Lipoprotein (a) increases in a low Vitamin C diet?

carnivore

#1

Continuing the discussion from Bob Harper host of Biggest Loser had a heart attack:

Pulling some research enquiry strings together from a few forum threads.

Précis: Lipoprotein (a) elevated on a blood test can be a risk indicator for cardiovascular disease.

Just listening to Joel Kahn, vegan cardiologist, who explains that elevated lipoprotein (a) is an inherited condition that can cause cardiovascular disease (in relation to Bob Harper’s heart attack). Yes, listening beyond the silo wall. They talk just like us. Kahn is a top shelf obfuscator.

https://podcasts.apple.com/au/podcast/plant-based-vs-ketosis-diet-wars-cardiologist-joel/id582272991?i=1000403419994

Whereas some research indicates the lower availability Vitamin C as involved in blood clotting may also be a stimulus for elevated lipoprotein (a). Carnivore enthusiasts indicate a theory that less Vitamin C is needed in the unique metabolic state of carnivore or keto-carnivore.

The unique metabolic state caveat seems very important in contextualising diet or nutrition discussion.


"Spoon-Fed" by Tim Spector
(Eric - The patient needs to be patient!) #2

Ep40 Dr Kendrick was a pretty solid podcast.


(Bob M) #3

In Episode 40, Ivor Cummins made an observation that he looked into Lp(a) at one point because his value was 180 nmol/L, but his CAC score was zero. Malcolm Kendrick made a comment that if your endothelium is healthy, Lp(a) might not be called upon to repair damage.

Here are my Lp(a) scores:

On 6/13/19, the day before I got 367 nmol/L, I got the following CAC score:

So, at least based on calcification of the arteries, my “high” Lp(a) (which is double Ivor’s) does not appear to be doing much. Or perhaps if it is doing something, I’m counteracting that by, e.g., diet and fasting and maybe exercise.

Note also that different testing facilities use different techniques and the Lp(a) results aren’t comparable. This is why I list the tester and the values they considered to be “high” at the time.

While I have taken vitamin C periodically in the past, I only took it infrequently. It makes me feel strange. Some posters on Malcolm Kendrick’s website have said they take vitamin C and it has lowered their Lp(a). I am not convinced, however, that large doses of vitamin C (or any vitamin, for that matter) are good for you. They may actually be bad for you.

It may also be that my high Lp(a) is killing me some other way, perhaps non-calcified plaque, or through some other deleterious effect. But I don’t know what those are to be able to test them.


#4

Your whole post is great stuff Bob. Thanks for sharing the knowledge and n=1 experience.

It makes sense that Lp(a) is not called into action unless there is arterial wall damage. And if a person is in a low insulin state that will reduce a lot of major risks. But I’m wondering about Vitamin C deficiency amping up the Lp(a) numbers. If Vitamin C drops low enough, maybe in the presence of a manganese* depleted or deficient state (longer term carnivore), it may set up the start of atherosclerosis?

  • Manganese being involved with Vitamin C in collagen synthesis and tissue repair.

(Bob M) #5

I have not taken enough data to determine whether taking vitamin C would decrease Lp(a). And the other issue is, let’s say this does work, what are the long term effects of taking vitamin C? I have heard (but have not researched) that too much vitamin C could be bad for you.

I find that I only take vitamin C if I think I"m getting a cold or other illness (and even there, I’m not sure about the studies).


(A fool and his bacon are soon parted) #6

There are plenty of threads around discussing recent research that implies we may have no need whatsoever for vitamin C on a well-formulated ketogenic diet. As Dr. Fung likes to point out, “If you’re no longer taking the poison, you no longer need the antidote.”

I believe you are involved in some of those threads to which I am referring, and I believe that it was in response to one of your posts that I posted a number of articles by Dr. Eric Verdin on the body’s ability to mobilise endogenous defenses against oxidative stress when we eat a ketogenic diet. Since the answers to a lot of your questions appear to reside in these articles, might I suggest that you might find it helpful to actually read them, instead of posting the same questions over and over again in different threads?


(PJ) #7

This is the theory that several brilliant scientists proposed more than half a century ago.

Chronically sub-acute (low but not by ‘current standards’) ascorbic leads to degradation of various ascorbic-dependent tissues, particularly to include arteries.

The pressure of blood from the heartbeat, at the point where the arteries have ‘turns’, gradually wears away (because the arteries are weakened) at the wall right where the turn is. This doesn’t happen everywhere. It happens where there is some degree of bend.

