Is a Thiamine Deficiency the trigger for Lactose Intolerance in Celiac's.

[Posterboy]

To All,

I recently rediscovered this research on Lactose Intolerance and a Thiamine deficiency and thought it deserved it's own topic.

Entitled "Effect of dietary thiamine deficiency (aka Vitamin B1) on intestinal functions in rats"

https://pubmed.ncbi.nlm.nih.gov/6465054/

I will quote the whole abstract because I think it is instructive.

Abstract

"The effect of dietary thiamine deficiency has been studied on intestinal functions and chemical composition of brush border membranes in rats. Intestinal uptake of glucose, glycine, alanine, and leucine was significantly stimulated in thiamin deficiency compared to pair-fed control group. Studies with glucose and glycine revealed that stimulation of the absorption process occurs only in the presence of Na+ but not in its absence. Km measured in the presence of 140 mM Na+ for glucose and glycine uptakes was reduced by 56 and 41%, respectively, but Vmax remained unaltered in vitamin deficiency. There was no change in these parameters in Na+-free medium (Km = 31.3 and 23.3 mM; Vmax = 17.2 to 19.7 and 13.5 to 16.4 mumol/10 min/g wet tissue, respectively) under these conditions. The activities of brush border sucrase, lactase, maltase, alkaline phosphatase, and leucine aminopeptidase were reduced by 42 to 66% in thiamine deficiency, compared to pair-fed controls. Kinetic studies with sucrase and alkaline phosphatase evinced that a decrease in Vmax (61 and 64%, respectively) with no change in Km (33.8 and 4.3 mM, respectively) was responsible for observed impairment in the enzyme activities in thiamine deficiency. Microvillus membrane proteins expressed on dry membrane basis were reduced by 20% in thiamine-deficient intestine. There was no difference in membrane sialic acid, cholesterol, phospholipids, and triglycerides fractions under these conditions. It is suggested that thinning of the microvillus membrane may be implicated in observed aberrations of intestinal functions in thiamine-deprived animals."

What do others think about this research is a Thiamine deficiency the trigger for Lactose Intolerance in Celiacs?

It seems to be consistent about what we know about how Low Thiamine levels can thin a Celiac's Villi?

See this article that explains this Thiamine connection in Celiac's?

Feed back and your thoughts are welcomed......it seems plausible in my mind what do you think???

If this is so.....then it could help those Celiac's still suffering from a Lactose Intolerance IMO....

Posterboy,

[Blue-Sky]

Here is some more information on nutritional deficiency and IBS.

https://onlinelibrary.wiley.com/doi/10.1111/jgh.15830

[Scott Adams]

It does make me wonder what comes first, the chicken or the egg (at least in celiac disease)? Does celiac disease get triggered by a virus or some other environmental factor in those with the genetic traits that make them susceptible to it, which then causes thiamine deficiency and further gut issues, or does thiamine deficiency, at least in some with the genetic traits, somehow help to trigger celiac disease?

[Posterboy]

Scott et All,

I don't think I could convenience you either way but I do know Celiac disease IBS, Chrons, UC, Heartburn (GERD) etc. happens when Low Stomach acid is ignored or overlooked in GI Disease(s) etc.

Howard Hughes Medical Institute aka HHMI debunked this theory years ago (20 years ago in fact to this year) but PPIs and H2 Blockers are as popular as ever it seems.

https://www.hhmi.org/news/excessive-growth-bacteria-may-also-be-major-cause-stomach-ulcers

I do think poor nutrition happens first (and why Celiac's are low in their minerals and B-Vitamins etc.) and I think Beri Beri is where the Link breaks.

Here are some links that might help you or who ever else who reads this.

Celiac disease is not the only trigger for Blunted Villi.....and this something Blue Sky already knows being an expert on Zinc....

But a  Zinc deficiency determines the Crypt height of our Villi.....not eating Gluten or Milk or Corn etc....

https://www.researchgate.net/figure/Influence-of-zinc-levels-on-gut-formation-Zinc-levels-mediate-villus-height-and_fig1_274013774

And a Niacin deficiency regulates our Zinc levels.....see this research entitled "Dietary nicotinic acid (aka Niacin or Vitamin B3) supplementation improves hepatic zinc uptake and offers hepatoprotection against oxidative damage"

https://www.cambridge.org/core/journals/british-journal-of-nutrition/article/dietary-nicotinic-acid-supplementation-improves-hepatic-zinc-uptake-and-offers-hepatoprotection-against-oxidative-damage/9D74C9569F29C909991AF47C7AFCE810

Oxidative damage or what we know as Villi Blunting comes from Low Zinc levels mediated by Low Niacin Levels.

We know our brush border enzymes are impaired WHEN Low in Thiamine and why I quoted it and underlined it.....to highlight this doesn't happen UNTIL the deficiency occurs.

