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Zag Enzyme, Lectins, Digestive Tract And Clogged Pores

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I took a very long break from the interwebs, to increase my productivity. It worked, a little too well - I started being accused of being a workaholic. So I'm dipping my toe back in tongue.png

When I went back and used better search terms, I was able to find some research about ZAG and desquamation. Interestingly, a couple of papers referred to the ZAG protein as "lectin-like", suggesting it binds to amino sugar signaling molecules. But it also has in vitro ribonuclease and protease activity. There's still no evidence that it directly degrades corneodesmosomes (that I could find), so its likely it plays some signaling role - like cathepsin D. In any case though, it's just one of many (and I mean many) enzymes involved. That's why I don't get the singular focus on it from Cordain ::shrugs::.

MMPs (there are at least 28 that we know of) all have a lot in common. They are active in the extracellular matrix, which means they inhabit the entire body in a wide range of conditions. They are all secreted as prohormones with a cysteine switch, meaning they have to be "activated" in some way before they can function. They all have a Zinc ion in the active site, and are endopeptidases (meaning they cut proteins somewhere in the middle, rather than at the very end of the sequence). They have several conserved structural and sequence features that aren't really relevant for us. They are all proteases that degrade major structural proteins, like collagen, elastin, laminin, and proteoglycans.

But that's where the likenesses end... their functions are all over the place. An easy way to think of the ECM is as a manager and support staff. It micromanages the cells it contains, telling them how and when to develop, what to develop into, where to move, and how to alter what they're doing and producing based on whats going on in the environment. As such, the functions of metalloproteinases are nigh impossible to summarize. The reason they're important for cancer researchers is because they're involved in cell development and differentiation, which is the key process that goes awry in cancerous cells. For the same reason, they're important to growth and remodeling, as well as wound healing and immune response. They're not just workhorses though - it's likely their most important functions are as signaling molecules, causing the release of cytokines and acting on cell-surface receptors for other reasons.

For example, some MMPs are strongly associated with the inflammatory response. We often tend to focus on the middlemen of the process, inflammatory mediators such as interferons, chemokines, histamines, leukotrienes, etc - in a sense, MMPs are one step earlier in the process. This is the reason doxy and minocycline are the antibiotics of choice for acne - they have anti-inflammatory effects on top of their antibiotic effect. We know that the causes of acne vary in importance from person to person - in people whose acne is primarily caused by an over-active inflammatory response to fairly benign levels of bacteria, sebum, and desquamation, anti-inflammatories are particularly useful. Doxy/minocycline have few side effects, and thickened skin or psoriatic skin isn't among them. This suggests some kind of specificity in the inhibition. Its also proven useful in particular cases of both chronic and acute inflammation, with a focus on MMP-9 and MMP-2 (aortic aneurysms, multiple sclerosis, arthritis, atherosclerosis).

The cysteine switch is pretty simple - it's a part of the MMP proteins that literally folds over and puts a cysteine in contact with Zn ion in the active site of the enzyme. In at least some cases, the switch is part of the "propeptide" sequence, the part of the MMP that gets broken off to "activate" the enzyme. Cysteine has interesting functions in active sites because it includes an S-H. This group is called an especially reactive group called a thiol, and can do fun things like bind to metal ions, form disulfide bridges, and strongly interact with the substrate. Suffice to say, if the cysteine is in the right place, it can be crucial to a protein's function. In the case of the switch, the thiol forms a bond with the Zn ion, preventing it and the active site from taking part in any enzymatic reactions.

However, there is no real danger of a cysteine "deficiency" without a general protein deficiency, and putting topical sulfur on doesn't have any effect on the amino acid in general, or the MMP switch. It just.. doesn't work that way. Elemental sulfur is not the same thing as a thiol group on an amino acid. Cysteine isn't an essential amino acid. It's produced from methionine, a common essential amino acid that contains sulfur. Introducing any other sulfur compound will have no obvious influence on the production or use of cysteine, and certainly not on the cysteine switch.

Okay break time tongue.png

PS: I wrote off Mercola as a scam artist a couple of years ago. I try really hard to give natural and alternative medicine proponents as much of the benefit of the doubt as I can, and of course there are those that are very honest, evidence based, and realistic. There are some that are honest, but clearly deluded and don't follow evidence-based practices. And then there are those like Mercola, who appear to purposely misguide people with scientific sounding mumbo jumbo that doesn't make any sense on the face of it to anyone with some scientific training. That blurb on sulfur is a perfect example.

