Would like to share my research with you...

Dwamma

WOW! Thank for the eye opener! Lost of good infor there!

Blessings! <><

PeggyWoodson

Hello,

This is my first day and I am just wondering how you all are losing weight? Is it just by tracking what you eat and exercising!?

Yes. I count carbohydrates and others count calories and I'm sure there are others who do other things on here to loose weight. I normally track my food and my exercise with this web site. I enjoy it and find it motivational.

MrsObundles

Very cool. Thanks for sharing!

12by311

Super interesting information. Do you suggest that people take a fiber and probiotic supplement daily?

samb330

Great post. Thanks for sharing. I know what I'm going to go out an buy tomorrow!:flowerforyou:

badgerbadger1

I'm sorry, when you refer to "leaky gut" between the intestinal cells are you talking about a leak into the vascular space, interstitial space or peritoneal space?

So everyone can stay in on the convo, I will stay it's a leak between the cells.

The cells in your intestine are too far apart because the proteins that keep them together aren't being made.

I guess I need the proper physiological explanation to fully digest what you're saying.

Okay...it appears to leak through the paracellular space. Enterocytes are held together by tight junctions...transmembrane receptors associate with one another across the paracellular junction and are held in place by anchor proteins attached to actin to allow for some contraction. LPS moves from the apical to the basolateral side of the enterocyte and empties into circulation if it's unbound, or into the lacteal if it's bound to a chylomicron. However, chylomicron-bound LPS is less of a risk as its lipid A portion is inactive when it's bound. Eventually the chylomicron is emptied and loses its ApoB48 apolipoprotein at which point it's considered LDL cholesterol. When oxidized this can bind the toll-like receptors competitively against LPS and doesn't cause such a severe inflammatory response. Or, the liver can take up the LDL along with its bound LPS (if it's still there and hasn't been picked up by a chylomicron in circulation) and acetylate the LPS, inactivating it. If the LPS is free and immediately enters circulation, it can bind to a TLR on skeletal muscle which causes the host of metabolic diseases associated with obesity. Free LPS can also bind TLRs in the intestine, but because the apical membrane is under constant LPS onslaught, TLR's are lowly expressed in normal conditions. However, obese individuals have greater TLR expression in the intestine which allows for some immune response (the TLRs are a major part of the innate immune system). Does that make more sense in terms of leakiness?

Yes. So you meant leaking into the vascular space. I thought we were making the jump to bacterial "leaking", which would of course result in a more severe reaction aka septicemia, however you're talking more at the biochemical/microbio level, so my confusion is thus alleviated. Thanks for sharing, and I'll have to research it further as it's relevant to my work.

jenniejengin

interesting, thanks

songbyrdsweet

I'm sorry, when you refer to "leaky gut" between the intestinal cells are you talking about a leak into the vascular space, interstitial space or peritoneal space?

So everyone can stay in on the convo, I will stay it's a leak between the cells.

The cells in your intestine are too far apart because the proteins that keep them together aren't being made.

I guess I need the proper physiological explanation to fully digest what you're saying.

Okay...it appears to leak through the paracellular space. Enterocytes are held together by tight junctions...transmembrane receptors associate with one another across the paracellular junction and are held in place by anchor proteins attached to actin to allow for some contraction. LPS moves from the apical to the basolateral side of the enterocyte and empties into circulation if it's unbound, or into the lacteal if it's bound to a chylomicron. However, chylomicron-bound LPS is less of a risk as its lipid A portion is inactive when it's bound. Eventually the chylomicron is emptied and loses its ApoB48 apolipoprotein at which point it's considered LDL cholesterol. When oxidized this can bind the toll-like receptors competitively against LPS and doesn't cause such a severe inflammatory response. Or, the liver can take up the LDL along with its bound LPS (if it's still there and hasn't been picked up by a chylomicron in circulation) and acetylate the LPS, inactivating it. If the LPS is free and immediately enters circulation, it can bind to a TLR on skeletal muscle which causes the host of metabolic diseases associated with obesity. Free LPS can also bind TLRs in the intestine, but because the apical membrane is under constant LPS onslaught, TLR's are lowly expressed in normal conditions. However, obese individuals have greater TLR expression in the intestine which allows for some immune response (the TLRs are a major part of the innate immune system). Does that make more sense in terms of leakiness?

Yes. So you meant leaking into the vascular space. I thought we were making the jump to bacterial "leaking", which would of course result in a more severe reaction aka septicemia, however you're talking more at the biochemical/microbio level, so my confusion is thus alleviated. Thanks for sharing, and I'll have to research it further as it's relevant to my work.

Ah, no, we are WAY lower than sepsis here, like 50 times lower. This is referred to as metabolic endotoxemia. People can have endotoxin levels up to 5 EU/mL plasma without feeling anything, and around 10 some issues arise. We generally see anywhere from 6-11 EU/mL after high-fat feeding in humans but we have taken some measurements much higher after a fat challenge (like 2 Jimmy Dean b-fast sandwiches in one meal). Some of our mice get low-dose LPS injections without entering sepsis as well.

songbyrdsweet

I am convinced now that I have a leaky gut and my intestines are being colonized and taken over by gooey evil.
Bleeeech. That said, can't say anything is probably more disgusting than the fat already there.

