Can Aerius trigger colitis flare

[wnorm]

I have collagenous colitis and mastocytic enterocolitis. I just started with an allergist who has an excellent reputation in Canada. He put me on a regimen of aerius about 11 days ago: 5 m/dayfor 3 days, then progress to 10 mg/day for 7 days if the 5 mg don't help with the diarrhea, abdominal pain, and finally progress to 20 mg/day for ~ 3 weeks if the 20 mg doesn't help. Over the past 10 days most of my abdominal systems have worsened dramatically. While the diarrhea may have diminished (because of Aerius or some other factor?), the cramping, bloating, gas etc are so much worse. I have been doubled up since last week. I did not think that Aerius could trigger these abdominal problems. In the past, I found that Allegra brought on these symptoms. My pharmacyst said that I should stop the Aerius for a week and then start it again to see if this drug was the trigger. I couldn't reach the doctor. Any thoughts? Also what can I do to feel better now?

[tex]

Hi,

Aerius is similar to Claritin. Normally, if an antihistamine is going to help GI symptoms, it will do so very quickly (within 24 hours or so), so it's not necessary to test it for weeks. I don't understand why your doctor started you on such a low dose. 5 mg is only a half dose compared with a normal 24-hour dose of Claritin, for example. Maybe he thinks that by starting slow and taking a long time to increase the dose, that will minimize the chances of having the side effects that you are having. But if you are already having those side effects on such a low dose, then it's unlikely that it will get any better.

Yes, antihistamines cause gas and bloating for many users. If the side effect symptoms you are having are as bad as you indicate, then you need to decide if they are worth putting up with, because they will probably get worse as you increase the dose.

I notice that you don't list gluten as one of your food sensitivities. Gluten is almost surely the cause of your continued symptoms (despite your negative test results for celiac disease). Have you tried eliminating gluten from your diet for a few months or so? It takes a while for gluten (anti-gliadin) antibodies to clear the system, because they have a 120-day half-life, so you may not see improvement for months, but as the gut heals, your symptoms should fade away.

Another thing to consider is your vitamin D level (the 25[OH]D3 test). Do you know what your level is? IBDs deplete vitamin D, and vitamin D is essential for reducing inflammation. Without adequate vitamin D the immune system cannot stop an autoimmune reaction. The active form of vitamin D suppresses the development of new mast cells and helps to keep the numbers down. Here's a quote from pages 51–56 of my book, Vitamin D and Autoimmune Disease, that provides a lot more information on what I'm talking about here:

As we review more recently-published research data, we can begin to see all sorts of connections to confirm what we have been suspecting. Way back in chapter 1 we discussed how mast cells release proinflammatory modulators when they are activated. And as we noted above, mast cells are capable of converting vitamin D3 into the active form, 1,25(OH)2D3. Researchers in Italy (Baroni et al., 2007) have shown that 1,25(OH)2D3 also plays a role in the regulation of the development and function of mast cells.12

So mast cells regulate vitamin D, and vitamin D regulates mast cells.
Specifically, mast cells can regulate the conversion of vitamin D from the inactive to the active form, and the active form of of vitamin D can regulate mast cells, by limiting their development. Baroni et al. (2007) showed that the active form of vitamin D not only initiates apoptosis, but it is also capable of limiting (in a dose-dependent manner) the ability of mast cell precursors to mature (into fully-capable mast cells), dependent upon the presence of vitamin D receptors. It doesn't get much more co-dependent, convoluted, and generally complex than that.

Is it any wonder that so many people, including physicians, are confused about how the immune system actually works?
It's a very complex and sophisticated system. And it can do wonderful things for us, provided that we just do our part to help keep it functioning properly. What this interdependent relationship implies then, is that vitamin D receptors must be present in adequate quantities in order for the active form of vitamin D to be able to prevent the production of excess numbers of mast cells when an inflammatory event is in progress. This is a mechanism that the immune system utilizes to prevent reactions from getting out of hand. Baroni et al. (2007) also demonstrated that VDR-deficient mice experience faster mast cell maturity rates than normal mice, and the mast cells that are produced are more easily-activated, compared with those produced by normal mice.

This phenomenon appears to explain why so many IBD patients tend to have mast cell activation disorder.
Mast cell activation disorder (MCAD) is a condition marked by inappropriate mast cell activation that results in the excessive release of histamine, cytokines, and other proinflammatory mediators by mast cells, for no legitimate (or at least no apparent) reason. It can cause many of the symptoms of mastocytosis or mastocytic enterocolitis, even though mast cell populations might be normal, or only slightly elevated.

