various issues listed remain extremely low. This is true because when a risk is very low to begin with, then even if the risk is multiplied, it still remains a very low risk, The fact that the absolute risks appear to remain so low has prompted some medical authorities to suggest that while clinicians should always be aware of these possibilities in younger patients, the evidence presented in the research does not justify any changes in current guidelines.
Additional information can be found in the article at the following reference:
Chronic constipation linked to dramatic hike in CRC risk
Smith, M. J. (2016, January 14). Gastroenterology & Endoscopy News. Retrieved from http://gastroendonews.com/In-the-News/Article/01-16/Chronic-Constipation-Linked-to-Dramatic-Hike-in-CRC-Risk/34869?ses=ogst
Although the main focus of the research article was colorectal cancer (CRC) risk, an increased risk of other adverse gastrointestinal events was also found. In addition to a significantly higher risk of CRC for patients presenting with only chronic constipation, increased risks for ischemic colitis, diverticulitis, and inflammatory bowel disease were also found. The study showed that chronic constipation patients had approximately 6 times the risk of having CRC, approximately 8 times the risk of having ischemic colitis, approximately a 5 times the risk of having diverticulitis, and approximately 1.5 times the risk of having an inflammatory bowel disease, compared with controls.
It should be noted however, that while the relative risks associated with this group of patients were significantly higher than the respective risks associated with a control group, the absolute risks of developing the various issues listed remain extremely low. This is true because when a risk is very low to begin with, then even if the risk is multiplied, it still remains a very low risk, The fact that the absolute risks appear to remain so low has prompted some medical authorities to suggest that while clinicians should always be aware of these possibilities in younger patients, the evidence presented in the research does not justify any changes in current guidelines.
Additional information can be found in the article at the following reference:
Chronic constipation linked to dramatic hike in CRC risk
Smith, M. J. (2016, January 14). Gastroenterology & Endoscopy News. Retrieved from http://gastroendonews.com/In-the-News/Article/01-16/Chronic-Constipation-Linked-to-Dramatic-Hike-in-CRC-Risk/34869?ses=ogst
A case study where microscopic colitis completely transitioned into giant cell colitis
Giant cell colitis (GCC) is a rare form of microscopic colitis (MC). A very interesting case study has been published in which a case of collagenous colitis evolved over a period of approximately 9 years into giant cell colitis (GCC), resulting in the disappearance of the diagnostic markers of both collagenous colitis (CC) and lymphocytic colits (LC). Though the diagnostic markers of both LC and CC disappeared, the clinical symptoms of MC persisted, apparently due to the mononuclear inflammation associated with the giant cells. Colonic biopsy samples taken at an intermediate stage, approximately 4 years after the initial diagnosis of CC, showed the presence of lymphocytic infiltration, and reduced collagen band thickening in some biopsy samples. Giant cells were present in samples taken where the collagen band thickening had been reduced back to near normal levels, but they were absent in areas where collagen band thickness diagnostic of CC was still present..
Biopsy samples examined at the 9-year point showed lymphocyte counts near normal levels (way below the diagnostic threshold for LC), and collagen band thickness consistently near normal levels (way below the diagnostic threshold for CC). Mononuclear inflammation and giant cells were present in the lamina propria of all segments of the colon that were examined. To date, giant cells have only been associated with CC (not LC), but they have also been found with ulcerative colitis (UC) and celiac disease.
Previous research has suggested that this pattern of inflammation (mononuclear inflammation associated with giant cells) begins as microscopic colitis with numerous macrophages, and over time the macrophages fuse to create giant cells. A reference can be found at:
Microscopic colitis with giant cells
Libbrecht, L., Croes, R., Ectors, N., Staels, F., & Geboes, K. (2002). Histopathology, 40(4), 335–338. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/11943017
Additional information about the case study discussed in this article can be found in the article at the following reference:
Evolution of microscopic colitis to giant cell colitis without significant intraepithelial lymphocytosis or thickened collagen plate
De Petris, G., & Chen, L. (2015). International Journal of Surgical Pathology, 23(3), 225–229. doi: 10.1177/1066896914542124. Epub 2014 Jul 7.