LOL fortunately the bacteria aren't visible so you are free from their gooeyness.

songbyrdsweet

YAY I was worried that I was overdosing on probiotics bc the box says take 1 but I always take two bc they are lower dosage then my previous pro-biotics but it looks like with some of your comments you cannot od on probiotics! That is great news! I have also heard pro-biotics are given to children help swing ADD, ADHD, and other behavioral disorders mood swings. Something about the happy hormones starting in the gut? Do you know anything about that?

Nah, you can't overdose. The gut is connected to the brain via nervous system and endocannabinoid system. Your gut can send signals to your brain about whether you need to eat and even can promote serotonin release. I wouldn't promote that over a Dr's rX though.

songbyrdsweet

You did a fabulous job breaking down scientific info AND footing questions (I teach high school Science). You have the making of a great professor! Good luck with your research!

That is a great compliment! Thank you!! And thank you for teaching!

songbyrdsweet

Super interesting information. Do you suggest that people take a fiber and probiotic supplement daily?

I sure do. Unless you get plenty of fiber from your diet, then you don't need to pay for extra.

LabRat529

Thanks so much for sharing!!

msunluckythirteen

Thanks! Great info! I recently come off of Prilosec and over use of Rolaids. I became gluten free and haven't really needed them since, but I wondered what kind of harm the Prilosec and Rolaids have done to my insides. I will certainly start taking some probiotics now.

grinch031

Everyone has a mix of healthy and harmful bacteria. Healthy bacteria keep your intestines covered in mucous, they digest fiber to make gas and some fatty acids for your intestinal cells to 'eat', and they kill harmful bacteria. Harmful bacteria are covered with something called lipopolysaccharide (LPS) which causes a type of inflammation in your body. This isn't like a bruise or an illness; it's almost undetectable, but it causes things like insulin resistance. It might also cause obesity and type 2 diabetes in the long run. When the harmful bacteria die, the LPS comes off of them and floats around in your intestine.

Everyone says that insulin resistance is caused by obesity, but you're saying that might not be true? What type of foods promote harmful bacteria growth?

docjoe

Interesting stuff, thanks for sharing. I do some oncology research, we are quite interested in probiotics therapeutically, opening a study in our pancreatic cancer patients. The FDA in their mighty wisdom has ruled we have to hold an IND for it which has been a bit of a setback (curious to know if you've run into this in your human trials,I think it's ridiculous). I think your research is great, it is really becoming more clear that the health of our bacteria impacts our personal health in far more profound ways than previously appreciated.

Interested in your mTor work since that is a big deal in my world. Have you been involved in oncology or is mTor being looked at in other arenas?

songbyrdsweet

Thanks! Great info! I recently come off of Prilosec and over use of Rolaids. I became gluten free and haven't really needed them since, but I wondered what kind of harm the Prilosec and Rolaids have done to my insides. I will certainly start taking some probiotics now.

Those are made to reduce aciditiy. While that's good in the esophagus, it's not great in the stomach or intestine as an acidic environment helps control the growth of harmful bacteria. So I think the probiotics are a good idea.

songbyrdsweet

Everyone has a mix of healthy and harmful bacteria. Healthy bacteria keep your intestines covered in mucous, they digest fiber to make gas and some fatty acids for your intestinal cells to 'eat', and they kill harmful bacteria. Harmful bacteria are covered with something called lipopolysaccharide (LPS) which causes a type of inflammation in your body. This isn't like a bruise or an illness; it's almost undetectable, but it causes things like insulin resistance. It might also cause obesity and type 2 diabetes in the long run. When the harmful bacteria die, the LPS comes off of them and floats around in your intestine.

Everyone says that insulin resistance is caused by obesity, but you're saying that might not be true? What type of foods promote harmful bacteria growth?

Well they are definitely linked. It's sort of a chicken-egg debate. Does the gut bacteria make you obese, or does the obesity cause the gut microbiome to change? It sort of goes like this:

Obesity--> increased fat cell size and gut leakiness --> inflammation --> metabolic inflexibility (unable to oxidize fats) & insulin resistance

But there are a BILLION subcategories within each area.

Toddrific

Hmm, when you eat yogurt you look for specific bacteria, are the probiotic supplements supposed to have key bacteria in them?

songbyrdsweet

Interesting stuff, thanks for sharing. I do some oncology research, we are quite interested in probiotics therapeutically, opening a study in our pancreatic cancer patients. The FDA in their mighty wisdom has ruled we have to hold an IND for it which has been a bit of a setback (curious to know if you've run into this in your human trials,I think it's ridiculous). I think your research is great, it is really becoming more clear that the health of our bacteria impacts our personal health in far more profound ways than previously appreciated.

Interested in your mTor work since that is a big deal in my world. Have you been involved in oncology or is mTor being looked at in other arenas?

Thank you! The IND is weird. O.o To my knowledge we didn't need that as this is not really a 'drug'. We're studying high-fat overfeeding with/without probiotics and taking anthropomorphic measurements as well as metabolic function stuff. I'm heading the metabolic function assays and the other lab is doing the clinical side.

I was studying mTOR regulation during endotoxemia. Many chronically ill patients experience cachexia and I was looking for the link between LPS, mTOR, and muscle wasting in a high-fat diet. Found some interesting changes in insulin receptor. I don't do anything with oncology but one of my co-workers studies sphingolipids and ovarian cancer, very cool stuff.