Could alopecia be as simple as a zinc deficiency?

[Baz493]

I recently learned that there are actually three different types of the 5-alpha reductase enzyme, which produces dihydrotestosterone, and that this is the key to understanding what is really happening. I think that this should provide a fairly complete picture of events now. It is a form of the enzyme which is called SRD5A1 which is expressed in skin, hair follicles, and especially the scalp.

Anyway, try doing a search online for diabetes and alopecia. The two often occur together for a reason. It's the insulin which is the connection. https://academic.oup.com/endo/article/151/10/5030/2456459?login=false The insulin triggers the prostaglandin D2 expression and GPR44 receptor triggering in male pattern baldness. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6296667/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3319975/ Because insulin is both a protein structure and a hormone the enzyme trypsin is required for both its production and breakdown. That's the reason that issues with insulin can result in the release of trypsin in sebum and issues with the integrity of skin structure. https://pubmed.ncbi.nlm.nih.gov/11423485/

People with coeliac disease, such as myself, tend to be at higher risk of developing diabetes. I assume that I must possess genetic factors which have successfully prevented this outcome in me but I must have experienced the issues with insulin and/or insulin resistance. While insulin tends to induce vasodilation in normal blood vessels, by increasing nitric oxide levels, it induces vasoconstriction in microcirculation (small blood vessels in tissues). https://journals.lww.com/jhypertens...ICTOR_EFFECTS_OF_INSULIN_IN_THE_HUMAN.82.aspx That's the reason that decreased blood flow is involved in hair loss. http://glenncorp.com/wp-content/uploads/2014/11/ProCircul8-TDS.pdf

I can't be absolutely certain about this but I am assuming that the galea aponeurotica, which forms the pattern of male pattern baldness, is filled with microcirculation vessels. While male pattern baldness can occur in women it is less common. Still, I can't help but wonder whether this article might help explain. https://www.tandfonline.com/doi/abs/10.3109/01612840.2011.625514?journalCode=imhn20

 

[Baz493]

I managed to find an article which explains the pattern of male pattern baldness. As I have previously described, the hair loss with this condition perfectly matches the shape of the galea aponeurotica, a sub-layer of fibrous collagen formed by fibroblasts. That was the key. Fibroblasts, from the galea aponeurotica, are normally converted into dermal adipocytes so something is obviously inhibiting the conversion of fibroblasts into fat cells. https://sciencebeta.com/fibroblasts-fat-cells/ https://pubmed.ncbi.nlm.nih.gov/28482134/ It turns out that the zinc dependent enzyme zfp423 is required for differentiation of dermal fibroblasts into dermal adipocytes. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2845731/ That is why zinc deficiency ultimately results in alopecia. It's also likely to be the reason that thyroid issues are involved in PCOS https://pubmed.ncbi.nlm.nih.gov/36753417/ as well as patchy types of hair loss. While the effects of dihydrotestosterone production doesn't appear to involve adipocytes it is central to fibroblasts and their function, with a much research on the variety of effects it has. I may have been premature in thinking that it was just the DHT enzymes which were involved in hair loss. This study of use of testosterone on cattle found that it reduced adipocyte production of zfp423. https://pubmed.ncbi.nlm.nih.gov/31476680/ That is seen as a positive thing with cattle, for increased muscle and reduced fat, but it means that the super-testosterone DHT is likely to reduce conversion of fibroblasts to adipocytes needed to sustain hair growth. What seems obvious is that adiposopathy, resulting from storage of toxins in fat cells, interferes with normal production of zfp423 by the adipocytes and reduces conversion of fibroblasts into adipocytes, so causing thinning of the dermal adipose layers underlying hair loss. Without sufficient adipose tissue or zinc to regenerate the top, protective, layers of the skin we develop the dermatitis associated with hair loss.

 

[Baz493]

In trying to get a final picture of how alopecia works I believe that I have put together something which most people will be able to try to resolve themselves, thanks to trying to help a friend with her PCOS which seems to revolve around the same set of factors. Adipocytes, underlying the upper layers of the skin, are converted into those upper layers as they are required so dysfunction in that fat layer undermines the entire process. Zinc is crucial to the health of all of the layers and figure 1, from this article, shows which zinc transporter proteins are involved at each level. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5852775/