Biopsy samples examined at the 9-year point showed lymphocyte counts near normal levels (way below the diagnostic threshold for LC), and collagen band thickness consistently near normal levels (way below the diagnostic threshold for CC). Mononuclear inflammation and giant cells were present in the lamina propria of all segments of the colon that were examined. To date, giant cells have only been associated with CC (not LC), but they have also been found with ulcerative colitis (UC) and celiac disease.
Previous research has suggested that this pattern of inflammation (mononuclear inflammation associated with giant cells) begins as microscopic colitis with numerous macrophages, and over time the macrophages fuse to create giant cells. A reference can be found at:
Microscopic colitis with giant cells
Libbrecht, L., Croes, R., Ectors, N., Staels, F., & Geboes, K. (2002). Histopathology, 40(4), 335–338. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/11943017
Additional information about the case study discussed in this article can be found in the article at the following reference:
Evolution of microscopic colitis to giant cell colitis without significant intraepithelial lymphocytosis or thickened collagen plate
De Petris, G., & Chen, L. (2015). International Journal of Surgical Pathology, 23(3), 225–229. doi: 10.1177/1066896914542124. Epub 2014 Jul 7.
New medical treatment guidelines issued for microscopic colitis
In mid-December, 2015, the American Gastroenterological Association Institute published new guidelines for the medical management of microscopic colitis. The new guidelines appear to include some significant departures from prior treatment protocols. These new recommendations, which focus on symptomatic patients of course, can be summarized as follows:
1. Treatment with budesonide is preferred over treatment using other anti-inflammatory medications for inducing clinical remission.
2. When treatment with budesonide is not feasible, treatment with mesalamine, bismuth salicylate, or prednisone is better than no treatment at all.
3. Treatment using a combination of cholestyramine and mesalamine (rather than mesalamine alone), is not recommended.
4. The association specifically does not recommend treatment with probiotics or Boswellia serrata, when attempting to induce clinical remission.
5. For patients whose symptoms relapse when a budesonide treatment regimen is completed, the guidelines recommend continued treatment with budesonide in order to maintain clinical remission.
Most clinicians who treat MC cases regularly were already well aware that budesonide typically produces superior results when compared with alternative anti-inflammatory medications. And many clinicians had already discovered that a maintenance dose of budesonide for patients who suffer a relapse of symptoms when initial budesonide treatment regimens are completed, can typically provide stable remission with a minimal risk of adverse side effects. But the recommendation against the use of probiotics for treating MC patients probably comes as a surprise to many GI specialists. Probiotics had been recommended for treating MC for decades, but apparently no one had bothered to do followup research to verify that they actually did provide benefits for MC patients. The reality is that a rather large body of epidemiological evidence indicates that not only is it uncommon for MC patients to recover more rapidly by using probiotics, but in many cases the use of probiotics actually makes symptoms worse, and can prevent some patients from achieving remission.
Additional information can be found in the Medscape article at the following link:
New Guideline Addresses Microscopic Colitis Management
If desired, a PDF copy of the original article can be downloaded by clicking this link.
1. Treatment with budesonide is preferred over treatment using other anti-inflammatory medications for inducing clinical remission.
2. When treatment with budesonide is not feasible, treatment with mesalamine, bismuth salicylate, or prednisone is better than no treatment at all.
3. Treatment using a combination of cholestyramine and mesalamine (rather than mesalamine alone), is not recommended.
4. The association specifically does not recommend treatment with probiotics or Boswellia serrata, when attempting to induce clinical remission.
5. For patients whose symptoms relapse when a budesonide treatment regimen is completed, the guidelines recommend continued treatment with budesonide in order to maintain clinical remission.