I don't think it is only one deficiency but probably 4 or 5 critical deficiencies but I do think it starts with Thiamine aka Vitamin B1 because we can't synthesize B1 when we get low in it.

We also know Thiamine helps regulate our Immune System via Acetylcholine triggering an auto-immune state.

See this article that explains how this happens....

https://www.medicalnewstoday.com/articles/321624#From-inflammatory-to-anti-inflammatory

Also an excessive intake of Carbs to Proteins has been shown to trigger metabolic Beri Beri and in today's HFCS modern laced diet of the Standard American Diet (SAD) it is easy to trigger the excessive 15 Carbs to 1 protein ratio needed to spare Thiamine from becoming deficient in the body.

See this nice article that summarizes this fact of the 15 to 1 ratio being established years ago and forgot years ago by modern medicine.

https://medium.com/war-is-boring/eating-too-much-rice-almost-sank-the-japanese-navy-f985772c81a6

quoting their paragraph the "Proof is in the Eating"....

"Sailors were consuming too many carbohydrates. Earlier German research had demonstrated that a healthy diet required at least one unit of protein per 15 units of carbohydrates. By contrast, the average Japanese sailor ate one unit of protein per 28 units of carbs."

And I think it hardly strange that today's HFCS standard American diet doesn't easily exceed that....

Add to that when we are low in Copper.....our thiamine is depleted.....and I can  easily believe a thiamine deficiency and a Zinc deficiency and a Niacin deficiency could easily be triggering a genetic disease (so called) or a poor nutritional status that is being diagnosed or confused for a Genetic disease instead.

I need to wrap this up so.....it doesn't get WTL again....

Here is Cooper deficiency, Fructose and Thiamine deficiency connection article...

Entitled "The fructose–copper connection: Added sugars induce fatty liver and insulin resistance via copper deficiency"

https://insulinresistance.org/index.php/jir/article/view/43/142

But I also wanted to cite this article because I think it is instructive if we want to heal our Leaky Guts then Niacin will be helpful to us...

Entitled "Intestinal permeability and oxidative stress in patients with alcoholic pellagra"

https://pubmed.ncbi.nlm.nih.gov/16713031/

where they say in conclusion "The results suggest that (supplementing with) niacin...  recovering to normal values after treatment with niacin".....IE the Leaky Gut and Intestinal Permeability returned to normal after supplementation....

And isn't that what we all want --- Normal.

I wrote a Posterboy blog post that goes into more detail about how Genetics, Nutrition and Stress can trigger an Immune reaction in Celiac's and other Severely Malnourished individuals (with GI problems) if any body wants to read it and has the time and interest to do so.  If it doesn't help Blue Sky or you....maybe it will help the next reader.....Lord Willing.

I hope this is helpful but it is not medical advice.

I am just trying to share what helped me.....in the hopes it will help the next person the Lord being my help.

Posterboy by the grace of God,

 

[Posterboy]

On 6/17/2022 at 6:28 PM, Posterboy said:

I don't think I could convenience you either way but I do know Celiac disease IBS, Chrons, UC, Heartburn (GERD) etc. happens when Low Stomach acid is ignored or overlooked in GI Disease(s) etc.

Scott, (et al)

If Thiamine was not the trigger (IMO) then your Thiamine levels would improve on a Gluten Free diet.....but just the opposite happens.

See this Australian study entitled "Nutritional inadequacies of the gluten-free diet in both recently-diagnosed and long-term patients with coeliac disease"

https://pubmed.ncbi.nlm.nih.gov/23198728/

Where they note quoting....

"The frequency of inadequacies was similar pre- and post-diagnosis, except for thiamine and vitamin A, where inadequacies were more common after Gluten Free Diet (GFD) implementation."

This was after eating Gluten Free for a 12 month period (IE a year)......when you replace one CARB (starch) for another.....the same results happen.......

When you are are get over 15 to 1 protein ratio......Beri Beri will develop.

Here is another blog post that might be  helpful to others who come across this thread .......where I discuss some of these Vitamin deficiencies in greater details....

If Celiac disease was the trigger and not the Vitamin/Mineral deficiency then eating gluten free would cure the Vitamin deficiencies (Presumably) and they (it) just don't/doesn't do it....

Even 10 years later the same deficiencies still exist......despite eating gluten free....

See this research entitled "Evidence of  (still) poor vitamin status in coeliac patients on a gluten-free diet for 10 years"

https://pubmed.ncbi.nlm.nih.gov/12144584/

Low stomach acid or NO Stomach Acid is a much more "Elegant" approach/way to think about GI problems of all kinds......not just Celiac disease or NCGS etc.

What your stomach acid can't dissolve your Villi won't be able to absorb!

I hope this is helpful but it is not medical advice.

