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The BEST explanation. All you gotta do is brush up on some notes if you haven't already and you're good. Or can also serve as a wonderful review to put everything together. Amazing!
It should be mentioned too, that LDL is not a cholesterol at all, but a cholesterol "transporter". We just call it LDL "cholesterol" for convenience but, it's not really correct.
it is said in the beggining of the video, that cholesterol is transported in lipoprotein particles and she talks about “low density lipoprotein - LDL” and not LDL cholesterol
@@michaell132 Yeah, I've always hated that term "bad" cholesterol. No such thing as bad cholesterol, just two different kinds of cholesterol. LDL is not necessarily "bad". I much prefer the more descriptive term of "small dense particles" and large. The large ones are harmless and just bounce around in the bloodstrream. Those small ones though, are the bad ones that lodge on artery walls, Atherosclerosis.
Hi, just wondering what your thoughts are on the different types of LDL - pattern A and pattern B which are increased in different diets? Also, thank you simplifying all these processes. Very helpful.
@MrBilld75 Agreed. I'm glad to see more people are catching up on that distinction. It is important to note that unbiased evidence indicates that LDL is "associative" in atherosclerotic plaque formation as opposed to being "causative". There's a huge difference between the two particularly with regard to prevention and treatment. We are still looking into this but the current evidence indicates that LDL can get damaged by glycation, oxidation and inflammation as a result of too much sugar/refined carbs intake, plant sterols (yes..in spite of the fact that it's ironically used to lower supposedly "bad" cholesterol) and a state of systemic inflammation (from the progression of insulin resistance for e.g.). I'm on the train right now so I can't type much...I'll try and elaborate on this another time. Damaged LDL are mostly of type B (dense). For example, one mechanism causing issues is the fact that the apoprotein B100 on LDL get damaged enough so that they can't be recognised and reabsorbed by the liver receptors for recycling. So they end up pooling in the circulation hence promoting adhesion to the vascular endothelium. Inflammation also makes the endothelium prone to that phenomenon. LDL is also a repair molecule so it will also migrate (by transcytosis using ATP) to sites of inflammation in an attempt to repair thus further exacerbating plaque formation over time as this process is repeated. Macrophages also try to engulf those inflammatory LDL complex resulting in foam cells and this also triggers more cytokines release (pro inflammatory). So you can see how this cascade can result in more plaque formation over time. Too long to elaborate on but hope that quick summary helps.
Learning this a while back is what made me want to limit/stop my intake of animal products. Over time, i have now been vegan for a good few years. No bad cholesterol in my diet 🙏
I'm experienced now high cholesterol is problem exist more than 20 from normal range, i am taking drug for this, as well as drugs for my hyperthyroidism, and high blood. And even my doctor tell me i have a liver problem too. I'm 38 yrs old heavy drunker before i diagnosed this problem, i completely stop drinking alcohol 6 months ago, i started exercise work today and diet, my next laboratory will be in February, hope there will be a good result. Thanks for the video.
At 1:40 the video states that chylomicrons go from the gut via blood to the liver. They do not. They are secreted by the intestinal cells into the lymphatic system, and drain via the thoracic duct into the venous circulation at the junction of the left subclavian and internal jugular veins, at the commencement of the brachiocephalic vein.
So now they are in the bloodstream and will go to the liver, right? We just skipped the details you mentioned to focus on the MAJOR steps of cholesterol metabolism. Sorry if the video gave the impression that they go directly from the intestine to the liver, they do not, but those steps are not essential for the scope of this video.