The erosion at the point of the bend ‘exposes’ (sort of) some molecules two of which happen to be high receptors for proline and for lysine.

The body creates a larger amount of Lipoprotein(a) in response to the degradation of the arteries. This is because it works well as a gummy-patch over the weakened area. As this situation continues, it patches over the patches until the patches themselves begin to occlude the artery in that location. (Also: other various crap sticks to that area and the L(a) as well. So it’s like a sticky junk pile, which also attracts calcium and calcifies (stiffens).)

Linus Pauling, a Nobel chemistry expert, realized eons ago that simply adding proline and lysine to the blood in a larger dosage – they are nutrients, amino acids – because they had a stronger pull than the receptors, would cause the patch material to bind one molecule at a time to the aminos and carried off.

However you should not do this unless you are also supplementing with ascorbic in order to strengthen the veins. The patches are there for a reason.

Measuring the L(a) tells you how well your arteries are doing in general (the higher, the worse), but that is more a statement on what the body thinks of their integrity, it only indirectly relates to lesions and patches. It does not tell you whether you have one or more patches which have accumulated to the point of endangering you. There is no way currently to know the state of all arteries in all areas in this regard. We get that by inference, by proxy, from other measures.

The theory is that way back in time when humans were not quite finished baking :slight_smile: a retrovirus affected them (and the primate family), and a few rare other creatures in that region, like a fruit bat. All the rest of the creatures on earth create ascorbic endogenously. Humans have the setup to create it – but at the end point, due to loss of a functional form of the last enzyme (l-gulono-1,4-lactone oxidase) of the biosynthesis pathway, it fails. It is suspected that the early humans who survived this, only did so because they lived in a region where the food supply was extremely high in vitamin C.

Before ascorbic was technically ‘discovered’ they had already decided it was a vitamin and ‘it cured scurvy.’ This created a paradigm in science which is dreadfully unfortunate for humanity and health. At the time it had not yet been synthesized in the lab and was extremely expensive to produce. So even what early research was done with it, was done with incredibly tiny amounts. Which sometimes still had impressive results – but nothing like an appropriate dose would.

Animal nutrition guidelines allot monkeys over 50 times the (comparative) ascorbic that the US RDA says humans need. Guinea Pigs, 40 to over 160 times. A goat’s body can make 15,000 mg on the spot to deal with a “sudden stress.” We are told we “need only a few milligrams of ascorbic” – not even a fraction what our body would naturally make on an easy day, were it not for that enzyme-deficiency. Insufficient ascorbic ensures our glucose handling, hormonal handling, and response to insult, injury and stress are dysfunctional.

Back in time, Diptheria was a big deal and ‘they’ (the science field, funded by interest in a worldwide immunization) were exploring ways of conquering this. Every animal they gave it to shook it off, unless they gave it in such high dose it just killed them outright. Then they discovered the guinea pig. Now this animal is far worse for science than mice and rats due to its lifespan. But it turns out, it cannot endogenously produce ascorbic either. Finally they had a lab rat that they could give the illness to, and then test drugs against. That’s where GP’s became the infamous lab animal, to the point that it’s even seeped into the public lingo where ‘guinea pig’ means ‘experimental test subject’.

So the body, although it gets a tiny amount from food, is not meant to get more than tiny amounts from it. We are supposed to create it internally in whatever dose we need. Ascorbic is not merely a vitamin to prevent scurvy. It does so many things in the body it would absolutely boggle your mind. With the exception of scurvy (including the sub-acute levels common now), everything it does is basically a “support” role. One study on olympic wrestlers showed it reduced cortisol by 20%. It recycles Glutathione and Vitamin E. It does all kinds of things – like I said, the list seems endless, and would be longer, much longer, were it a patentable substance. If you are not aware, ascorbic has seen more bias in every possible way in the science field than any other substance.

As an aside, Szent-Gyorgyi won the Nobel prize for discovering a primary role – more info here:

Ascorbic, like magnesium, has an osmotic effect in the intestines. If you take more than you can absorb at one time, it will pull water in and flush. Ascorbic acid absorbs about 16%. Sodium or Potassium or Magnesium Ascorbate in the low 20’s. Of course, if you are very ill, your body may well use the ascorbate before it even has a chance to reach the end of your intestines, in which case you can take dramatically higher doses. Cathcart did early research on this. You can find more about the flush and dosages here:

The best form is liposomal. Because this is encapsulated inside fats, it is pulled in through the peyer’s patches in the upper intestine, and sent to the liver. This drastically increases the amount one can take at once. The second-best form is a “micro-emulsified” form which is partially liposomal. You can make this at home in quantity using ascorbic acid, sunflower lecithin, and a sonicator, all available online.