Most clinicians who treat MC cases regularly were already well aware that budesonide typically produces superior results when compared with alternative anti-inflammatory medications. And many clinicians had already discovered that a maintenance dose of budesonide for patients who suffer a relapse of symptoms when initial budesonide treatment regimens are completed, can typically provide stable remission with a minimal risk of adverse side effects. But the recommendation against the use of probiotics for treating MC patients probably comes as a surprise to many GI specialists. Probiotics had been recommended for treating MC for decades, but apparently no one had bothered to do followup research to verify that they actually did provide benefits for MC patients. The reality is that a rather large body of epidemiological evidence indicates that not only is it uncommon for MC patients to recover more rapidly by using probiotics, but in many cases the use of probiotics actually makes symptoms worse, and can prevent some patients from achieving remission.
Additional information can be found in the Medscape article at the following link:
New Guideline Addresses Microscopic Colitis Management
If desired, a PDF copy of the original article can be downloaded by clicking this link.
Scientists declare that certain ingredients in processed foods are associated with the development of autoimmune disease
German and Israeli researchers have published data in the journal Autoimmunity Reviews suggesting that the consumption of processed foods significantly increases the risk of developing various autoimmune diseases. While claiming that approximately 100 autoimmune (AI) diseases are involved, some specific examples of common AI diseases were listed, including autoimmune hepatitis, celiac disease, inflammatory bowel disease, lupus erythematosus, multiple sclerosis, myesthenia gravis, type 1 diabetes, and scleroderma.
The scientists presented evidence that many processed foods tend to weaken the natural resistance of the digestive system to bacteria, various toxins, and other harmful items, some of which are nutritional, while others are non-nutritional. This occurs because certain ingredients in processed foods cause increased intestinal permeability (sometimes referred to as "leaky gut"). When these ingredients cause the tight junctions between the cells of the lining of the intestine to open wide enough for partially-digested peptides to pass through into the bloodstream, this causes an immune system reaction that results in food sensitivities and inflammation. The inflammation opens the door to the risk of autoimmune disease development.
The report mentioned at least 7 common food additives that have been shown to weaken the tight junctions, resulting in an increased risk for the development of AI diseases. Sugars, salt, fat emulsifiers, organic acids, microbial transglutaminase (which is an enzyme that is used as a food protein adhesive), and nanometric particles were specifically named.
Additional information can be found in the article at the following link:
http://www.news-medical.net/news/20151231/Processed-foods-may-increase-likelihood-of-developing-autoimmune-diseases.aspx
The scientists presented evidence that many processed foods tend to weaken the natural resistance of the digestive system to bacteria, various toxins, and other harmful items, some of which are nutritional, while others are non-nutritional. This occurs because certain ingredients in processed foods cause increased intestinal permeability (sometimes referred to as "leaky gut"). When these ingredients cause the tight junctions between the cells of the lining of the intestine to open wide enough for partially-digested peptides to pass through into the bloodstream, this causes an immune system reaction that results in food sensitivities and inflammation. The inflammation opens the door to the risk of autoimmune disease development.
The report mentioned at least 7 common food additives that have been shown to weaken the tight junctions, resulting in an increased risk for the development of AI diseases. Sugars, salt, fat emulsifiers, organic acids, microbial transglutaminase (which is an enzyme that is used as a food protein adhesive), and nanometric particles were specifically named.
Additional information can be found in the article at the following link:
http://www.news-medical.net/news/20151231/Processed-foods-may-increase-likelihood-of-developing-autoimmune-diseases.aspx
Research shows that coconut oil can be used to treat or prevent yeast overgrowth
A research team at Tufts University has demonstrated how ordinary coconut oil can be used in the diet to effectively control a Candida albicans overgrowth. This research was done on mice, but the implication is clear that it should also be effective for humans because of the similarities in digestive system behavior. Coconut oil is known to have antifungal properties, so it was used in studies that also compared the use of beef tallow and soybean oil.
The researchers found that a diet rich in coconut oil reduced the amount of C. albicans in the gut by more than 90 % when compared with a diet rich in beef tallow. The effectiveness was even maintained when coconut oil was combined with beef tallow. This obviously supports Hippocrates claim made roughly 2,000 years ago — food can be used as medicine.