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I took a very long break from the interwebs, to increase my productivity. It worked, a little too well - I started being accused of being a workaholic. So I'm dipping my toe back in tongue.png

When I went back and used better search terms, I was able to find some research about ZAG and desquamation. Interestingly, a couple of papers referred to the ZAG protein as "lectin-like", suggesting it binds to amino sugar signaling molecules. But it also has in vitro ribonuclease and protease activity. There's still no evidence that it directly degrades corneodesmosomes (that I could find), so its likely it plays some signaling role - like cathepsin D. In any case though, it's just one of many (and I mean many) enzymes involved. That's why I don't get the singular focus on it from Cordain ::shrugs::.

Because it supports his demonizing of all seeds. And it's his claim that lectins inhibit ZAG that I can't find support for, other than that one study that may be saying that. And that study is about a specific lectin in the common bean, not lectins in general or lectins in grains as Cordain claims. I think Cordain makes a lot of suspect statements. Including the usual Paleo claim that humans didn't eat grains until the development of aggriculture. They wouldn't have learned to cultivate them if they didn't eat them. And I can cite an example of a people who ate such significant amounts of a wild grass seed that they consider them sacred - the Ojibwe people and the wild rice they gather, not cultivate.

ZAG and Capthepsin D are the two enzymes identified as impacting cell differentiation and desquammation in psoriasis.

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The cysteine switch is pretty simple - it's a part of the MMP proteins that literally folds over and puts a cysteine in contact with Zn ion in the active site of the enzyme. In at least some cases, the switch is part of the "propeptide" sequence, the part of the MMP that gets broken off to "activate" the enzyme. Cysteine has interesting functions in active sites because it includes an S-H. This group is called an especially reactive group called a thiol, and can do fun things like bind to metal ions, form disulfide bridges, and strongly interact with the substrate. Suffice to say, if the cysteine is in the right place, it can be crucial to a protein's function. In the case of the switch, the thiol forms a bond with the Zn ion, preventing it and the active site from taking part in any enzymatic reactions.

However, there is no real danger of a cysteine "deficiency" without a general protein deficiency, and putting topical sulfur on doesn't have any effect on the amino acid in general, or the MMP switch. It just.. doesn't work that way. Elemental sulfur is not the same thing as a thiol group on an amino acid. Cysteine isn't an essential amino acid. It's produced from methionine, a common essential amino acid that contains sulfur. Introducing any other sulfur compound will have no obvious influence on the production or use of cysteine, and certainly not on the cysteine switch.

But topically applied sulfur is a keratolytic agent. You don't think that has anything to do with this? Also, there's a big difference between not deficient and optimal. Maybe we need more.

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I wonder. Since IgA binds up lectins, then should we also look into ways that aid IgA production? Function?

IgA are the antibodies that live and function within our mucosa, which is why they are the antibodies that must be tested for gluten intolerance. They are also our first line of defense against infectious disease. (Don't take cold and flu meds that reduce mucus)

http://www.krispin.com/lectin.html scroll to the bottom.

searching on 'boosting IgA' produces a lot of results. And it seems that probiotics, anything that produces endorphins (laughter, music, affection, sex) That sex boosts endorphins and therefore IgA seems to have sparked many articles.

http://www.yeastinfe...upplements.html lots about NK cells which it says, in addition to their assassination duties, play a regulatory role in the immune system. Also a lot about the essential glyconutrients we've been discussing here.

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So, about all those glyconutrients we spent so much time researching. They are also important for the immune system and cell repair and are anti-aging.

Glyconutrients boost T-Cell and Natural Killer cell production and activity. NK cells destroy all the bad invaders - fungi, bacteria, virii, etc. And cancer cells. And they signal other cells that make up the body's immune response to tell them to get to work.

Glyconutrients also boost production of the Stem Cells that can repair any damaged tissue. http://www.natural-h...onutrients.html And may also increase the extremely important antioxidants glutathionine and SOD superoxide dismutase . Which along with Zinc creates ZSOD (which you may have heard of in Databased's threads/theory about it's deficiency being the root cause of acne and the treatment is an extremely natural circadian/melatonin cycle of bright outdoor light all day and darkness at night.)