For anybody with real interest in this, these links are to an old blog of mine (no ads), and this is the very long but “how we got to current point” introduction to ascorbic:

For those who have interest in creating the micro-emulsified/partly-liposomal version at home (for expense/quantity options), there is a page here, but you should read the introduction page linked above first so it makes more sense:

Trivia: in 2001 I was hospitalized for my lungs due to chronic infections that turned out to be (I later learned) a grain-proteins reaction. During that I was assigned a cardiologist due to a moment of very high stress, pain, and crazy heart rate for a few seconds, and that’s the guy who wrote me a prescription to The Protein Power Life Plan book that eventually (much later) I followed and it saved my life. At that time, allegedly I had crazy high “bad cholesterol” though unfortunately I do not recall details (I wasn’t even given them actually, just the reference from the doc).

About a year prior to heart surgery I did some of the “Pauling Protocol” which I will put below, for clearing out the arteries. I only did it off and on. I had a lot of other stuff going on frankly (birth defect issue with the valve, in a terrible state). When I got to the surgery, the surgical team told me I had the cleanest veins they’d seen on an adult in eons and even better than many young people. I had zero bypasses as a result. The surgery took half the normal time and I was a day ahead of ideal goal recovery for the next two weeks until I left the hospital for a couple weeks at a care center (my pleading to the doc to assign me this so insurance would cover it) before going home.

I can’t say that protocol helped but something certainly did.

Vitamin C is the main component of the three ingredients in Linus Pauling’s patented preventive cure for Lp(a) related heart disease, the other two being the amino acid lysine and nicotinic acid (a form of Vitamin B3).

Othomolecular protocols:

  1. Take Vitamin C as ascorbic acid or sodium ascorbate up to bowel tolerance (3 to 18 g) daily.
  2. Take Lysine, 2 to 3g daily for prevention and from 3 to 6 g daily for the greatest therapeutic benefit.
  3. Take Proline from 250 mg to 2000 mg daily. (This added factor may lower elevated Lp(a) within 6 to 14 months.)
  4. Follow Pauling’s general heart and cardiovascular recommendations provided in his book How to Live Longer and Feel Better. Linus Pauling’s Basic Vitamin Program: Vitamin E – 800 to 3200 IU, Vitamin A - 20,000 to 40,000 IU. Super B-Complex, esp. Vitamins B6 and B3
  5. Supplement Coenzyme Q10 (100 - 300 mg) (High vitamin C and several vitamins will help stimulate your own synthesis of CoQ10 which is vital for proper heart function.)
  6. Supplement the mineral Magnesium (300 to 1500 mg) and avoid Manganese (No more than 2 mg. USDA researchers report that elevated manganese, more than 20 mg daily, competes with magnesium uptake in the heart causing irregular heart beats.)
  7. Supplement the amino acids Taurine,Arginine and Carnitine (I to 3 g).
  8. Avoid refined carbohydrates, especially sugars which crowd out the similar vitamin C molecule in cells.
  9. Avoid supplemental calcium.
  10. Add a good mineral/ multivitamin - to cover all possible nutritional needs.

Edited to add: you need a lot MORE vitamin C if you are eating badly. And: L(a) “covers for” lack of ascorbic to a small degree which if you are eating well, is plenty to keep you alive. Lastly: as noted, the vast majority of what ascorbic does is behind the scenes, see the page on Szent-Gyorgyi. Ascorbic is like “inner sunshine.” You can live through cloudy and rainy days and never know the difference. But ascorbic tends to make everything better. We live just fine without it making things better, but when we are faced with almost any kind of assault, it helps a great deal. Most doctors and public only think of it as a prevents-scurvy and anti-oxidant. (Actually it’s also a pro-oxidant. See the Szent-Georgi ref.) It is vastly more.

Some notes on the excellent book by Dr. Thomas Levy about ascorbic which goes through the research that has been done so far for what it helps/does.