Study in mice suggests coconut oil can control overgrowth of a fungal pathogen in GI tract
Tufts Now. (2015, November 18). Tufts University News Release. Retrieved from http://now.tufts.edu/news-releases/study-mice-suggests-coconut-oil-can-control-overgrowth-fungal-pathogen-gi-tract
The researchers found that a diet rich in coconut oil reduced the amount of C. albicans in the gut by more than 90 % when compared with a diet rich in beef tallow. The effectiveness was even maintained when coconut oil was combined with beef tallow. This obviously supports Hippocrates claim made roughly 2,000 years ago — food can be used as medicine.
Study in mice suggests coconut oil can control overgrowth of a fungal pathogen in GI tract
Tufts Now. (2015, November 18). Tufts University News Release. Retrieved from http://now.tufts.edu/news-releases/study-mice-suggests-coconut-oil-can-control-overgrowth-fungal-pathogen-gi-tract
New research suggests that use of a probiotic strain Lactobacillus reuteri may suppress intestinal inflammation
This research seems interesting at first glance, because until guidelines were recently changed, probiotics were generally recommended as part of a medical treatment regimen for microscopic colitis. So the idea that a certain strain of probiotic bacteria might suppress inflammation in the intestines seems appealing, and possibly even logical. But the official guidelines were changed to recommend against the use of probiotics when attempting to induce clinical remission of MC symptoms, and the guideline changes were published in the same month that this research article was published.
Unfortunately the research report contains a glaring problem for MC patients. The article (cited below) states:
However, the mechanisms of probiosis are not clear. Our current studies suggest that supplementation with hdc+ L. reuteri, which can convert l-histidine to histamine in the gut, resulted in suppression of colonic inflammation.
This is a problem because L-histidine is a precurser to histamine. In other words, histamine is produced by the body from L-histidine. So how did increasing histamine production in the intestines suppress inflammation (as claimed by the researchers)? That claim is contradictory to the actual experiences of many, many MC patients who experience a relapse of symptoms or perpetuated symptoms whenever histamine levels increase above certain threshold levels. Therefore, the researchers need to answer that question before the research will have any clear value for MC patients. The problem with the treatment concept suggested by the research is that most MC patients seem to already have too much residual histamine in their intestines, and in their bloodstream. For someone who happens to be low on histamine though, taking Lactobacillus reuteri might possibly be helpful.
Histamine H2 receptor-mediated suppression of intestinal inflammation by probiotic Lactobacillus reuteri
Gao, C., Major, A., Rendon, D., Lugo, M., Jackson, V., Shi, Z., . . . Versalovica, J. (2015). mBio, (6)6, e01358-15.
http://mbio.asm.org/content/6/6/e01358-15.full
Unfortunately the research report contains a glaring problem for MC patients. The article (cited below) states:
However, the mechanisms of probiosis are not clear. Our current studies suggest that supplementation with hdc+ L. reuteri, which can convert l-histidine to histamine in the gut, resulted in suppression of colonic inflammation.
This is a problem because L-histidine is a precurser to histamine. In other words, histamine is produced by the body from L-histidine. So how did increasing histamine production in the intestines suppress inflammation (as claimed by the researchers)? That claim is contradictory to the actual experiences of many, many MC patients who experience a relapse of symptoms or perpetuated symptoms whenever histamine levels increase above certain threshold levels. Therefore, the researchers need to answer that question before the research will have any clear value for MC patients. The problem with the treatment concept suggested by the research is that most MC patients seem to already have too much residual histamine in their intestines, and in their bloodstream. For someone who happens to be low on histamine though, taking Lactobacillus reuteri might possibly be helpful.
Histamine H2 receptor-mediated suppression of intestinal inflammation by probiotic Lactobacillus reuteri
Gao, C., Major, A., Rendon, D., Lugo, M., Jackson, V., Shi, Z., . . . Versalovica, J. (2015). mBio, (6)6, e01358-15.
http://mbio.asm.org/content/6/6/e01358-15.full
Another proposed remedy for gluten sensitivity
Many research groups are hard at work trying to cash in on the popular trend to treat every health issue with a pill. There are already several products on the market, and researchers continue to come up with ideas for trying to neutralize, or at least minimize the effects of gluten on the digestive system of people who are sensitive to gluten because their immune system produces antibodies to it.