There are 8 essential glyconutrients. Many are easy to get if you eat lots of veggies, but a few are not so easy to get. Go back to around pages 4-6 or so for more info, links to sources and what these nurients do lectin-wise. Here's another article about a glyconutrient rich diet: http://www.glyconutr...onutrients.html

8 saccharides which play a critical role in cell to cell communication. They are not digested for energy and do not convert to glucose but go to the cells to connect with glycoproteins.

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this information is overwhelming and seems to be inconclusive. I can tell you that when I eat any soy products (soybean oil, soy protein isolate, soy crisps etc....) i break out, so I know that something in soy is bad. phytoestrogens? lectins? what... anyone have information about the correlation between lectins and flax?

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this information is overwhelming and seems to be inconclusive. I can tell you that when I eat any soy products (soybean oil, soy protein isolate, soy crisps etc....) i break out, so I know that something in soy is bad. phytoestrogens? lectins? what... anyone have information about the correlation between lectins and flax?

If you break out soon after consuming any amount of soy, you probably have an allergy. If you start to break out when you have a lot of soy as part of your diet, then it could be the lectins and/or the phytoestrogens. If you also break out from flax, another estrogenic food, I'd say you want to avoid/limit estrogenic foods.

And yes, we only have Dr Loren Cordain's word that the lectins impair normal exfoliation and lead to clogged pores. There is plenty of other evidence that the lectins damage the digestive tract. And soy is estrogenic. And it's very common to be allergic to soy. So there are many ways it can affect acne.

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urine actually contains zag according to these studies:

http://www.nature.com/jid/journal/v119/n2/full/5601575a.html

"The normal functions of ZAG are unclear; however, ZAG has been isolated from the urine of human cancer patients with cachexia and can function as a lipid-mobilizing factor. ZAG purified from human or mouse serum or human cancer patient urine induces lipolysis resulting in glycerol release and also increases lipid utilization in both human and mouse adipocytes"

http://www.jci.org/articles/view/108371

"One of the major proteins, identified Zn-alpha2-glycoprotein (Zn-alpha2), was isolated from the urine and partly characterized."

though its not clear what zag actually does and all of the research is aimed towards cancer, zag is definetly present in not only semen but urine. Check out these astounding reviews on urine therapy. Sounds totally desperate and also disgusting but urine therapy is when you either topically apply urine to the face or internally ingest urine daily. It really does work for alot of people.

http://www.acne.org/urine-therapy-reviews/524/page1.html

there's 256 reviews!!

Also if you have time:

and

what do you think?

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^Is that about topical use or oral? I haven't watched the videos as my sound card doesn't work. I have a long list of videos I've been meaning to watch on my iphone or something.

But just remember that urine is also full of things your body just worked so hard to eliminate.

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This maybe the mechanism behind Semen Therapy also. Both topical and oral. Zinc alpha2 glycoprotein

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ZAG, Capthepsin D and the enzyme named here are involved in desquammation.

http://www.acne.org/messageboard/index.php/topic/298075-recent-advances-in-acne-pathogenesis-information/page__st__20#entry3257144 And apparently PH affects the function of those enzymes. And water so perhaps also a factor in people with dry skin and acne.

Psoriasis is a T cell-mediated inflammatory disease characterized by hyperproliferation and by aberrant differentiation. We found cathepsin D and zinc-α2-glycoprotein, two catalytic enzymes associated with apoptosis and desquamation, to be present in the stratum corneum of the normal epidermis but absent from the psoriatic plaque. Psoriasis is characterized by an altered response to interferon-γ (IFN-γ), including the induction of apoptosis in normal but not in psoriatic keratinocytes, often with opposite effects on gene expression of suprabasal proteins. We found that IFN-γ binding and signaling were attenuated in psoriasis: The IFN-γ receptor, the signal transducer and activator of transcription STAT-1, and the interferon regulatory factor IRF-1 were strongly up-regulated by IFN-γ in normal keratinocytes, but not in psoriatic ones. IFN-γ strongly up-regulated the expression of the catalytic enzymes cathepsin D and zinc-α2-glycoprotein in normal keratinocytes but down-regulated them in psoriatic ones; the reverse was true of the apoptotic suppressor bcl-2. We believe that the aberrant response to IFN-γ plays a central role in the pathophysiology of psoriasis, particularly the disruption of apoptosis and desquamation.—Chen, S.-H., Arany, I., Apisarnthanarax, N., Rajaraman, S., Tyring, S. K., Horikoshi, T., Brysk, H., Brysk, M. M. Response of keratinocytes from normal and psoriatic epidermis to interferon-γ differs in the expression of zinc-α2-glycoprotein and cathepsin D.
http://www.fasebj.or...t/14/3/565.full