(PJ) #8

PS: Fung is attacked for supporting fasting. He is accurate that you need a lot less ascorbic (re: scurvy) if you’re not eating badly, and that you need a lot less anti-oxidant if you’re not eating badly. I suspect he is uninformed about the great detail related to this ascorbic topic, which is the norm. Medical school is like an indoctrination in many regards, and it’s amazing when doctors like him actually finally start discovering alternative views. Ascorbic is pretty obscure in the modern world of info. Or, he is simply only addressing the point people are making, when attacking fasting (and ketogenic) for allegedly driving up L(a). Lower ascorbic will increase L(a) so that it can support the body better in compensation. But you can have a fairly low ascorbic and if you aren’t eating like crap, that may be plenty to keep the arteries healthy. You just can’t compare people on a toxic diet to people eating well, when looking at the measures of these things and what matters. The high L(a) is unlikely to matter much if the person is eating well.


(Bob M) #9

I think Lp(a) goes up while fasting because it’s like LDL, it has an energy transport process part. This is what Dave Feldman has shown. And I showed it was true. Using Dave’s protocol, I raised my Lp(a) while fasting and then lowered it on three days high fat, high calorie. See this post:

https://www.ketogenicforums.com/t/the-feldman-protocol-thread/7789/71?u=ctviggen

You can see that LDL and Lp(a) go down basically exactly the same percentage. Nothing to do with vitamin C, only eating more fat and calories.


(PJ) #10

That lack of ascorbic and degradation of arteries causes L(a) to increase, does not mean that nothing else can cause it to increase, you know. I saw that – it’s excellent that anything at all is being done in research with ascorbic which is very difficult to get funded or published (and it’s usually biased in protocol to find negative results). But one of the posts was specifically talking about heart disease, so I was addressing that. :slight_smile: Other forms of reason for increase are, obviously, not heart disease. If you see what I mean.


(Bob M) #11

My point is that no one really knows what these lipoproteins do. For instance, I have very high Lp(a) yet a zero CAC score. If Lp(a) “causes” heart disease, how does it do if if not through calcification? If my arteries are “degrading”, why does that not show up on a CAC scan? If you can fast and that causes Lp(a) to go up, maybe a high Lp(a) goes up for other reasons, too, which are totally unrelated to heart disease? Lp(a) is associated with heart disease, but maybe it doesn’t CAUSE heart disease.

So, there could be theory after theory after theory why Lp(a) “causes” heart disease, but I am one person where my high Lp(a) does not seem to be causing heart disease (that I know of, anyway). If lipidologists were true scientists, this one data point that does not fit their hypothesis means their hypothesis is wrong. It’s wrong. I’m the black swan.

The problem with lipidologists (and epidemiologists) is that they can see one, two, many studies that do not fit their theory, yet their theory keeps going.

So, how do you reconcile your knowledge of vitamin C and Lp(a) with my very high Lp(a) and zero CAC score?


(PJ) #12

Howdy,

No… I didn’t say that. I said WHEN (if-in-the-condition-that) arteries are damaged (which is usually indirectly through bad diet further-depleting ascorbic, which in turn causes issues with tissues such as arteries - subclinical scurvy), L(a) binds to the proline/lysine receptors in that location.

There may be several reasons why L(a) can increase in the bloodstream. One of them is because it is an excellent patch, but there are likely others – you pointed one out in the paper above. That particular substance hasn’t had a ton of time to be the focus of research yet.

If arterial damage is not present, then binding to the damaged areas is obviously not an issue… since there is not damage.

In which case, L(a) in that instance does not appear to have anything to do with heart disease. But in the presence of heart disease, it absolutely does.

It (L(a)) does not cause it (heart disease). It functions as the body’s duct-tape-repair of a crisis situation in the arteries. It probably has other functions too, but that is one of them.


#13

The clots on the arteries don’t need to be calcified to be a risk.
Calcification is a maturation stage of the clot or haematoma as the scar tissue matures.
An arterial embolism can occur from non-calcified clot.


#14

Bob, how did your triglycerides compare when the Lp(a) was tested? Have you been tested for lipoprotein lipase enzyme genetics?


#15

Wonderful post PJ. It raises more questions.
I can see that both you and Bob can be correct.
It is good stuff to pull apart.

For now it seems evident that when people are fed in a highly nutritious state that a variety of metabolic options can be enacted to compensate in pathways where components may be in short supply. Complex human physiology appears to be a multiplicity of metabolic pathways and metabolic detours or bypasses. The pathways that are active are dependent on the base metabolic state. As long as there is no absolute deficient state of an essential nutrient a compensatory pathway seems probably available to maintain health.