The goal of the research discussed in the article at the link below is to utilize a protein found in egg yolk that will bind to gluten peptides so that hopefully they will not be recognized by the immune system, thus averting a major reaction. At least that's what the researchers hope to accomplish. The problem with products such as this is that they are never 100% effective, and for many MC patients who are sensitive to gluten, it only takes tiny trace amounts to trigger a reaction. Therefore, whether or not the final product that comes out of this research will actually be useful may depend on the relative sensitivity level of potential users. Unfortunately, in many cases trace amounts of gluten may not cause clinical symptoms, but they are still sufficient to increase the inflammation level in the intestines. This can perpetuate a state of subclinical inflammation that can cause long-term damage, even though it is just below the threshold at which an immune system reaction might be triggered.
In such a state, where inflammation is perpetually maintained at just below the threshold at which a reaction might be triggered, a small upset may be sufficient to trigger a flare. On the other hand, if all food sensitivities are totally avoided, so that the intestines can actually heal, a minor glitch in the diet might not cause any more than minor, fleeting symptoms.
That said, if a product such as this is used to help insure against possible damage caused by accidental cross-contamination by trace amounts of gluten in a meal (such as commonly occurs in some restaurant settings), rather than using it to justify eating gluten-based foods, it may be quite helpful. Using such products as a means to justify eating whatever one desires, however, is probably a very risky proposition that will likely lead to adverse consequences at some point in the future, if using them to justify eating gluten becomes a regular, routine practice.
'Cracking' gluten intolerance -Researchers use egg yolks to create supplement that could improve lives of people with celiac disease
Pysklywyc, S. (2015, July 15) [Web log message] University of Alberta
http://uofa.ualberta.ca/news-and-events/newsarticles/2015/july/cracking-gluten-intolerance
The goal of the research discussed in the article at the link below is to utilize a protein found in egg yolk that will bind to gluten peptides so that hopefully they will not be recognized by the immune system, thus averting a major reaction. At least that's what the researchers hope to accomplish. The problem with products such as this is that they are never 100% effective, and for many MC patients who are sensitive to gluten, it only takes tiny trace amounts to trigger a reaction. Therefore, whether or not the final product that comes out of this research will actually be useful may depend on the relative sensitivity level of potential users. Unfortunately, in many cases trace amounts of gluten may not cause clinical symptoms, but they are still sufficient to increase the inflammation level in the intestines. This can perpetuate a state of subclinical inflammation that can cause long-term damage, even though it is just below the threshold at which an immune system reaction might be triggered.
In such a state, where inflammation is perpetually maintained at just below the threshold at which a reaction might be triggered, a small upset may be sufficient to trigger a flare. On the other hand, if all food sensitivities are totally avoided, so that the intestines can actually heal, a minor glitch in the diet might not cause any more than minor, fleeting symptoms.
That said, if a product such as this is used to help insure against possible damage caused by accidental cross-contamination by trace amounts of gluten in a meal (such as commonly occurs in some restaurant settings), rather than using it to justify eating gluten-based foods, it may be quite helpful. Using such products as a means to justify eating whatever one desires, however, is probably a very risky proposition that will likely lead to adverse consequences at some point in the future, if using them to justify eating gluten becomes a regular, routine practice.
'Cracking' gluten intolerance -Researchers use egg yolks to create supplement that could improve lives of people with celiac disease
Pysklywyc, S. (2015, July 15) [Web log message] University of Alberta
http://uofa.ualberta.ca/news-and-events/newsarticles/2015/july/cracking-gluten-intolerance
Mast cells in the intestines
The role of mast cells in gastrointestinal disease has been well documented. When an inflammatory bowel disease (IBD) is active, mast cell numbers and activity tend to increase. When they are activated, mast cells promote inflammation by means of the release of inflammatory mediators. This mode of inflammation is separate and distinct from the T-cell-based inflammation so commonly associated with IBDs.