@@junemercado Cholesterol does not just float around freely in your bloodstream. Cholesterol is like a fat and your blood is like water. And we know fat and water don't mix. Therefore, the cholesterol we typically learn about in our blood work (i.e. LDL-C, HDL) is carried within LDL particles that transport cholesterol throughout your body. In simple terms, there are two types of particles, small dense particles and large buoyant particles. Many experts now believe it is the nature of the particles, not the cholesterol they are carrying, that really matters when it comes to things like heart disease. The particles themselves can be measured with advanced lipoprotein testing, typically NMR (nuclear magnetic resonance) testing. It sounds intimidating but can be done via a routine blood test that is sent to labs to do this sort of testing (which are becoming more commonplace as time goes on). Most often the particle numbers are reported in nmol/L (nanomoles per liter). Optimally, you want results showing a total LDL particle number of about 1000 nmol/L or less. And you want your small (dense) particle number to be 200 nmol/L or less (optimally). The large buoyant portion, which your NMR result will also provide, is not the number to focus on according to some experts, as they are not atherogenic. But the small dense particles (so the theory goes) can get into the endothelium of your coronary arteries and contribute to the heart disease process. Why is that? Well, large LDL particles have a relatively short time duration, say 24 hours, and are "dispensed" with fairly quickly, but small LDL particles are not easily recognized by the liver and hence float around in your circulation much longer (e.g. a week or so) giving them more time to do their damage. You can appreciate therefore why standard cholesterol measurements (like LDL-C) never seem to correlate well to the occurrence of heart disease. Cardiologist Dr. Stephen Sinatra, who operated on thousands of patients and actually saw their arteries with his own eyes, used to say many patients with very high LDL-C would have beautiful, pristine arteries, yet many with low LDL-C had prolific heart disease. We now know the nature of LDL particles can be very much in our control by lifestyle and diet. Diets high in carbohydrates, wheat, grains, sugar etc. provoke the occurrence of abundant, dangerous small LDL particles. But low-carb diets (even if high in fat), support metabolic health and most often will result in a healthy small LDL particle sub-fraction (along with increased HDL by the way), thereby lowering your cardiovascular disease risk. To sum up, heart disease is a metabolic disease. Cholesterol is not the problem. And the sooner less attention is paid to cholesterol and the focus gets changed to metabolic health, the sooner we will see some progress in reducing heart disease. C'mon, we've been doing it wrong for 50 years. Let's change the paradigm now so we can start making strides.
@@Malcolm-Achtman Beautifully explained!! A lot of useful information can be gained from videos from Ivor Cummins on this subject. As you explained, LDL in itself is not bad, and high values of measured LDL are not dangerous. The problem arises when these LDL particles become "coated" with "sugary" molecules or oxidized. This changes the appearance of LDL and it is not recognized by special receptors on the liver that control the re-absorption of LDL. It remains floating in the blood for extended periods, causing the discussed health issues. Metabolic disease is caused by sugar- and refined carb loaded products as you explained. Also vegetable or seed oils are abundantly used in the food industry, because very cheap. Think of canola, cottonseed, sunflower, safflouer, soy, peanut and other oils and margerines. These products are highly processed and have nothing in common with the seeds they were taken from. The oils are easily oxidized inside and outside the body (compare this with a sliced apple, parts are browning fast when exposed to air). This oxidized oil leads to chronic low grade inflation in the body and changing the surface of LDL particles, after which they are not recognized by the liver for reuptake. The often demonized natural occurring saturated oils and fats have absolutely no impact on health. They contain no unsaturated (double) carbon-carbon bonds and are more or less inert to oxygen on body temperature. Also in the kitchen their smoke point is high. Unsaturated fatty acids like the omega varieties (e.g. in fatty fish) are heart healthy. It is best to consume fish, as capsules with oil are more easily oxidized.
@@TheVafa95 If you obtain a routine lipid panel it will include your triglyceride and HDL values. A crude but potentially good way to establish your metabolic health would be to calculate your triglyceride/HDL ratio. Ideally, that ratio should be 1.5 or less. For example, if your trigs were 70 mg/dL and your HDL was 55 mg/dL, the ratio would be 70/55 = 1.27. That's pretty good. Another key blood test to get is fasting insulin. Also get fasting glucose. So, be sure to fast for about 12 hours before getting these tests. You can drink water, but no juice or coffee or food. A very good fasting insulin result would be about 3 uIU/mL. A good fasting glucose result would be 80 - 90 mg/dL. Try to get HbA1c tested as well. An optimal value is 5.0% or close to that.
Very good. It would be even more helpful if intracellular processing of LDL cholesterol was included. One point would be to explain how cholesterol is exported from lysosomes. How many pathways are there? One pathway is via the lysosomal membrane protein NPC1 that allows transport of cholesterol to the ER facilitating homeostasis . Defects in this pathwat result in Niemann-Pick type C disease, a severe and fatal condition.
