Anal Fissure

Dan W

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So, the bigger question is - what labs would accept nails for analysis?
I came across one located in Germany:

111€ for aluminum, antimony, arsenic-total, barium, beryllium, bismuth, boron, cadmium, calcium, chromium, cobalt, copper, germanium, iodine, iron, lead, lithium, magnesium, manganese, mercury, molybdenum, nickel, palladium, platinum, selenium, silver, strontium, thallium, tin, titanium, tungsten, uranium, vanadium, zinc, zirconium.

144€ for the above plus cerium, cesium, dysprosium, erbium, europium, gadolinium, gallium, iridium, lanthanum, lutetium, praseodymium, rhenium, rhodium, ruthenium, samarium, tantalum, tellurium, thorium, thulium, ytterbium.
 

haidut

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I came across one located in Germany:

111€ for aluminum, antimony, arsenic-total, barium, beryllium, bismuth, boron, cadmium, calcium, chromium, cobalt, copper, germanium, iodine, iron, lead, lithium, magnesium, manganese, mercury, molybdenum, nickel, palladium, platinum, selenium, silver, strontium, thallium, tin, titanium, tungsten, uranium, vanadium, zinc, zirconium.

144€ for the above plus cerium, cesium, dysprosium, erbium, europium, gadolinium, gallium, iridium, lanthanum, lutetium, praseodymium, rhenium, rhodium, ruthenium, samarium, tantalum, tellurium, thorium, thulium, ytterbium.

Thanks. What about more general analysis including steroids, like the hair analysis companies do?
 

Amazoniac

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The thing about taking vitamin D supplements is you throw large doses at the intestines. Now I know cholecalciferol is not generally thought to be active until it reaches the kidneys, but I had read one experiment showing epithelial cells capable of transforming cholecalciferol into active calcitriol.

I had thought perhaps that taking supplements could lead to an unusually high calcium absorption for this reason. I use it transdermally now once in a while, on the skin, and can feel the hormonal effects (but not that hypercalcemic, stiff joint feeling I notice from taking it orally.)
Apparently it affects lead as well:
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"The present study demonstrates that vitamin D markedly stimulates the absorption of lead ions from the small intestine. Surprisingly, however, this enhancement was noted only in the distal segments of small intestine, while greatest stimulation of calcium transport by vitamin D is found in the proximal duodenum of the rat (12,13). It would, therefore, appear that lead and calcium absorption do not share a common mechanism as often assumed. Vitamin D does stimulate phosphate transport especially in the distal small intestine (18-21) suggesting that the lead transport may be related in some way to phosphate absorption. Of some interest is the fact that high doses of vitamin D do not markedly enhance the absorption of lead above that achieved with physiological doses of the vitamin. However, it is known that intestine is saturated with small doses of vitamin D in contrast to the bone resorption system (22). Thus it is not surprising that high doses of vitamin D had no remarkable effect on lead absorption from the small intestine.
The methods of assessing lead absorption developed here directly reflect those developed for studying calcium absorption (14, 23). Obviously, however, much less lead was absorbed than calcium. For this reason and because tissue takes up sizeable amounts of lead, it was not possible to obtain evidence for concentrative or active transport. Nevertheless, the methods described should prove useful in the study of factors involved in lead absorption and toxicity."​

Now I couldn't tell if this can be explained by what you mentioned above, or if the same thing would've occurred from topical application. But I think out of safety, it's best to use it topically indeed.
"The total bodily amount of lead does not affect lead absorption. Thus, lead does not have a feedback mechanism which limits absorption."
Bones serenading vit D.
Avoiding lead acetate supplementation is another thing to try.

@Leader
 
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Travis

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Apparently it affects lead as well:
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"The present study demonstrates that vitamin D markedly stimulates the absorption of lead ions from the small intestine. Surprisingly, however, this enhancement was noted only in the distal segments of small intestine, while greatest stimulation of calcium transport by vitamin D is found in the proximal duodenum of the rat (12,13). It would, therefore, appear that lead and calcium absorption do not share a common mechanism as often assumed. Vitamin D does stimulate phosphate transport especially in the distal small intestine (18-21) suggesting that the lead transport may be related in some way to phosphate absorption. Of some interest is the fact that high doses of vitamin D do not markedly enhance the absorption of lead above that achieved with physiological doses of the vitamin. However, it is known that intestine is saturated with small doses of vitamin D in contrast to the bone resorption system (22). Thus it is not surprising that high doses of vitamin D had no remarkable effect on lead absorption from the small intestine.
The methods of assessing lead absorption developed here directly reflect those developed for studying calcium absorption (14, 23). Obviously, however, much less lead was absorbed than calcium. For this reason and because tissue takes up sizeable amounts of lead, it was not possible to obtain evidence for concentrative or active transport. Nevertheless, the methods described should prove useful in the study of factors involved in lead absorption and toxicity."

Now I couldn't tell if this can be explained by what you mentioned above, or if the same thing would've occurred from topical application. But I think out of safety, it's best to use it topically indeed.