The intestines are known to have relatively high populations of mast cells. MCAD can result in additional symptoms (due to IgE-based reactions) that cause complications, and add confounding issues to certain types of autoimmune diseases, such as IBDs. In the case of microscopic colitis (of which lymphocytic colitis and collagenous colitis are the most common types) for example, MCAD appears to be capable of causing virtually any of the clinical gastroenterological symptoms traditionally associated with the disease, plus the addition of classic IgE-based allergy symptoms such as nasal discharge, watery eyes, and itching skin or tongue, in some cases. These symptoms are usually somewhat attenuated (compared with classic allergic reactions), and they may even be overlooked, unless the patient is aware of this possibility, and remains alert, in order to notice the symptoms. But whether these symptoms are relatively minor, or severe, the additional mast cell activity typically results in increased severity of gastrointestinal symptoms normally associated with an IBD, and in some situations, this type of mast cell activity can even trigger a flare when an IBD has been in remission.

The observations noted in the above paragraph are based on an ongoing epidemiological study of hundreds of people who have microscopic colitis and who share their experiences freely as members of an Internet discussion and support group.13 This collection of real-life experiences is arguably the largest database in the world of specific information devoted to the understanding and treatment of microscopic colitis and related issues. The discussion board has been active (including continued participation by many of the original founding members) for approximately 10 years at this point in time, so a lot of real-life, down-to-earth data are available.

Presumably, this may also apply to the other IBDs, including Crohn's, ulcerative colitis, and celiac disease, although this possibility certainly hasn't yet been verified by random, double-blind research trials. Not all IBD patients experience these IgE-based symptoms, but for those who do, this observation should answer a lot of questions.

So a deficiency of either vitamin D receptors, or vitamin D in it's active form can lead to a hypersensitive condition where not only are mast cells more likely to degranulate (releasing proinflammatory agents), but additional mast cells are produced more rapidly, and more of them are ultimately produced, so that a state of severe hypersensitivity (resulting in massive inflammation) may be the result.

This condition appears to meet the definition of at least mast cell activation disorder, and it might possibly be the primary cause of mastocytic enterocolitis. It also may be associated with mastocytosis, which is a serious systemic form of mast cell disorder.

Other researchers have validated this discovery, and demonstrated how powerful the effect of vitamin D can be.
Additional compelling data about the association between VDRs and inflammation were established when Kong et al. (2008) showed that when normal mice, and mice with compromised vitamin D receptor function, were fed dextran sodium sulfate in order to intentionally attempt to induce colitis, the mice with compromised vitamin D receptors developed much more severe symptoms than the mice with normal vitamin D receptors.14 The mortality rate in the mice with compromised VDR function ranged up to 70 %, whereas there was no mortality, and only relatively minor symptoms in the mice with normal VDR function. Needless to say, that's a striking difference in the results displayed by the comparison of the 2 groups of test subjects.

During a colonoscopy exam, gastroenterologists often take biopsy samples of the interior lining (known as the epithelia) of the colon, and these samples are later examined under a microscope by a pathologist in order to search for microscopic physical changes in the structure of the cells. Certain specific changes are considered to be diagnostic of certain digestive system diseases.

Researchers have shown that patients who have Crohn's disease and ulcerative colitis are indeed deficient in VDRs.
Liu et al. (2013) studied colonic biopsies in order to compare the status of vitamin D receptors in Crohn's disease and ulcerative colitis patients with the VDR status of normal subjects. Compared with the relatively high quantities of vitamin D receptors found in normal colonic epithelial tissue, the researchers found that Crohn's disease and ulcerative colitis were associated with a significant reduction in the number of VDRs.15 By utilizing gene splicing techniques in mouse intestinal epithelial tissue, they demonstrated that a sufficient number of human VDRs expressed in mouse intestinal epithelial cells will protect mice from developing colitis.

The researchers concluded that, "Together, these results demonstrate that gut epithelial VDR signaling inhibits colitis by protecting the mucosal epithelial barrier, and this anticolitic activity is independent of nonepithelial immune VDR actions" (p. 3,982) (Liu et al. 2013). Obviously this is an extremely important observation, as it provides compelling evidence of a possible way to prevent inflammatory bowel disease.