Right. Here is a Wikipedia article on lacteals that better describes the route taken by chylomicrons: en.m.wikipedia.org/wiki/Lacteal Chylomicrons actually travel through the lymphatic system first before being released into the bloodstream at the thoracic ducts for transit back to the liver. While traveling back to the liver, some triglycerides are removed from the chylomicrons thereby creating a more dense chylomicron remnant that contains a higher concentration of lipoprotein. This remnant is what actually gets reabsorbed into the liver. More triglycerides are then added to this denser structure to form VLDL.
return to liver of chylomicron how to become VLDL The process you’re referring to involves the metabolism and transformation of lipoproteins within the body. When chylomicrons, which transport dietary fats, return to the liver after delivering fatty acids to tissues, the liver processes their remnants. The liver repackages these remnants into very low-density lipoproteins (VLDL). Here’s a simplified breakdown: Chylomicron Remnants: After chylomicrons deliver triglycerides to peripheral tissues, they return to the liver as chylomicron remnants. Processing in the Liver: The liver takes up these remnants and reprocesses them. The liver cells (hepatocytes) remove remaining lipids and cholesterol from the chylomicron remnants. Formation of VLDL: The liver synthesizes new VLDL particles by combining triglycerides and cholesterol. These VLDL particles are then secreted into the bloodstream. VLDL serves the purpose of transporting triglycerides from the liver to various tissues in the body. As VLDL particles circulate in the bloodstream, they gradually lose triglycerides, becoming intermediate-density lipoproteins (IDL) and eventually low-density lipoproteins (LDL), which are often referred to as “bad cholesterol.” Feel free to ask if you want to dive deeper into any specific part of this process! Message Copilot
It might be a bit late to ask, but Im curious whether dietary cholesterol generally is processed more into LDL, since there was a lot of controversy regarding dietary cholesterols.
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Explained to me in 4 minutes what my lecturers couldn't explain me to in 1 hour. Thank you
Danny Williams
It’s very limitedly informative but good for premed beginners tho (not even enough for premed)
@@xufenghuang yeah ! But for example, i will be working on lipid metabolism disorders and I am here to get some info before that
In harper it is given nicely....and after that you can see Lippincott for revision too
Very true
Seems like someone is a bit stupid
What an incredible, clear and concise run through of lipid transport. The best I've seen. Thank you
Hands down the best explanation with best visuals I've seen yet! Thank you so much for sharing!
The BEST explanation. All you gotta do is brush up on some notes if you haven't already and you're good. Or can also serve as a wonderful review to put everything together. Amazing!
Best video in 4 mins. Let's show some love here.
you're the real MVP! short & simple way to review! THANKS!
Oh my god. This video just packed together an entire day of gibberish so it made sense. Its SO FUCKING GOOD.
Learned something new about the difference between HDL and LDL. Thanks!
content that is compact and easy to understand. I Stan
thank you for explaining this biochemistry and pharmacology stuff in such simple way!
It should be mentioned too, that LDL is not a cholesterol at all, but a cholesterol "transporter". We just call it LDL "cholesterol" for convenience but, it's not really correct.
Absolutely.....
it is said in the beggining of the video, that cholesterol is transported in lipoprotein particles and she talks about “low density lipoprotein - LDL” and not LDL cholesterol
@@nikoletavassova3927 Hmmm, I must have missed that part. Thank's for pointing that out.
Also listen at 3:05 where it’s stated that LDL is known as bad cholesterol
@@michaell132 Yeah, I've always hated that term "bad" cholesterol. No such thing as bad cholesterol, just two different kinds of cholesterol. LDL is not necessarily "bad". I much prefer the more descriptive term of "small dense particles" and large. The large ones are harmless and just bounce around in the bloodstrream. Those small ones though, are the bad ones that lodge on artery walls, Atherosclerosis.
5 hours lectures in 3min you saved my semester!!
Great VDO! Highly knowledgable was that stuff! 🤩
The Video I've been looking for. Great job
Such explanations are useful to all medical professionals& I expect more such useful information
crazy how much you can learn in 4 minutes, while ive been reading for hours not getting it
because school is meant to enslave and confuse you.
Amazing video. Thank you so much.
I love that the video that was the easiest and clearst to understand was narrated by a woman :)
Thank you so much Vicky!!
Good summary of all the processes involved in Lipid transport ...
This is amazing and so helpful!!!!
It gives a fundamental knowledge about lipid metabolism to comman men and students. Thankyou very much with appreciations.