So cathepsin D is also something to look into. And just looking at the wikipedia article and skimming through the references cited, there's a lot of mention of estrogens and that estrogen regulates cathepsin D levels. Which could be how estrogen is a factor. Most research into cell proliferation and apoptosis is going to be about cancer and breast cancer is one of the more common research topics.

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A whole lot of studies on the badness of the WGA lectin http://www.greenmedinfo.com/page/opening-pandoras-bread-box-critical-role-wheat-lectin-human-disease#_ftn12. Such as:

Antinutritive effects of wheat-germ agglutinin and other N-acetylglucosamine-specific lectins.

Source

Rowett Research Institute, Bucksburn, Aberdeen.

Abstract

Incorporation of N-acetylglucosamine-specific agglutinins from wheat germ (Triticum aestivum; WGA), thorn apple (Datura stramonium) or nettle (Urtica dioica) rhizomes in the diet at the level of 7 g/kg reduced the apparent digestibility and utilization of dietary proteins and the growth of rats, with WGA being the most damaging. As a result of their binding and endocytosis by the epithelial cells of the small intestine, all three lectins were growth factors for the gut and interfered with its metabolism and function to varying degrees. WGA was particularly effective; it induced extensive polyamine-dependent hyperplastic and hypertrophic growth of the small bowel by increasing its content of proteins, RNA and DNA. Furthermore, an appreciable portion of the endocytosed WGA was transported across the gut wall into the systemic circulation, where it was deposited in the walls of the blood and lymphatic vessels. WGA also induced the hypertrophic growth of the pancreas and caused thymus atrophy. Although the transfer of the gene of WGA into crop plants has been advocated to increase their insect resistance, as the presence of this lectin in the diet may harm higher animals at the concentrations required to be effective against most pests, its use in plants as natural insecticide is not without health risks for man.

-------------------

Effects of wheat germ agglutinin on human gastrointestinal epithelium: insights from an experimental model of immune/epithelial cell interaction.

Dalla Pellegrina C, Perbellini O, Scupoli MT, Tomelleri C, Zanetti C, Zoccatelli G, Fusi M, Peruffo A, Rizzi C, Chignola R.

Source

Department of Biotechnology, University of Verona, Strada Le Grazie 15-CV1, I-37134 Verona, Italy.

Abstract

Wheat germ agglutinin (WGA) is a plant protein that binds specifically to sugars expressed, among many others, by human gastrointestinal epithelial and immune cells. WGA is a toxic compound and an anti-nutritional factor, but recent works have shown that it may have potential as an anti-tumor drug and as a carrier for oral drugs. To quantitate the toxicity threshold for WGA on normal epithelial cells we previously investigated the effects of the lectin on differentiated Caco2 cells, and showed that in the micromolar range of concentrations WGA could alter the integrity of the epithelium layer and increase its permeability to both mannitol and dextran. WGA was shown to be uptaken by Caco2 cells and only approximately 0.1% molecules were observed to cross the epithelium layer by transcytosis. Here we show that at nanomolar concentrations WGA is unexpectedly bioactive on immune cells. The supernatants of WGA-stimulated peripheral blood mononuclear cells (PBMC) can alter the integrity of the epithelium layer when administered to the basolateral side of differentiated Caco2 cells and the effects can be partially inhibited by monoclonal antibodies against IL1, IL6 and IL8. At nanomolar concentrations WGA stimulates the synthesis of pro-inflammatory cytokines and thus the biological activity of WGA should be reconsidered by taking into account the effects of WGA on the immune system at the gastrointestinal interface. These results shed new light onto the molecular mechanisms underlying the onset of gastrointestinal disorders observed in vivo upon dietary intake of wheat-based foods.

And much more, such as how WGA can act as a neurotoxin. But many are extremely complicated for non-molecular biologists, neruoscientists and oncologists to understand and without any clear statements describing the badness for me to highlight. And others are about various lectins showing similar harm such as those in soy and peanuts.