In essence, the researchers have demonstrated that an adequate level of vitamin D (and sufficient numbers of vitamin D receptors) can prevent the development of inflammatory bowel disease. And if this is true in the gut, then there is good reason to believe that future research may verify that it is also true in other organs (including joints) affected by autoimmune-associated inflammation.

And here are the medical references cited in that quote:

12. Baroni, E., Biffi, M., Benigni, F., Monno, A., Carlucci, D., Carmeliet, G., . . . D’Ambrosio, D. (2007). VDR-dependent regulation of mast cell maturation mediated by 1,25-dihydroxyvitamin D3. Journal of Leukocyte Biology, 81(1), 250–262. doi:10.1189/jlb.0506322

13 Discussion and Support Forum for Collagenous Colitis, Lymphocytic Colitis, Microscopic Colitis, Mastocytic Enterocolitis, and Related Issues. (2014). perskyfarms.com. Retrieved from http://www.perskyfarms.com/phpBB2/index.php

14. Kong, J., Zhang, Z., Musch, M. W., Ning, G., Sun, J., Hart, J., . . . Li, Y. C. (2008). Novel role of the vitamin D receptor in maintaining the integrity of the intestinal mucosal barrier. American Journal of Physiology - Gastrointestinal and Liver Physiology, 294(1), G208–G216. doi:10.1152/ajpgi.00398.2007

15. Liu, W., Chen, Y., Golan, M. A., Annunziata, M. L., Du, J., Dougherty, U., . . . Li, Y. C. (2013). Intestinal epithelial vitamin D receptor signaling inhibits experimental colitis. Journal of Clinical Investigation, 123(9), 3,983–3,996. doi:10.1172/JCI65842

If you're not familiar with using digital object identifier (doi) designations for references, here are conventional links for the references that are listed as doi addresses:

12. http://www.jleukbio.org/content/81/1/250.full

14. http://ajpgi.physiology.org/content/ear ... 00398.2007

15. http://www.jci.org/articles/view/65842

Tex

[wnorm]

Thank-you very much for your prompt response. I am feeling better since I stopped the Aerius. My understanding is that a dosage of 5 mg Aerius, or desloratadine, is equivalent to 10 mg Claritin,or loratadine. Usually the side effects with loratadine are worse than with desloratadine. For years I took Aerius regularly without any significant abdominal side effects.
I was suprised to experience these side effects now. On the recommendation of the pharmacist, I stopped Aerius and will resume taking it after a week to determine if , indeed, the Aerius was causing these symptoms.
I take 10,000 mg vit.D/week, as prescribed by my doctor. I have been taking this dosage for many years. I did an self-directed elimination study several years ago and found out my specific triggers: soya, egg whites, citrus, etc. I am quite diligent in following a low histamine, low fibre diet. Plus, I have tested positive for nuts, etc and therefore avoid all offending foods. I have a master's degree in toxicology and am familiar with the importance of following specific protocols. Documentation is extremely important, as is eliminating conflicting variables. I avoid most commercial foods and eat out rarely. However, stress and medications can often play havoc with my system.
I had avoided gluten for only ~ 3 weeks and did not find it to be a significant factor in my condition. I understand that a 120 day elimination protocol is required. However, I have so many allergies and intolerances. I cannot include any whole grains,corn,beans,nuts,soya, all fresh fruit and vegetables,nearly all cooked fruits and vegetables, etc.
I consume: moderate quantities of-
peeled and cooked apples,
squash,
potatoes,
carrots;
lactose-free skim milk and cottage cheese,
poultry
beef
very fresh ocean
homemade white bread,
white pasta,

and small quantities of
sugar,
herbs such as basil, fennel, thyme, coriander, oregano, etc.
whole eggs
low fat cheeses
cooked minced garlic and
cooked blueberries(?)

I cannot tolerate/or am allergic to - codeine, aspirin, all nsaids, reglan, reactine, allegra, levaquin, metamucil, robaxin, chloroquin, all migraine meds, biaxin, penicillin, latex and all foods that have proteins that cross-react with latex (such as bananas), sorbital,
etc.
You have mentioned doing tests with Enterolab in the past. However, if I cut out all gluten containing foods, my diet would be too limited. I also cannot tolerae xanthan gum, guar gum, etc. which one generally needs to make gluten-free bread. My dietician put me on a very resticted diet for a while in 2011 (chicken, white rice, apple sauce, potatoes, etc) and I ended up quite sick with the flu and brochitis for months afterwards.I had to inhale steroids for months. My gastroenterologist told me not to restrict myself in that manner again. I had surgery for uterine cancer last year and have been kind of fragile since then.
Any suggestions would be appreciated.