Hat's off to u champ👏
Great explanation 👍
Hi, just wondering what your thoughts are on the different types of LDL - pattern A and pattern B which are increased in different diets? Also, thank you simplifying all these processes. Very helpful.
@MrBilld75 Agreed. I'm glad to see more people are catching up on that distinction. It is important to note that unbiased evidence indicates that LDL is "associative" in atherosclerotic plaque formation as opposed to being "causative". There's a huge difference between the two particularly with regard to prevention and treatment. We are still looking into this but the current evidence indicates that LDL can get damaged by glycation, oxidation and inflammation as a result of too much sugar/refined carbs intake, plant sterols (yes..in spite of the fact that it's ironically used to lower supposedly "bad" cholesterol) and a state of systemic inflammation (from the progression of insulin resistance for e.g.). I'm on the train right now so I can't type much...I'll try and elaborate on this another time.
Damaged LDL are mostly of type B (dense). For example, one mechanism causing issues is the fact that the apoprotein B100 on LDL get damaged enough so that they can't be recognised and reabsorbed by the liver receptors for recycling. So they end up pooling in the circulation hence promoting adhesion to the vascular endothelium. Inflammation also makes the endothelium prone to that phenomenon. LDL is also a repair molecule so it will also migrate (by transcytosis using ATP) to sites of inflammation in an attempt to repair thus further exacerbating plaque formation over time as this process is repeated. Macrophages also try to engulf those inflammatory LDL complex resulting in foam cells and this also triggers more cytokines release (pro inflammatory). So you can see how this cascade can result in more plaque formation over time. Too long to elaborate on but hope that quick summary helps.
just wow! soo simplified! thank you :)
The voice is so soothing!!
Kudos on an awesome informative video. Thanks!!
So helpful 🥺♥️ thank U to make the Arabic translateor
Awesome Video! Had a much clearer concept about LDL & HDL now. Thank you!
A huge love form India...🙏
Omg thank-you i got confused, this is very helpful
this is amazing! thank you for this video!!!
Informative and Straight forward
What you're doing is excellent. Thank you 💕.
Thanks for the video it's very helpful ^^
really good explanation, thanks
Thank you for explaining cholesterol metabolism
je suis en 2e année de médecine en France et je comprenais rien grâce a toi j'ai compris la base de mon cours, MERCII
Very clearly explained...🥰
to the point, simple, clear. G-d sent! tysm!
You guys are awesome!! Keep it up with the good work.
Great explanation👍👍👍
Short and excellent explanation... thanks for the video 😊
Learning this a while back is what made me want to limit/stop my intake of animal products. Over time, i have now been vegan for a good few years. No bad cholesterol in my diet 🙏
Absolutely great!
Excellent video. It helped me a lot. Thank you. 🙂
Wow! Thank you! Was so well explained ,thank you
You're very welcome!
Great explanation.. Keep up the good work.. 👍👍👍👍
Its is so helpful, thanks!
I learned in less than 5 minutes about Lipoproteins instead of 5 hours of biochemistry
Thank you for the lovely video, very helpful
You are so welcome!
Such a good video
Thank you so much ❤
Best video ever
This is so beautiful
best explained........thanks a lottt
Best Vedio and its very helpful😊😊😊😊
Welldone. Good job.Hat off
LDL is not the enemy. It is the inflammation.
what is the enemy then
@@aysumutcan Insulin resistance causes inflammation.
Yes its the inflammation
this is amazing, this vid is SO GOOD
Love how you explained this. Thank you
Glad you enjoyed it!
Good work👍👍👍
WOW so good, it was so helpful
You are missing the transition from VLDL to LDL ( IDL ). Still great job
Jose Cordova, also the difference between liver derived LDL vs LDL derived from VLDL degradation.
It's amazing video, thank you so much really
I'm experienced now high cholesterol is problem exist more than 20 from normal range, i am taking drug for this, as well as drugs for my hyperthyroidism, and high blood. And even my doctor tell me i have a liver problem too. I'm 38 yrs old heavy drunker before i diagnosed this problem, i completely stop drinking alcohol 6 months ago, i started exercise work today and diet, my next laboratory will be in February, hope there will be a good result. Thanks for the video.
Hi, you may also want to change from a carb loaded menu to low carb. Check out Jason Fung and/or Paul Mason .
wow, for me am highly educated by this info thanks
Glad to hear!
Very helpful, thanks.
