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What is myanteric plaxus? I thought it was a muscle at first, but then you said decreases tone so what is it? And what is tone exactly bc it's confusing

I was addicted to opioids and that stuff made it so you can't sht. I would drink like 5 mugs of coffee before I could poop. Interesting that Loperamide is in the same category.

2:03 damn that chick is hot

I'm here because I was confused 😂 I had nasty diarrhoea after a big night of drinking and I took gastro stop and my stohmach would be very very noisy gurgling non stop I'd go to the toilet thinking it was just the diarrhoea but nothing would then happen

You are absolutely 100% wrong about Lomotil being addictive. I've been on and off of it for 30 years and have steadily taken it for the last 15. It has no business being a scheduled drug. It is non addictive and has zero abuse potential. Your medical textbooks have misled you.

The explanation is amazing that complicated concept can be explained by your simple wordings.

Wait, 50 mg each of NMN and Nicotinamide…according to your previous graphic, those are the same thing. I’m confused how these two are different.

Thank you for this video. I’ve always wanted to know how Imodium worked. You are the only channel I found that shows a model and you explained it very well. Thanks again.

Histamine 2?

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Mitachondria are the powerhouse of the cell

Extremely good video. Thank you for your time and sharing your knowledge

How many minutes takes to go to toilet? 8hrs?

It’s the only thing that makes me sleep.

Low dose flush niacin is best and most cost effective to raise NAD levels

Thank You 💯🦾

You make the best pharmacology videos, very thorough!

I’m faded off the lope hope I don’t croak

This is a very informative video! Thank you!

Wow, thanks for the info!

Thankyou

Is loperamide an opioid just like codeine ? Does it make you addicted ?do you get withdrawals from loperamid? Because it does I don t want to use it

And who are you again?

great video

Osmotic laxative may not only induce an electrolyte inbalance, but especially Epsom salt may lead to the kidney kidney in the case of a false dosage.

So….. you dont know anything. As sodium do not cause these effects.

Best explanation of this on TH-cam

Thank you very clear .

Not a student but i take lopramid regularly, i ve always wondered how it works and how long do i wait to see it s results, now i understand how i should use it to get the effects i want, thank you so much for making a video that is easy to understand even for someone unrelated to medicine

I just wanted to know how immodium works lol thanks

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Great revision. Would you have a video on the action of NSAIDS and COX-2 inhibitors and gastric ulcers?

Throughout this chapter, we've learned quite a bit about the cellular receptors by using the medications from the drug class termed opioids. We've also learned the most important safety issues regarding the treatment of diarrhea. Right now, we're going to finalize the chapter with a few last points about the specific opioid termed loperamide, starting with the mechanism by which it works. In the gastrointestinal tract, we have the nervous system cells, and they communicate with the brain, and they also have an effect on what's happening in the GIT. This very large network of nerves is called the enteric nervous system, and it can speed up or slow down the peristaltic actions in the GIT, and it can also affect the secretion of products such as mucus into the GIT. Peristaltic actions are wave-like muscular contractions of the muscles in the GIT. Also in the GIT, we have opioid receptors in the cells, and when our body's natural opioids bind to those opioid receptors, there's a decrease in peristaltic actions within the GIT. And you can see from that the endogenous opioids are one of the tools in which we regulate the gastrointestinal tract. In the presence of endogenous opioids, the peristaltic actions will decrease, and that will allow more time for the absorption of fluids from the GIT, so the fecal contents get drier. So, loperamide is an opioid agonist that acts on those same receptors as natural endogenous opioids. That slows down the GIT, and as such, relieves diarrhea. Remember that we're taking a pharmacological dose of the agent, so it has much more of a profound action than our natural release of opioids would. To be clear, loperamide is not the only medication for diarrhea. Most of our opioid medications will decrease diarrhea, and there's also other medications known as anticholinergic agents, so against acetylcholine, that are useful for diarrhea as well. But loperamide is normally the preferred medication because most of it stays in the gastrointestinal tract and simply works locally. Right now, I'd like you to try to hypothesize about what an opioid antagonist would do and what its applications would be. Why would we want to block the opioid receptors in the GIT, and why would we want to block the opioid receptors in other parts of the body? And you were right if you had said to reverse the effects of too many opioids in the body. We have a couple different kinds of opioid antagonists. One is called methyl naltrexone. Methyl naltrexone is an opioid receptor antagonist that has a very poor capacity to be absorbed. So you can think of it as being pretty much the exact opposite of loperamide. And it's specifically given to decrease the constipating effects of the opioids. We don't give it for any kind of constipation, but rather, for instance, if a person has taken high doses of opioid medications for cancer pain, the physician may need to block some of those receptors in the GIT so the person is relieved of their severe constipation. And another opioid antagonist is naloxone. Naloxone is an opioid antagonist that's used for people who are experiencing the opioid-related respiratory depression that comes along with overdose of opioids. Naloxone binds so strongly to the opioid receptors that it actually knocks off other opioids that are already there, and quickly reverses the life-threatening side effects of opioid overdose. The important thing about naloxone is that it is extremely short-lived in the body. Or in other words, it has a very short half-life. And it needs to be re-administered a couple times before the other opioids will be out of the system.