Reminder: WGA = wheat germ agglutinin.

WGA is bound up by:

N-Acetylglucosamine (N-acetyl-D-glucosamine, orGlcNAc, or NAG) is a monosaccharide derivative ofglucose. It is an amide between glucosamine and acetic acid. And a major component of many of your body's tissues. (Acetic Acid? I'd never come across this before. Is this why another way vinegar improves digestion?)

and

Sialic acid - another major component of your body's tissues.

Such as those lining your digestive tract.

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i think there are better ways of approaching this, even if it does work, who really wants pee or semen on them? i could think of maybe one time that would it be necessary, and thats after being stung by a jelly fish.

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i think there are better ways of approaching this, even if it does work, who really wants pee or semen on them? i could think of maybe one time that would it be necessary, and thats after being stung by a jelly fish.

????? I've no idea why you've even made such a silly comment comment. Of course there are better approaches. Such as the many, many pages of discussion about proper preparation to reduce lectins and traditional food combinations involving nutrients that bind up lectins. While there has been a post or two mentioning urine and semen, that is not what this thread is about and there is 12 pages filled with other information.

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i think there are better ways of approaching this, even if it does work, who really wants pee or semen on them? i could think of maybe one time that would it be necessary, and thats after being stung by a jelly fish.

????? I've no idea why you've even made such a silly comment comment. Of course there are better approaches. Such as the many, many pages of discussion about proper preparation to reduce lectins and traditional food combinations involving nutrients that bind up lectins. While there has been a post or two mentioning urine and semen, that is not what this thread is about and there is 12 pages filled with other information.

i was distracted by it, sorry...i agree with the rest though, food is one way to approach clogged pores...there are several more

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Hah! I just noticed something. In the first post I had stated that the ZAG enzyme was found in bodily fluids including sweat. Perhaps this is a factor in why working up a sweat helps many people. I don't sweat much, which can be a symptom of hypo-thyroidism or low functioning thyroid, and perhaps the reduced sweating and therefore the reduced ZAG enzyme on the surface of the skin is a factor in why people with hypothyroidism often get acne. ???

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From the 2009 report titled Recent Advances in Acne Pathogenesis Information

http://piel-l.org/bl...al-alliance.pdf

Sebum contains several matrix metalloproteinases (MMPs) which play important roles in the inflammatory process of acne. The levels of MMPs are significantly reduced in the acne lesions following treatment.

See, I wondered what enzymes might be in normal sebum but my quick searches didn't produce any results.

Metalloproteinases (or metalloproteases) constitute a family of enzymes from the group of proteases, classified by the nature of the most prominent functional groupin their active site. These are proteolytic enzymes whose catalytic mechanism involves a metal. Most metalloproteases are zinc-dependent, but some usecobalt. - wikipedia def

So, they might just be talking about the ZAG, at least with the zind-dependent ones. But did Cordain ever tell us that ZAG was found in your sebum?

This is a better wikipedia article on the metalloproteinase matrix. Doesn't specifically mention the ZAG enzyme. A little bit about cell differentiation. And a bit about a 'cysteine switch.' Cysteine is a sulfur containing amino acid and we hopefully all know by now how beneficial sulfur is, in the diet and topically.

Also talks of inhibitors, especially synthetic ones i.e. drugs. Names doxycycline. Isn't this prescribed for acne? And it inhibits the enzymes that allow normal exfoliation? And even more important things affected by proper cell proliferation and death?

There's a study cited in that wikipedia article about the cysteine switch but I'm afraid I get nothing from the abstract. At least not without a lot of thought into what it might mean.

Wow, this might be it for me! I was on doxycycline hyclate 100mg 2x a day for 4 months, and now i have tons of dead skin all over my face everyday (also on shoulders/back). I wonder how i can reintroduce these enzymes which would allow for normal exfolition hmm...

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From the 2009 report titled Recent Advances in Acne Pathogenesis Information

http://piel-l.org/bl...al-alliance.pdf

Sebum contains several matrix metalloproteinases (MMPs) which play important roles in the inflammatory process of acne. The levels of MMPs are significantly reduced in the acne lesions following treatment.

See, I wondered what enzymes might be in normal sebum but my quick searches didn't produce any results.