Amazing and easy revision
Nice video, great lecture, understand able.
Good explanation
Great work!
At 1:40 the video states that chylomicrons go from the gut via blood to the liver. They do not. They are secreted by the intestinal cells into the lymphatic system, and drain via the thoracic duct into the venous circulation at the junction of the left subclavian and internal jugular veins, at the commencement of the brachiocephalic vein.
So now they are in the bloodstream and will go to the liver, right? We just skipped the details you mentioned to focus on the MAJOR steps of cholesterol metabolism. Sorry if the video gave the impression that they go directly from the intestine to the liver, they do not, but those steps are not essential for the scope of this video.
@@Alilamedicalmedia First they visit fat cells.
Thank you so much
Fantastic explanations. Thanks!
Glad you enjoyed it!
Amazing video thanks very much
Awesome 👍 saved me 🙏
Ldl is off two types - small dense ldl and large buoyant ldl
So what does it mean?
@@junemercado Cholesterol does not just float around freely in your bloodstream. Cholesterol is like a fat and your blood is like water. And we know fat and water don't mix. Therefore, the cholesterol we typically learn about in our blood work (i.e. LDL-C, HDL) is carried within LDL particles that transport cholesterol throughout your body. In simple terms, there are two types of particles, small dense particles and large buoyant particles. Many experts now believe it is the nature of the particles, not the cholesterol they are carrying, that really matters when it comes to things like heart disease. The particles themselves can be measured with advanced lipoprotein testing, typically NMR (nuclear magnetic resonance) testing. It sounds intimidating but can be done via a routine blood test that is sent to labs to do this sort of testing (which are becoming more commonplace as time goes on). Most often the particle numbers are reported in nmol/L (nanomoles per liter). Optimally, you want results showing a total LDL particle number of about 1000 nmol/L or less. And you want your small (dense) particle number to be 200 nmol/L or less (optimally). The large buoyant portion, which your NMR result will also provide, is not the number to focus on according to some experts, as they are not atherogenic. But the small dense particles (so the theory goes) can get into the endothelium of your coronary arteries and contribute to the heart disease process. Why is that? Well, large LDL particles have a relatively short time duration, say 24 hours, and are "dispensed" with fairly quickly, but small LDL particles are not easily recognized by the liver and hence float around in your circulation much longer (e.g. a week or so) giving them more time to do their damage. You can appreciate therefore why standard cholesterol measurements (like LDL-C) never seem to correlate well to the occurrence of heart disease. Cardiologist Dr. Stephen Sinatra, who operated on thousands of patients and actually saw their arteries with his own eyes, used to say many patients with very high LDL-C would have beautiful, pristine arteries, yet many with low LDL-C had prolific heart disease. We now know the nature of LDL particles can be very much in our control by lifestyle and diet. Diets high in carbohydrates, wheat, grains, sugar etc. provoke the occurrence of abundant, dangerous small LDL particles. But low-carb diets (even if high in fat), support metabolic health and most often will result in a healthy small LDL particle sub-fraction (along with increased HDL by the way), thereby lowering your cardiovascular disease risk. To sum up, heart disease is a metabolic disease. Cholesterol is not the problem. And the sooner less attention is paid to cholesterol and the focus gets changed to metabolic health, the sooner we will see some progress in reducing heart disease. C'mon, we've been doing it wrong for 50 years. Let's change the paradigm now so we can start making strides.
@@Malcolm-Achtman Beautifully explained!!
A lot of useful information can be gained from videos from Ivor Cummins on this subject.
As you explained, LDL in itself is not bad, and high values of measured LDL are not dangerous.
The problem arises when these LDL particles become "coated" with "sugary" molecules or oxidized. This changes the appearance of LDL and it is not recognized by special receptors on the liver that control the re-absorption of LDL. It remains floating in the blood for extended periods, causing the discussed health issues.
Metabolic disease is caused by sugar- and refined carb loaded products as you explained. Also vegetable or seed oils are abundantly used in the food industry, because very cheap. Think of canola, cottonseed, sunflower, safflouer, soy, peanut and other oils and margerines. These products are highly processed and have nothing in common with the seeds they were taken from. The oils are easily oxidized inside and outside the body (compare this with a sliced apple, parts are browning fast when exposed to air). This oxidized oil leads to chronic low grade inflation in the body and changing the surface of LDL particles, after which they are not recognized by the liver for reuptake.