(Bunny) #16

Wow that was fascinating, I got lost in every word here are some highlights:

Ivor 01:13:56 You know what? I think it was circa, it would have been 2013. I spent a little while on Lp(a) because my Lp(a) is through the roof. It’s 118 nanomole. It’s huge, like my particle count, but I have zero CAC at 48. And I have my reasons for not worrying about that. But Lp(a), I found a paper and it was old enough to be photocopied rather than a proper electronic copy. I purchased it, and it showed exactly that. It showed that the LDL type components in the plaque are overwhelmingly of the Lp(a) type. How that fact is not openly discussed by lipidologists and poured over is extraordinary to me.

Malcolm 01:14:44 Well, it’s not extraordinary, because it’s the same thing. Once you go down that route, you’re left thinking, “So, we’re wrong.” We thought we were finding… without the cholesterol crystals coming from LDL, no, they don’t. We thought that a lipoprotein we’re finding is LDL. No, it isn’t. Well, there’s the hypothesis gone, isn’t it?

01:15:05 I mean, yes. As you know, Lp(a), lots of people say we don’t know why it’s there. Well, you do because you’ve been told, right? You know why it’s there. It’s there, because. If you have a lack of vitamin C, which is called scurvy or called scorbutic. If you have a low level of vitamin C, or you have damaged the artery walls due to a low level of vitamin C, Lp(a) is attracted to areas of damaging craps, sticks to it very tightly, and cannot be easily removed. And that stops you bleeding to death, because that’s why you die if you’ve got scurvy. So people gums used to bleed and then it would bleed internally, and then they would die.

01:15:53 Vitamin C is required to make collagen, collagen is quite lightly reinforcing roads in concrete. Get rid of the collagen and your arteries start to splinter. So when that starts to happen, well, nature came along because we can’t synthesize… humans can’t synthesize vitamin C. We lost that ability, apparently, 40 million years ago. I never quite know how they can work out this up up 40. But what you were around at the time, did you see it happen, I presume is somewhere you can do this and track it back. But anyway, for some reason, human beings, great apes, couple of other animals I can’t remember, and guinea pigs can’t synthesize vitamin C. So we need it in the diet. If we don’t get it, we die. Which seems a bad design flaw to me. There we go. You know, why would this happen? Anyway, there must be some…

01:16:46 Anyway, that’s evolution for you. So we can’t produce it. So therefore, the theory was by some people that we’ve got, most people have got ineffective, a lot of us are slightly vitamin C deficient at all times so our arteries are slightly cracking open. And then the Lp(a) comes along and sticks to it, and cannot be removed. This was Linus Paulings’s idea, initially. And it wasn’t Linus Pauling’s ideas; Matthias Rath’sidea, and Linus Pauling thought it was a really good idea. So he said, “If you want to prevent heart disease, eat lots of vitamin C, you won’t get cracks in your arteries, and you will live forever.” I don’t know if you eat a lot of vitamin C or not. But of course, if you don’t get cracks in your arteries, it doesn’t matter. Because the Lp(a) does nothing, it just floats around.

01:17:31 This is found, the [Inaudible 01:17:36] don’t synthesize vitamin C. That’s it. And the Lp(a) is designed to cause any damage to the arteries to be covered over and not leak. And then it gets incorporated into the artery as it must do because it gets re-endothelialized. And the reason why Lp(a) is so effective at doing this is because that protein that’s attached to it called Apolipoprotein(a) is almost exactly the same structure as another protein called plasminogen. Plasminogen is incorporated into all clots as they form. And when plasminogen is changing to plasmin, it then slices fibrin apart and chops the clots apart so it shaves it down. But if you’ve got lots of Apolipoprotein(a), this blocks the movement from plasminogen to plasmin, and therefore the clot can’t be got rid of.