Metalloproteinases (or metalloproteases) constitute a family of enzymes from the group of proteases, classified by the nature of the most prominent functional groupin their active site. These are proteolytic enzymes whose catalytic mechanism involves a metal. Most metalloproteases are zinc-dependent, but some usecobalt. - Collectively, they are capable of degrading all kinds of extracellular matrix proteins, but also can process a number of bioactive molecules. They are known to be involved in the cleavage of cell surface receptors, the release of apoptotic ligands (such as the FAS ligand), andchemokine/cytokine in/activation.[3] MMPs are also thought to play a major role on cell behaviors such as cell proliferation, migration(adhesion/dispersion), differentiation, angiogenesis, apoptosis, and host defense.

So, they might just be talking about the ZAG, at least with the zinc-dependent ones. But did Cordain ever tell us that ZAG was found in your sebum?

This is a better wikipedia article on the metalloproteinase matrix. Doesn't specifically mention the ZAG enzyme. A little bit about cell differentiation. And a bit about a 'cysteine switch.' Cysteine is a sulfur containing amino acid and we hopefully all know by now how beneficial sulfur is, in the diet and topically.

Also talks of inhibitors, especially synthetic ones i.e. drugs. Names doxycycline. Isn't this prescribed for acne? And it inhibits the enzymes that allow normal exfoliation? And even more important things affected by proper cell proliferation and death?

There's a study cited in that wikipedia article about the cysteine switch but I'm afraid I get nothing from the abstract. At least not without a lot of thought into what it might mean.

Wow, this might be it for me! I was on doxycycline hyclate 100mg 2x a day for 4 months, and now i have tons of dead skin all over my face everyday (also on shoulders/back). I wonder how i can reintroduce these enzymes which would allow for normal exfolition hmm...

Your body produces the enzymes. Just stop inhibiting them. Also your skin needs to be acidic for them to function, so stop stripping your acid mantle away with soap. See also the linoleic acid thread. It's an important part of the acid mantle and mammals with skin problems of all sorts have been found to be deficient.

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i think there are better ways of approaching this, even if it does work, who really wants pee or semen on them? i could think of maybe one time that would it be necessary, and thats after being stung by a jelly fish.

this approach makes a ton of sense though

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Screw soaking and then toasting nuts. I just eat em raw' outta the pack.

I recently found the joys of eating beans too! Sure, soaking your own would be easier and delicious but I usually just make a quick curry or salad and it's delicious! They are soaked in salt only (I tried to find salt free, failed, you can find sugar free in abundance though).

FYI: Salt displaces some of the magnesium in the skins. This is what makes the skin more tender and why people do it. But I don't want my magnesium displaced.

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alternativista, I have been recently diagnosed with graves disease and have often wondered what and how it contributes to my skin issues. Im very confused and overwhelmed at all the info you posted about the ZAG enzyme and its relationship to cell differentation.. Clogged pores plague me something awful. Its not just a normal clogged pore or two but they are embedded in my chin by the hundreds. I thought I had seb derm issues but have tried anti fungals and changing my diet drastically but my skin cell turnover will not regulate. I am on Armour thyroid medicine and take good supplement and dont know what else to try. What are your thoughts?

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alternativista, I have been recently diagnosed with graves disease and have often wondered what and how it contributes to my skin issues. Im very confused and overwhelmed at all the info you posted about the ZAG enzyme and its relationship to cell differentation.. Clogged pores plague me something awful. Its not just a normal clogged pore or two but they are embedded in my chin by the hundreds. I thought I had seb derm issues but have tried anti fungals and changing my diet drastically but my skin cell turnover will not regulate. I am on Armour thyroid medicine and take good supplement and dont know what else to try. What are your thoughts?

Doesn't graves cause an over active thyroid? In which case, why would you take thyroid hormones? Has anything changed since you started taking it?

I think what you should take away from this thread is to soak and cook your beans properly and ideally soak, sprout or ferment what grains you consume. And avoid or limit the most harmful. And eat your glyconutrients. There is that bit about colostrum obtaining zag and so it might be beneficial topically. There's another enzyme involved in dissolving the cell matrix and Its regulated by estrogens. and zag production is regulated by glucocorticoids which is what spironolactone is which may be a big factor in how its helpful in acne.

Did you try topical linoleic acid? It plays a vital role in the production of these enzymes and pretty much every thing else to do normal skin function. And your thyroid affects the lipid composition of your sebum.

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