I know a person that took 100 and was hurt.

New meds, waiting for it...3/11

You don't need 1-4 grams of NA to significantly raise NAD+. Just a fraction of that will be the same as much higher concentrations of NR and NMN (NMN has to be broken down into NR to be transported into cells). So if you take under 100 mg of NA, then almost all people will have no flushing and the claimed insulin resistance increase is not significant at that lower level. What's more the existing evidence points to NMN and NR being almost all degraded by the gut microbiome intor nicotinamide. The claims in this video that only 125 mg of NMN is needed to get an effect are just complete nonsense. Sinclair himself takes at least a 1000mg or more to raise NAD+. As to the claimed benefits, there has been no studies proving that at all, just clinical studies providing evidence of safety. Of course NO list of references to back up those big claims for NMN. Experiments inhibiting the conversion to nicotinamide also remove the increase in NAD+. So NMN and NR are a BIG waste of money. Supplementing with Nicotinamide is known to inhibit the synthesis of NAD+ so without references, doubt those claims as well. There has been research showing the benefit of taking D-ribose along with NA, both of these supplements are cheap building blocks of NAD+. But since companies can't patent them and they are so cheap, there is no profit in talking about them. The use of exercise at least is the one thing this video gets right. Suggesting using NMN is just garbage advice.

i just did take Mineral oil and detergent laxatives at same time :(

Thanks 🙏

Do the second generation 'drugs' also aid sleep?

Niacin 60mg was equivalent to 1000mg NMN in raising NAD. Don't waste your money.

Another Top way to increase NAD or to preserve it is to lower cd38 levels. CD38 Rises as we age and depletes NAD. Quercetin and apigenin do this nicely. They suppress cd38 but do not overly reduce it . They bring it down to youthfull levels. Also TMAO from gut bacteria will cause a rise of CD38 which again, uses up NAD. Garlic and Berberine will knock down the bacteria that turn dietary choline into tmao. You should also use equal amounts of trimethyl gycine with b vitamins ( TMG) so as not to deplete methyl doners in the liver. Over time it will harm your health. I dont bother with NMN. Its too greaking expensive. Its also almost exclusively turned into niacinamide in the gut and liver anyways. I use high dose niacinamide , quercetin, agigenin and berberine along with a tsp of TMG. Apigenin is also showing promise in slowing azheimers disease. It lowers blood pressure , is neuroprotective, reduces anxiety and more. And dont forget all the other b vitamins too. Nothing works in isolation. Biological pathways are extremely complex and even one fsctor that is missing can stall or impair your normal biological processes.

I hate those cheesy stock videos that every TH-camr seems to be using.

Can these osmotic laxatives be administered anally, supp or small volume enema? At a very cautious dose, so only the very hard dehydrated stool in or near the rectum is affected. Are these osmotic laxatives also not for prolonged use? Does psyllium husks created an osmotic pull into the bowel? Or just use up and retain the water in the bowel?

Glorious video thank you!

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NA nicotinic acid flushing niacin is the most effective NAD precursor actually

Hi, my English is not good. Do you think taking 500mg NAM (Niacinamide) is good for improving NAD level?

very informative, thank you. Looks like I need to stop taking sodium bicarbonate. I already have a high daily sodium intake and hypertension.

Thank you professor ❤