Hi,

Aerius is similar to Claritin. Normally, if an antihistamine is going to help GI symptoms, it will do so very quickly (within 24 hours or so), so it's not necessary to test it for weeks. I don't understand why your doctor started you on such a low dose. 5 mg is only a half dose compared with a normal 24-hour dose of Claritin, for example. Maybe he thinks that by starting slow and taking a long time to increase the dose, that will minimize the chances of having the side effects that you are having. But if you are already having those side effects on such a low dose, then it's unlikely that it will get any better.

Yes, antihistamines cause gas and bloating for many users. If the side effect symptoms you are having are as bad as you indicate, then you need to decide if they are worth putting up with, because they will probably get worse as you increase the dose.

I notice that you don't list gluten as one of your food sensitivities. Gluten is almost surely the cause of your continued symptoms (despite your negative test results for celiac disease). Have you tried eliminating gluten from your diet for a few months or so? It takes a while for gluten (anti-gliadin) antibodies to clear the system, because they have a 120-day half-life, so you may not see improvement for months, but as the gut heals, your symptoms should fade away.

Another thing to consider is your vitamin D level (the 25[OH]D3 test). Do you know what your level is? IBDs deplete vitamin D, and vitamin D is essential for reducing inflammation. Without adequate vitamin D the immune system cannot stop an autoimmune reaction. The active form of vitamin D suppresses the development of new mast cells and helps to keep the numbers down. Here's a quote from pages 51–56 of my book, Vitamin D and Autoimmune Disease, that provides a lot more information on what I'm talking about here:

As we review more recently-published research data, we can begin to see all sorts of connections to confirm what we have been suspecting. Way back in chapter 1 we discussed how mast cells release proinflammatory modulators when they are activated. And as we noted above, mast cells are capable of converting vitamin D3 into the active form, 1,25(OH)2D3. Researchers in Italy (Baroni et al., 2007) have shown that 1,25(OH)2D3 also plays a role in the regulation of the development and function of mast cells.12

So mast cells regulate vitamin D, and vitamin D regulates mast cells.
Specifically, mast cells can regulate the conversion of vitamin D from the inactive to the active form, and the active form of of vitamin D can regulate mast cells, by limiting their development. Baroni et al. (2007) showed that the active form of vitamin D not only initiates apoptosis, but it is also capable of limiting (in a dose-dependent manner) the ability of mast cell precursors to mature (into fully-capable mast cells), dependent upon the presence of vitamin D receptors. It doesn't get much more co-dependent, convoluted, and generally complex than that.

Is it any wonder that so many people, including physicians, are confused about how the immune system actually works?
It's a very complex and sophisticated system. And it can do wonderful things for us, provided that we just do our part to help keep it functioning properly. What this interdependent relationship implies then, is that vitamin D receptors must be present in adequate quantities in order for the active form of vitamin D to be able to prevent the production of excess numbers of mast cells when an inflammatory event is in progress. This is a mechanism that the immune system utilizes to prevent reactions from getting out of hand. Baroni et al. (2007) also demonstrated that VDR-deficient mice experience faster mast cell maturity rates than normal mice, and the mast cells that are produced are more easily-activated, compared with those produced by normal mice.

This phenomenon appears to explain why so many IBD patients tend to have mast cell activation disorder.
Mast cell activation disorder (MCAD) is a condition marked by inappropriate mast cell activation that results in the excessive release of histamine, cytokines, and other proinflammatory mediators by mast cells, for no legitimate (or at least no apparent) reason. It can cause many of the symptoms of mastocytosis or mastocytic enterocolitis, even though mast cell populations might be normal, or only slightly elevated.

The intestines are known to have relatively high populations of mast cells. MCAD can result in additional symptoms (due to IgE-based reactions) that cause complications, and add confounding issues to certain types of autoimmune diseases, such as IBDs. In the case of microscopic colitis (of which lymphocytic colitis and collagenous colitis are the most common types) for example, MCAD appears to be capable of causing virtually any of the clinical gastroenterological symptoms traditionally associated with the disease, plus the addition of classic IgE-based allergy symptoms such as nasal discharge, watery eyes, and itching skin or tongue, in some cases. These symptoms are usually somewhat attenuated (compared with classic allergic reactions), and they may even be overlooked, unless the patient is aware of this possibility, and remains alert, in order to notice the symptoms. But whether these symptoms are relatively minor, or severe, the additional mast cell activity typically results in increased severity of gastrointestinal symptoms normally associated with an IBD, and in some situations, this type of mast cell activity can even trigger a flare when an IBD has been in remission.