01:18:35 So if you’ve got quite a lot of Lp(a) in your system, and a lot of that is arriving in your arteries and covering over clots, then basically you have an immovable or less easily removable clot that is stuck the artery wall. Now, people have looked and said, you know, I’ve seen people say, “We don’t really know Lp(a) does. But why does it look so much like plasminogen? In fact, why is it only changed by three amino acids in a tree ring sequence?” “Well, that’s interesting. What’s that got to do with heart disease?” Well, everything actually, because this is what happens. The Lp(a) is attracted to areas of arterial damage. It forms a clot that is much more difficult to remove. It becomes incorporated into the artery as part of the clot. It looks like LDL and all you idiot say is, “Look, we’ve got LDL inside the plaque.” We go, “No, you don’t. You’ve got Lp(a) inside, which is a completely different thing, or some completely different because it’s exactly the same apart from this protein.” And then they go, “Oh, look, LDL must cause heart disease.” And you think, “Well, that’s one way of looking at it.” But it’s almost like a weird… I remember giving a couple of talks and saying, don’t know if you’ve ever seen the film 12 Angry Men. …More


Woah.. I was banned on facebook.. No idea why
(Bunny) #17

I wonder how long that glycocalyx sheild holds up after a vitamin C deficiency? Even if you get a microscopic crack in the vein or artery itself?

Fascinating because I never seen that term before?

Too much refined sugar (types of sugar/carbohydrates?) in the diet can act as if it were (mimics) Vitamin C?

Thus canceling out the real Vitamin C?

So if you have this (L(a)) stuff floating around constantly patching holes on the walls could that lead (a precursor?) to cardiovascular CHD and CVD (risk?) later in life?

Could the carnivores (carnivore diet?) be getting the real Vitamin C? (that is why carnivores thrive?)

Footnotes:

[1] The glycocalyx is a carbohydrate-enriched coating that covers the outside of many eukaryotic cells and prokaryotic cells, particularly bacteria. When on eukaryotic cells the glycocalyx can be a factor used for the recognition of the cell. On bacterial cells, the glycocalyx provides a protective coat from host factors. …More

[2] Endothelial cell metabolism: A novel player in atherosclerosis? Basic principles and therapeutic opportunities

[3] Diabetic Retinopathy: Breaking the Barrier

[4] Methylglyoxal-Induced Endothelial Cell Loss and Inflammation Contribute to the Development of Diabetic Cardiomyopathy

[5] Effects of Methylglyoxal, TNF-α and IL-1α on Proteoglycan Synthesis in Human Endothelial Cells in vitro

[6] Role of matrix metalloproteinases and histone deacetylase in oxidative stress-induced degradation of the endothelial glycocalyx

[7] The sugar-protein glycocalyx coats all healthy vascularendothelium. It is an integral part of the vascular barrier [1, 2]. The presence of a protein layer on the endothelium was first postulated by Danielli in 1940 …More

[8] ”…The glycocalyx modulates adhesion between cells and also surface characteristics that determine adhesion and flow properties. The layer consists of a network of fibrous proteins with sugar-based side chains. The layer acts as a size-selective molecular sieve that impedes the passage of plasma proteins. …” …More

[9] “…A basic understanding of physiology tells us that it is high cholesterol in conjunction with elevated inflammation and damaged arterial lining (the glycocalyx) that allows cholesterol to product damage. Elevated inflammation and damaged arterial lining occurs when we eat a lot of carbohydrates, especially processed carbohydrates. …” …More

[10] “…The glycocalyx composition varies according to the tissue and cell type, but it is composed primarily of glycosaminoglycans (GAGs) and proteoglycans (PG). The main GAGs are heparan sulfates, chondroitin sulfates and hyaluronan. Heparan sulfates and chondroitin sulfates are carried by PG that belong to two main families: syndecans and glypicans. While syndecans may carry both heparan sulfate and chondroitin sulfate, glypicans only carry heparan sulfate.(20; 21) Hyaluronan is a large secreted GAG that remains in association with the endothelial surface and is thought to be a major structural component of the glycocalyx(22) (Figure 1). …” …More

[11] “…The outer surface of all animal cells is covered by a glycocalyx composed of oligosaccharides (glycans) of glycoproteins and glycolipids and a layer of secreted mucus particularly in the gastrointestinal, respiratory, and urogenital tracts. The biological roles of the glycocalyx are diverse. In general terms, it exerts stabilising and protective functions. Specific functions are related to the glycan structure and cell type and to specific recognition and interaction of glycans with other molecules. Certain glycans are important for development and differentiation of organs through modulation of cell-cell and cell-matrix interactions and signalling. They also can function as receptors for certain pathogens or may represent ligands for various receptors and can be involved in turnover and trafficking of molecules. …” …More

[12] Protein Controversies in Diabetes