Bones serenading vit D.
Avoiding lead acetate supplementation is another thing to try.

@Leader
This is not surprising. I think it's well‐known that lead (Pb²⁺) and calcium (Ca²⁺) have similar properties. The chelator EDTA, for instance, chelates both with high‐affinity; and lead does partition towards the bonds more than ions such as aluminum and mercury. These are similar enough as to almost consider lead (Pb²⁺) the 'inimical counterion' of calcium (Ca²⁺), in analogy to its 'biological counterion' magnesium (Mg²⁺).

It's well known that vitamin K chelates calcium by creating a post-translational modification on proteins: a calcium-chelating domain called γ-carboxyglutamate with the help of an enzyme. This is absolutely non-mysterious and intuitive. Also known is that the parathyroid has a calcium-sensing domain on one of its proteins, having a disulfite bridge. Although its still an open question how this actually senses calcium, experimental evidence proves that it does.

But calcium follows phosphate. Calcium can be found in the bones bound to phosphate (PO₄²⁻), and will precipitate with phosphate everywhere in the event of low vitamin K. So does vitamin D effect calcium (Ca²⁺) or does it effect phosphate (PO₄²⁻)? Does it activate a membrane pore similar to aldosterone (Na⁺/K⁺), or does it work 100% transcriptionally to create proteins which shift the Ca²⁺/Mg²⁺/PO₄²⁻ balance? I do know that the most upregulated gene induced by vitamin D is the enzyme which inactivates it; there is an enzyme which adds the fourth hydroxyl (–OH⁻) group to vitamin D, making it even more water‐soluble and priming it for excretion; vitamin D induces mRNA for this enzyme at ~10× the concentrations of any other.

Vitamin D also induces transcription of bone morphogenic protein. But since the PCR data I had looked was focused on inflammation, and not calcium, I'm not sure what other relevant Ca²⁺ proteins it induces; I think we'd have to look at the 'calcium proteome' of vitamin D to get a clear picture. But since aldosterone works on a pore and transcriptionally, it is tempting to think that vitamin D does likewise:

And I think I found the perfect article:

Fleet, James C. "Genomic and proteomic approaches for probing the role of vitamin D in health." The American journal of clinical nutrition (2004)
'Although we have learned a great deal about vitamin D metabolism and function since it first became apparent that this factor was required for bone health, there are still many gaps in our understanding, at both the basic science (eg, the molecular actions and targets of vitamin D) and applied (eg, what “adequate” vitamin D status means) levels. For example, although the identification of extrarenal 1α-hydroxylase activity suggests that autocrine/paracrine actions of 1,25-dihydroxyvitamin D complement the classic endocrine actions of the hormone, the practical implications of this finding are only now being explored. In addition, studies showed that 1,25-dihydroxyvitamin D rapidly activates signal transduction pathways in addition to the classic transcriptional activation pathways that require the vitamin D receptor. These new modes of vitamin D action may be crucial to our understanding of both the traditional calcium-regulating actions of vitamin D and the anticancer actions of this essential mediator. Recent developments in genomics and proteomics have provided new opportunities for us to identify molecular targets of vitamin D action. ' ―Fleet
It seems like it could have an immediate function besides its transcriptional (genomic) effects. This makes sense, as many other steroids have similar dual roles. Besides aldosterone previously mentioned, pregnenolone and progesterone form a physical boundary in nerves; myelin consists mostly of progesterone and pregnenolone. And judging by how androgens effect male nerves, it wouldn't surprise me if they didn't have microtubule‐stabilizing properties of their own.

'Elevated serum 1,25(OH)₂D₃ concentrations then stimulate the expression of vitamin D-responsive genes within the primary target tissues that control calcium homeostasis (ie, TRPV6 and calbindin D₉ in intestine, osteocalcin and RANKL in bone, and TRPV5 and calbindin D₂₈ in kidney) through activation of the vitamin D receptor (VDR). Although this system is clearly functional and biologically important during periods of calcium stress, it may not be sufficient to explain all of the biological actions of vitamin D.' ―Fleet

Osteocalcin is a γ-carboxyglutamate protein, so would be a vitamin K‐dependent Ca²⁺-binding protein with clear molecular function. The calbindins appear a bit different, as explained in an excerpt from Nutritional Biochemistry of the Vitamins:

calbindin.png
Don't bother clicking: Image is already fully embiggened

So it looks like it chelates calcium between two turns of a protein a α-helix, physically mediated by 'side-chain oxygen atoms.' I think it would be fair to assume that these are carboxyl groups, and not hydroxyl groups. Would a person expect many glutamate and aspartate residues in calbindin?

So it looks as if vitamin D mainly chelates calcium through calbindin proteins, which are vitamin K-independent. These calbindins appear responsible for the extra Ca²⁺ absorption seen after vitamin D supplementation, and are probably synthesized by intestinal cells or the pancreas. You would expect, like EDTA, that calbindin₉k also binds lead ions (Pb²⁺).

calbindin.png calbindin.png click to embiggen

This Ca²⁺-binding pocket of calbindin₉k seems dominated by aspartate, but also containing one glutamate. The negative charges of these carboxyl groups are the only ones suitable for binding divalent cations.