The observations noted in the above paragraph are based on an ongoing epidemiological study of hundreds of people who have microscopic colitis and who share their experiences freely as members of an Internet discussion and support group.13 This collection of real-life experiences is arguably the largest database in the world of specific information devoted to the understanding and treatment of microscopic colitis and related issues. The discussion board has been active (including continued participation by many of the original founding members) for approximately 10 years at this point in time, so a lot of real-life, down-to-earth data are available.

Presumably, this may also apply to the other IBDs, including Crohn's, ulcerative colitis, and celiac disease, although this possibility certainly hasn't yet been verified by random, double-blind research trials. Not all IBD patients experience these IgE-based symptoms, but for those who do, this observation should answer a lot of questions.

So a deficiency of either vitamin D receptors, or vitamin D in it's active form can lead to a hypersensitive condition where not only are mast cells more likely to degranulate (releasing proinflammatory agents), but additional mast cells are produced more rapidly, and more of them are ultimately produced, so that a state of severe hypersensitivity (resulting in massive inflammation) may be the result.

This condition appears to meet the definition of at least mast cell activation disorder, and it might possibly be the primary cause of mastocytic enterocolitis. It also may be associated with mastocytosis, which is a serious systemic form of mast cell disorder.

Other researchers have validated this discovery, and demonstrated how powerful the effect of vitamin D can be.
Additional compelling data about the association between VDRs and inflammation were established when Kong et al. (2008) showed that when normal mice, and mice with compromised vitamin D receptor function, were fed dextran sodium sulfate in order to intentionally attempt to induce colitis, the mice with compromised vitamin D receptors developed much more severe symptoms than the mice with normal vitamin D receptors.14 The mortality rate in the mice with compromised VDR function ranged up to 70 %, whereas there was no mortality, and only relatively minor symptoms in the mice with normal VDR function. Needless to say, that's a striking difference in the results displayed by the comparison of the 2 groups of test subjects.

During a colonoscopy exam, gastroenterologists often take biopsy samples of the interior lining (known as the epithelia) of the colon, and these samples are later examined under a microscope by a pathologist in order to search for microscopic physical changes in the structure of the cells. Certain specific changes are considered to be diagnostic of certain digestive system diseases.

Researchers have shown that patients who have Crohn's disease and ulcerative colitis are indeed deficient in VDRs.
Liu et al. (2013) studied colonic biopsies in order to compare the status of vitamin D receptors in Crohn's disease and ulcerative colitis patients with the VDR status of normal subjects. Compared with the relatively high quantities of vitamin D receptors found in normal colonic epithelial tissue, the researchers found that Crohn's disease and ulcerative colitis were associated with a significant reduction in the number of VDRs.15 By utilizing gene splicing techniques in mouse intestinal epithelial tissue, they demonstrated that a sufficient number of human VDRs expressed in mouse intestinal epithelial cells will protect mice from developing colitis.

The researchers concluded that, "Together, these results demonstrate that gut epithelial VDR signaling inhibits colitis by protecting the mucosal epithelial barrier, and this anticolitic activity is independent of nonepithelial immune VDR actions" (p. 3,982) (Liu et al. 2013). Obviously this is an extremely important observation, as it provides compelling evidence of a possible way to prevent inflammatory bowel disease.

In essence, the researchers have demonstrated that an adequate level of vitamin D (and sufficient numbers of vitamin D receptors) can prevent the development of inflammatory bowel disease. And if this is true in the gut, then there is good reason to believe that future research may verify that it is also true in other organs (including joints) affected by autoimmune-associated inflammation.