2 Timothy 2:7  “Consider what I say; and the Lord give thee understanding in all things” this included.

Posterboy by the grace of God,

[Blue-Sky]

6 hours ago, Posterboy said:

"The frequency of inadequacies was similar pre- and post-diagnosis, except for thiamine and vitamin A, where inadequacies were more common after Gluten Free Diet (GFD) implementation."

I think it is saying they aren't eating to match the DV. (Maybe by 1% less than DV or a lot more I don't know). The absorption rate could be improved on a GFD though. That could explain changes in the homocysteine levels (along with malabsorption) I think, without resolving the chick or egg problem.

[Posterboy]

Scott and Blue Sky Et Al,

Here is the research that shows where Virus (IE Environment) can trigger a Celiac diagnosis in Science Magazine I thought once......now it is Science.org

Entitled "Reovirus infection triggers inflammatory responses to dietary antigens and development of celiac disease"

https://www.science.org/doi/10.1126/science.aah5298

In their comment section or response to this article now behind a paywall (so I can't cite it) but I didn't capture their (someone's) response so this article earlier so I will quote it because it is intriguing, interesting and helpful I think.

I would like to know @knitty kittythoughts on this as well....

This is by Leslie Klevay the Professor Emeritus of the North Dakota School of Medicine who had a similar thought about 5 years ago and what made me think I was on the right tract with the Vitamin/Mineral deficiency triggering the Genetic disease.

quoting the full correspondence.

"RE: Cooperative mechanisms in human illness

Leslie M. Klevay, Prof. Emeritus, Department of Internal Medicine University of North Dakota School of Medicine and Health Sciences

(19 May 2017)

Bouziat et al.(1) found that reovirus infection may disrupt intestinal immune homeostasis and initiate loss of oral tolerance to gluten leading to celiac disease. The findings may explain the epidemiologic association between viral infection and onset of food sensitivity(2).

Three decades ago(3, 4) it was suggested that four classes of etiologic agents---toxicity, heredity, infection, deficiency---plus cooperations between and among members of the classes can explain much variability of human disease (a sequel is currently under editorial review).

Here reovirus seems to change gluten from an innocuous dietary component into a toxin. The complicated mechanism is somewhat different from the original infectious intoxications described (3), e.g., in cholera the organism elaborates an enterotoxin that produces illness directly by inhibiting sodium absorption causing great, and often fatal, loss of fluid and electrolytes.

Some patients with celiac disease absorb too little dietary copper and become deficient(5, 6). In the original classification scheme, celiac disease would have been considered a toxic deficiency (3) similar to Wernicke’s encephalopathy in which excessive ingestion of ethanol induces thiamine deficiency. Now some celiac disease can be considered a three-way cooperation among an infection, a toxin and a deficiency. Other three- and four-way cooperations have been identified(3).

Bouziat et al.(1) found that reovirus infection may disrupt intestinal immune homeostasis and initiate loss of oral tolerance to gluten leading to celiac disease. The findings may explain the epidemiologic association between viral infection and onset of food sensitivity(2).

Three decades ago(3, 4) it was suggested that four classes of etiologic agents---toxicity, heredity, infection, deficiency---plus cooperations between and among members of the classes can explain much variability of human disease (a sequel is currently under editorial review).

Here reovirus seems to change gluten from an innocuous dietary component into a toxin. The complicated mechanism is somewhat different from the original infectious intoxications described (3), e.g., in cholera the organism elaborates an enterotoxin that produces illness directly by inhibiting sodium absorption causing great, and often fatal, loss of fluid and electrolytes.

Members of the four classes of known, etiologic agents can cooperate to modify and induce human illness. More attention to cooperative mechanisms may lead to better understanding of seemingly incomprehensible illnesses. Viruses that do not lead to overt clinical pathology may be worth investigation(1) as contributing to a new type of infectious intoxication. Perhaps associations of illnesses with members of the microbiome involve cooperations that may be mediated via toxins or deficiencies of essential nutrients."

And that is exactly what we find in the research IMO especially where Vitamin deficiencies like Thiamine, Riboflavin, Niacin, Zinc and/or Copper deficiencies as well as Low Tryptohan levels (to name many of the usual suspects) can and do effect GI Health!

And that is exactly what new genetic research approx. two and a half years ago found to be true.

https://www.genengnews.com/news/dna-has-relatively-little-say-in-disease-risk-usually/

The problem is.....most people can't wait another 20+ years before this new thinking (working Theory) in Science works it way down to the clinical level.

quoting from the Genetic Engineering news article about this topic.

“It is becoming increasingly clear,” explained Wishart, “that the risks for getting most diseases arise from your metabolism, your environment, your lifestyle, or your exposure to various kinds of nutrients, chemicals, bacteria, or viruses.”