But you'd think it would bind lead ions (Pb²⁺) too, right? The image on the left is with divalent (Mg²⁺), so it would be difficult to make the case that it's specific for calcium (Ca²⁺) alone.
 

Broken man

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So can thiamine and charcoal, also searchable but more easily found through a Google search on the forum :):
Thiamine Reverses Diabetic Kidney Damage In Humans
Thiamine Reverses Diabetic Kidney Damage In Humans

Anything that keeps FFA low will protect kidneys from degeneration. Raising NAD/NADH ratio was recently shown to reverse aging in any organ studied. Steroids like androsterone have been known as kidney-anabolic since the 1940s. It is also anti-aging for heart, liver, and skin. Progesterone and DHEA share many of the same effects as do testosterone and DHT.
The Anabolic Effects Of Androsterone
I think taurine and vitamin E, niacinamide too.
 

Kunder

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Let me chip in on this. Our daughter had a fissure since the age of about 3 for about one amd a half to two years. Nothing worked, it was EXTREMELY frustrating and stressful as you can imagine. We tried everything.

What worked in the end was a special healing gel called Hemagel. It is Czech and somehow very unique, though I dont know why or how. It was developed by the Czech academy of sciences, so outside of the big pharma scope.

Not sure where you can get it or how, but that’s what worked for us. There’s no doubt this was the cure, as there was nothing else going on concurently. The fissure has never returned since.
 
OP
raypeatclips

raypeatclips

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One thing to note is that I feel my bowel movements are very thick, maybe excessively thick. I feel like the sheer size of them could be causing the blood I see when I wipe. I would say some of them are similar in girth to a cucumber, maybe even bigger, but around half the length, or around 1/3 in length. Around 2-3 on the Bristol stool chart, sausage shaped but usually with cracks.

Does anyone know the cause of this?
 

Koveras

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We check urinary albumin, creatinine, and ACR for everyone. Tests are always done in the morning.

Any test can be useful given the proper context. What sort of context are you considering blood Mg/Ca for?

I have also never heard of nail testing, but it does sound interesting. I don't know what it would offer that hair doesn't though.

Thanks, for some reason this quote would not show up on a Google search or a forum search. Maybe it was just not indexed yet.
So, the bigger question is - what labs would accept nails for analysis?

Keratinous matrices for the assessment of drugs of abuse consumption: a correlation study between hair and nails.

However, nail analysis can offer multiple advantages over hair analysis [1, 12].

First, the average growth rate of nails is substantially lower compared to hair (3 and 1 mm/month for finger- and toenails, respectively, compared to 1 cm/month for head hair); which would allow a more significant accumulation of substances [13, 14]. This can be relevant in situations where low concentrations are expected (e.g. low dosages).

Secondly, while hair is characterized by a cyclic growth rate with different stages, nails grow at a constant rate, which facilitates the interpretation of results [15]. Hair strands that have been in a resting stage might result in the detection of more remoted consumption.

Third, in contrast to hair, nails do not contain melanin. Since drug incorporation might be influenced by melanin concentrations, hair pigmentation becomes an important source of bias when interpreting detected drug concentrations [16, 17].

Fourth, nails can provide an alternative option in cases where hair is not (sufficiently) available (e.g., alopecia, newborns).

Fifth, cosmetic hair treatments have been proven to reduce drug content in hair, which can be overcome through nail analysis [18, 19].

Possible disadvantages linked to the use of nails as matrix can be insufficient sample amount in cases of (finger)nail biting, presence of nail diseases (e.g. bacterial or fungal infections), and effects of nail polishing or cleaning. Also, drugs are incorporated into hair via the blood flow in the hair follicle, while incorporation into nails occurs by a dual mechanism of deposition into the root via blood flow in the nail matrix and the nail bed [1]. The vertical and horizontal incorporation into nails might complicate the interpretation of results.
 

Tenacity

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One thing to note is that I feel my bowel movements are very thick, maybe excessively thick. I feel like the sheer size of them could be causing the blood I see when I wipe. I would say some of them are similar in girth to a cucumber, maybe even bigger, but around half the length, or around 1/3 in length. Around 2-3 on the Bristol stool chart, sausage shaped but usually with cracks.

Does anyone know the cause of this?

Less frequent bowel movements? Too mich fibre?
 

Velve921

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A friend of mine has fissures now that are extremely painful. Could progest e on the fissures be helpful with healing?
 
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Hmm speaking of calcification and cracked heels- when I added vitamin K recently , I noticed that my heels healed up . When I take D without K , I have less than stellar ...how to I say ... smooth moves. I would really try adding lots of K AND lots of vitamin C ( orange juice ) to your diet and see if it helps.
 
EMF Mitigation - Flush Niacin - Big 5 Minerals

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