Mast cells are mostly located near nerve terminals in the subepithelial layer of the intestinal mucosa known as the lamina propria. Activation is accomplished by means of locally-secreted neuropeptides. Neuropeptides are small protein molecules produced and secreted by neurons. Neuropeptides function as signaling mechanisms, allowing communications with the nervous system and the brain. All together, they comprise the most diverse class of signaling molecules known, for coordinating many physiological functions with the brain. To date, almost 70 genes in the genome of mammals (including humans) have been determined to engage in the process of encoding neuropeptide precursors involving a wide range of bioactive neuropeptides.
Research in this area helps to illuminate many aspects of the inflammation associated with IBDs that are either unexplained by, or are counterintuitive to our understanding of the reaction processes or symptoms traditionally associated with T-cell-based inflammation. The article cited below explores and defines why mast cell issues have been underappreciated in the past, and why they will probably play a major role in research focused on diseases involving intestinal inflammation in the future.
Mast cells in gastrointestinal disease
(2010). Gastroenterology and Hepatology, (6)12, 772–777.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3033552/
Mast cells are mostly located near nerve terminals in the subepithelial layer of the intestinal mucosa known as the lamina propria. Activation is accomplished by means of locally-secreted neuropeptides. Neuropeptides are small protein molecules produced and secreted by neurons. Neuropeptides function as signaling mechanisms, allowing communications with the nervous system and the brain. All together, they comprise the most diverse class of signaling molecules known, for coordinating many physiological functions with the brain. To date, almost 70 genes in the genome of mammals (including humans) have been determined to engage in the process of encoding neuropeptide precursors involving a wide range of bioactive neuropeptides.
Research in this area helps to illuminate many aspects of the inflammation associated with IBDs that are either unexplained by, or are counterintuitive to our understanding of the reaction processes or symptoms traditionally associated with T-cell-based inflammation. The article cited below explores and defines why mast cell issues have been underappreciated in the past, and why they will probably play a major role in research focused on diseases involving intestinal inflammation in the future.
Mast cells in gastrointestinal disease
(2010). Gastroenterology and Hepatology, (6)12, 772–777.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3033552/
Oral vitamin d sprays shown to be as effective as oral capsules
Because IBD patients tend to have a limited ability to absorb vitamins and minerals in their diet, and most IBD patients are deficient in certain vitamins and minerals, there is a significant amount of interest in the possible use of alternative vitamin supplements that can bypass the malabsorption problems caused by digestive system issues. In a side by side comparison trial, where subjects started with an average serum vitamin D level of 23 ng/ml, one group used conventional capsules, while the other used an oral spray. After 4 weeks of treatment using 3,000 IU of vitamin D daily, serum vitamin D levels were measured again. The group using capsules showed an average vitamin D level of 36 ng/ml, and the group using the oral spray averaged 34 ng/ml. The difference was small enough that the treatments could be considered to be equivalent, for most practical purposes.
Vitamin D3 supplementation in healthy adults: a comparison between capsule and oral spray solution as a method of delivery in a wintertime, randomised, open-label, cross-over study.
Todd, J. J., McSorley, E. M., Pourshahidi, L. K., Madigan, S. M., Laird, E., Healy, M., & Magee, P. J. (2016). British Journal of Nutrition, 116(8), 1402-1408. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/?term=Vitamin+D3+supplementation+in+healthy+adults%3A+a+comparison+between+capsule+and+oral+spray+solution+as+a+method+of+delivery+in+a+wintertime%2C+randomised%2C+open-label%2C+cross-over+study.
Vitamin D3 supplementation in healthy adults: a comparison between capsule and oral spray solution as a method of delivery in a wintertime, randomised, open-label, cross-over study.
Todd, J. J., McSorley, E. M., Pourshahidi, L. K., Madigan, S. M., Laird, E., Healy, M., & Magee, P. J. (2016). British Journal of Nutrition, 116(8), 1402-1408. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/?term=Vitamin+D3+supplementation+in+healthy+adults%3A+a+comparison+between+capsule+and+oral+spray+solution+as+a+method+of+delivery+in+a+wintertime%2C+randomised%2C+open-label%2C+cross-over+study.