Notice that Wishart referred to most diseases. According to Wishart and colleagues, these include many cancers, diabetes, and Alzheimer’s. In fact, for such diseases, the genetic contribution to disease risk is just 5–10%. There are diseases, however, for which the genetic contribution is about 40–50%. These diseases include Crohn’s disease, celiac disease, and macular degeneration."

Which means many diseases only have a 10 to 20% genetic risk (unlike putatively (commonly) believed) and you often hear repeated.

Heck I have another "Genetic" disease called Hemochromosis (Genetically high Iron) that I beat with the proper and appropriate supplementation.

IF the doctor's will do or would do the research Nutritionist could teach them a thing or too!  But they won't sadly....

The doctor who treated me for my high Iron got MAD at me for the research HE/THEY should of been doing.

Here is the research my high iron was triggered by a Vitamin deficiency of Copper and Vitamin A.

https://www.sciencedirect.com/science/article/abs/pii/S0899900708005029#:~:text=Vitamin A deficiency increased liver hepcidin mRNA and,and significantly increases divalent metal transporter-1 mRNA levels.

Maybe your doctor(s) will be kinder to YOU when you bring the research to them!

Sadly about once a month or once a quarter he loses patients who Iron levels are over 1K and as high as 5K leading to Iron overload in their organs and eventually organ failure and death.......treatable by appropriate supplementation(s).

Or at least  in my case.......I have found I have keep another "Genetic" disease at bay (and doctor's) with Vitamins and Minerals.

I also wanted to say.....and that is exactly what we find when Pellagra (a Niacin/Tryptophan deficiency) treats/improves accelerates Villi health/healing in Celiacs!

https://www.news-medical.net/news/20201022/Tryptophan-found-in-turkeys-can-accelerate-intestinal-healing-in-people-with-celiac-disease.aspx

I hope this is helpful but it is not medical advice.

I wish us all good luck and good health on our/your continued journeys in health and life!

2 Corinthians (KJV) 1:3,4 3) “Blessed be God, even the Father of our Lord Jesus Christ, the Father of mercies, and the God of all comfort;

4) who comforteth us in all our tribulation, that we may be able to comfort them which are in any trouble (starfish/sufferer), by the comfort wherewith we ourselves are comforted of God.”

Posterboy by the Grace of God,

[Blue-Sky]

 Meat depending on the type  and quantity might result in worse bacteria compared to fruits and vegetables. More limited high tryptophan foods or supplements are probably beneficial.

Ahr ligands, niacin and other things sensitize dendritic cells which can switch to tolerant dendritic cells. I know vitamin d plays a role in this process also. Short chain fatty acids (like acetate and propionate) from fermentable soluble and insoluble fiber might be the main stimulators of this process if someone eats a normal diet.

Here is another link on the topic:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5917019/

https://www.youtube.com/watch?v=DSawB-MlChk

[Wheatwacked]

On 6/14/2022 at 12:39 PM, Scott Adams said:

It does make me wonder what comes first, the chicken or the egg

A small dinosaur egg mutated and gave us the chicken as a result. 😉

Oldest known velociraptor relative was a chicken-sized feather-covered predator

 

[Posterboy]

Wheatwacked Et Al,

I was going to start a thread about this article I came across recently ( and might still do since it really is a  fascinating  article/interview of Dr. Alessio Fasano....but haven't had the chance yet entitled "Alessio Fasano, MD: How a Cholera Researcher Became an Expert on Autoimmune Disease"

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6396758/

And it had some interesting information I did not know that might help answer the "was it the chicken or egg question"???

It was the deficiency of Zonulin according to his research that came first (or the research he quoted)

quoting from the article.....read it all when you get a chance...

"Of course, at that point, we reasoned, like for anything that has a physiological function, what the problem would be when you push it to the extreme and you propel from physiology to pathology. As I mentioned before, autoimmune diseases are considered conditions in which you lose the capability to keep these enemies at bay and prevent autoimmunity from occurring. Because celiac is the only autoimmune disease for which we know the trigger—that is, gluten—it was only logical for us to look first and foremost at celiac disease and ask the question: “Is the zonulin pathway involved?” If it is, do we have any evidence that these people have an increased amount of zonulin, and therefore an exaggerated permeability, compared to normal people? The answer turns out to be most definitely, yes. They produce 10 times more zonulin than normal people do and, consequently, their intestine is more permeable even before the intestine is damaged by the autoimmune process. So the reason we choose to study celiac is because it is the only autoimmune condition that you can turn off—no gluten in the diet—or on—reintroducing gluten in the diet—at will."

He says the deficiency of Zonulin comes first......which if the research from the Live Journal blog is to be believed then Zonulin  a marker of a Niacin deficiency comes first then the Gut begins to leak!....

https://alobar.livejournal.com/2930798.html#%2F2930798.html

I hope this is helpful but it is not medical advice.

Posterboy,

[Scott Adams]

Very interesting research for sure!