The often demonized natural occurring saturated oils and fats have absolutely no impact on health. They contain no unsaturated (double) carbon-carbon bonds and are more or less inert to oxygen on body temperature. Also in the kitchen their smoke point is high.
Unsaturated fatty acids like the omega varieties (e.g. in fatty fish) are heart healthy. It is best to consume fish, as capsules with oil are more easily oxidized.
@@Malcolm-Achtmanthanks for your explanation. How would you measure metabolic health at low cost?
@@TheVafa95 If you obtain a routine lipid panel it will include your triglyceride and HDL values. A crude but potentially good way to establish your metabolic health would be to calculate your triglyceride/HDL ratio. Ideally, that ratio should be 1.5 or less. For example, if your trigs were 70 mg/dL and your HDL was 55 mg/dL, the ratio would be 70/55 = 1.27. That's pretty good. Another key blood test to get is fasting insulin. Also get fasting glucose. So, be sure to fast for about 12 hours before getting these tests. You can drink water, but no juice or coffee or food. A very good fasting insulin result would be about 3 uIU/mL. A good fasting glucose result would be 80 - 90 mg/dL. Try to get HbA1c tested as well. An optimal value is 5.0% or close to that.
Excellent
Best explanation so for.
Very good. It would be even more helpful if intracellular processing of LDL cholesterol was included. One point would be to explain how cholesterol is exported from lysosomes. How many pathways are there? One pathway is via the lysosomal membrane protein NPC1 that allows transport of cholesterol to the ER facilitating homeostasis . Defects in this pathwat result in Niemann-Pick type C disease, a severe and fatal condition.
Thx that was v. Helpful
G even I can follow this. Great presentation
Chylomicron is not always transported to the liver , some times the chylomicrons move from small intestine to peripheral tissues
Right. Here is a Wikipedia article on lacteals that better describes the route taken by chylomicrons:
en.m.wikipedia.org/wiki/Lacteal
Chylomicrons actually travel through the lymphatic system first before being released into the bloodstream at the thoracic ducts for transit back to the liver.
While traveling back to the liver, some triglycerides are removed from the chylomicrons thereby creating a more dense chylomicron remnant that contains a higher concentration of lipoprotein. This remnant is what actually gets reabsorbed into the liver. More triglycerides are then added to this denser structure to form VLDL.
Hats off 🙌
Excellent.
Just wooooow
Thanks ❤❤❤❤❤❤
Perfect thank you so much
Loved it awsmmmmmm💯
Wonderful. ,,... thx
OMG THANK YOU!
return to liver of chylomicron how to become VLDL
The process you’re referring to involves the metabolism and transformation of lipoproteins within the body.
When chylomicrons, which transport dietary fats, return to the liver after delivering fatty acids to tissues, the liver processes their remnants. The liver repackages these remnants into very low-density lipoproteins (VLDL). Here’s a simplified breakdown:
Chylomicron Remnants: After chylomicrons deliver triglycerides to peripheral tissues, they return to the liver as chylomicron remnants.
Processing in the Liver: The liver takes up these remnants and reprocesses them. The liver cells (hepatocytes) remove remaining lipids and cholesterol from the chylomicron remnants.
Formation of VLDL: The liver synthesizes new VLDL particles by combining triglycerides and cholesterol. These VLDL particles are then secreted into the bloodstream.
VLDL serves the purpose of transporting triglycerides from the liver to various tissues in the body. As VLDL particles circulate in the bloodstream, they gradually lose triglycerides, becoming intermediate-density lipoproteins (IDL) and eventually low-density lipoproteins (LDL), which are often referred to as “bad cholesterol.”
Feel free to ask if you want to dive deeper into any specific part of this process!
Message Copilot
thank you ❤
Yes
It might be a bit late to ask, but Im curious whether dietary cholesterol generally is processed more into LDL, since there was a lot of controversy regarding dietary cholesterols.
Honestly you slayed it. Let me know if you'd like to collab!
I have been on Tirzepatide for 8 weeks. I have lost 20lbs. My cholesterol was 400 and is now 168!!!
So helpful. Thanks!
Perfect thank you Guys for being here
great lecture, thanks.
I have a quesiton:
Cholesterol is an example of what type of lipid?
a) lipid
b) fat oil
c) phospholipid
d) sterol
Superb