And here are the medical references cited in that quote:

12. Baroni, E., Biffi, M., Benigni, F., Monno, A., Carlucci, D., Carmeliet, G., . . . D’Ambrosio, D. (2007). VDR-dependent regulation of mast cell maturation mediated by 1,25-dihydroxyvitamin D3. Journal of Leukocyte Biology, 81(1), 250–262. doi:10.1189/jlb.0506322

13 Discussion and Support Forum for Collagenous Colitis, Lymphocytic Colitis, Microscopic Colitis, Mastocytic Enterocolitis, and Related Issues. (2014). perskyfarms.com. Retrieved from http://www.perskyfarms.com/phpBB2/index.php

14. Kong, J., Zhang, Z., Musch, M. W., Ning, G., Sun, J., Hart, J., . . . Li, Y. C. (2008). Novel role of the vitamin D receptor in maintaining the integrity of the intestinal mucosal barrier. American Journal of Physiology - Gastrointestinal and Liver Physiology, 294(1), G208–G216. doi:10.1152/ajpgi.00398.2007

15. Liu, W., Chen, Y., Golan, M. A., Annunziata, M. L., Du, J., Dougherty, U., . . . Li, Y. C. (2013). Intestinal epithelial vitamin D receptor signaling inhibits experimental colitis. Journal of Clinical Investigation, 123(9), 3,983–3,996. doi:10.1172/JCI65842

If you're not familiar with using digital object identifier (doi) designations for references, here are conventional links for the references that are listed as doi addresses:

12. http://www.jleukbio.org/content/81/1/250.full

14. http://ajpgi.physiology.org/content/ear ... 00398.2007

15. http://www.jci.org/articles/view/65842

Tex

[AnnW]

Consider taking digestive enzymes, prescription strength if you can get them (with your doctor's permission of course). Incomplete digestion will result in the development of more gut sensitivities/allergies over time. VDR genetic defects are very common even in the general population, but seemingly more so in IBD patients. 5,000 - 7,000 IU of Vitamin D/day is the recommended supplemental dose for those with malabsorption issues. I would definitely consider having your the 25[OH]D3 levels tested. 30-50 ng/ml is considered normal.
Dr. Ann

[wnorm]

Thank-you, AnnW. You offered some excellent suggestions. I have taken pancreatic enzymes in the past without success. I definitely will ask my physician about testing for D3 levels. I have not been tested for over 12 years. At that time I was found to be deficient and was put on the 10,000 i.u. / week regimen.I have been reading about VDR defects this week and you offer a plausible solution. Thank-you again.

Consider taking digestive enzymes, prescription strength if you can get them (with your doctor's permission of course). Incomplete digestion will result in the development of more gut sensitivities/allergies over time. VDR genetic defects are very common even in the general population, but seemingly more so in IBD patients. 5,000 - 7,000 IU of Vitamin D/day is the recommended supplemental dose for those with malabsorption issues. I would definitely consider having your the 25[OH]D3 levels tested. 30-50 ng/ml is considered normal.
Dr. Ann

[AnnW]

Are you taking a multi-vitamin/mineral supplement? I ask because the longer someone is on such a restricted diet the more deficiencies they will tend to develop. These deficiencies then slow or prevent the gut from healing. This results in more inflammation, more malabsorption, and the increased likelyhood of developing even more intolerances. It can become a vicious downward spiral. Try finding a multi you can tolerate and start taking it oh so slowly. Maybe taking just one per week, then gradually increasing the dose.

I see this happen so often in MC patients! They have so many intolerances that their nutrition suffers. Then they wonder why they are not getting any better. It is normal to want to stay away from food intolerences. Who wants to feel bad?! Obviously, you cannot keep eating foods that inflame or irritate the gut. However, avoidance should be temporary for at least some of these foods. Many can be re-introduced after the gut begins to heal. We all need to keep in mind that without adequate nutrition, we can (inadvertantly) inhibit the very healing we desire.

If you cannot cut out all gluten containing foods than at least look for a digestive enzyme supplement that helps digest gluten. However, I have found gluten to be a problem in every MC/IBD patient I have worked with. Here is a gluten-free flour mix I found that you can use for baking that is free of both xanthan and guar gum. Substitutions for each flour are in parentheses.

1¼ cups/170 g brown rice flour (sorghum flour)
1¼ cups/205 g white rice flour (millet flour)
1 cup/165 g sweet rice flour (potato flour)
1 cup/120 g tapioca flour (potato starch)
2-4 tsp powdered unflavored gelatin

Dr. Ann

[wnorm]

Thank-you Dr.Ann. I have always taken a multivitamin. I take the Cosco one for seniors.
I am not familiar with a digestive enzyme that digests gluten. I'll have to look it up.
Thank-you for the recipe for a gluten-free flour mixture. I will certainly try it. Obtaining the
gelatin might be a problem. I keep kosher. The only available gelatin, imported from Israel, is made from fish bones and costs over $5 for 2 tiny packets, probably about a tsp each packet. Also usually the store does't have any. Is there anything else that I can substitute for gelatin?