There is a strange thing which occurs when there are mineral deficiencies in the body. Levels of the minerals will all be low or in normal range in the blood but can reach toxic levels in the tissues because of how the zinc transporter proteins work. One example is the ZIP14 in figure 1 from that last article, which 'feeds' the adipocytes zinc. Both iron and zinc compete for the protein so a deficiency of zinc may lead to an excess of supply of iron to the fatty tissues, particularly if you are supplementing with it. Normal function of those fatty layers depends upon zinc and excessive levels of iron will induce ferroptosis of cells, a type of cell death induced by iron. That is known to relate to skin conditions like dermatitis, which lead to hair loss. As this next article details, when zinc is deficient in the body, nickel can be mistaken for zinc by our bodies yet doesn't work like it. https://www.drmyhill.co.uk/wiki/Nickel_-_toxicity_and_detoxing I'm guessing that this is why nickel has such a high affinity for the filaggrin proteins in the top layer of our skin, undermining the structural integrity and protection which it provides.

I have read, in medical research articles, about the same processes being involved in men with prostate cancer and women with breast cancer and PCOS, with dysfunction of the fatty tissues resulting in the diseases.

 

[Ken Lassesen]

https://pubmed.ncbi.nlm.nih.gov/20523772/ When I went bald, during my late teens, I had no idea that the primary cause of my condition was coeliac disease. That took me decades to learn. I also had no idea that dandruff is a sign of skin conditions resulting from either bacterial (staphylococcus) or fungal (malassezia) infections. Funny thing about all of these is that they induce, among other things, zinc deficiency in the skin. Zinc is required not only for preventing sebum from blocking pores of the skin (comedogenic) but also for a wide range of factors affecting both skin health and hair growth. Stem cells, throughout our bodies, change into cells which are required at the time and may revert to being stem cells if the body signals that it requires different cells. Not only does that signaling become disrupted when zinc deficiency occurs but the normal process, stabilising the workhorse cells they have become and preventing them from reverting, lacks the essential zinc needed to maintain it. https://pubmed.ncbi.nlm.nih.gov/35172118/ Conditions such as atopic dermatitis occur in the skin and even the bone of the skull can lose integrity, due to the same stem cell differentiation which occurs in the skin. The normal pattern of alopecia develops because of the galea apotoneurotica, a fibrous mat of collagen which connects the muscles on either side of the scalp. This mat contains numerous fibroblasts, which all require lots of zinc to both maintain their own stem cell stability and to produce all of the required collagen to maintain the apotoneurosis. The scalp on top of the head is like a zinc sponge, requiring constant feeding. So if you add conditions like coeliac disease, inducing nutrient deficiencies, and/or disruption of the top layer of the skin (stratum corneum) allowing infections to enter the skin then that zinc sponge suddenly becomes an open drain. The hair bulges, containing stem cells which produce the hair, rise to the surface of the skin and differentiate into skin keratinocytes and the skin thins. Hair canals need to be at least 4mm deep inside the skin in order to be able to produce mature hair. Ironically, dietary zinc levels don't necessarily equate to tissue zinc levels. Some people have SLC30 or SLC39 gene mutations which reduce the levels of proteins which transport zinc, and other minerals, around the body. Once a zinc deficiency occurs you become even more vulnerable to allergic reactions as zinc helps to prevent Th2 allergic response from switching into Th17 response. https://www.researchgate.net/public...the_Dermis_Particularly_around_Hair_Follicles https://pubmed.ncbi.nlm.nih.gov/20215335/ You always hear people blaming dihydrotestosterone for hair loss but it is the Th2 and Th17 responses which are actually responsible. Interleukin signaling, involved in Th2 and Th17 responses, tells stem cells in the hair bulges to enter resting stage of hair growth. https://pubmed.ncbi.nlm.nih.gov/34281739/ Dihydrotestosterone actually tries to reduce that signaling. https://pubmed.ncbi.nlm.nih.gov/1830499/ As I have read about cases of excessive dietary zinc inducing alopecia I am cautious regarding supplementing the diet. Find a way to reduce the underlying factors inducing zinc deficiency in the scalp and the problem will hopefully be eliminated.

There is also a microbiome aspect. The zinc could be influencing the microbiome in some cases.

National Library of Medicine Citations for Alopecia (Hair Loss)

 

[Baz493]

Ken, Because I am now aware that my hair loss was initiated by gluten intolerance/coeliac I have done a bunch of research about how the microbiome can be involved. Certain bacteria are required for the breakdown of gluten so an increase in unhealthy bacteria levels increases the gluten intolerance. My health issues became gradually worse as I grew older, fitting with such a progression. Since dysregulated microbiome results in reduced mineral absorption and increased heavy metal presence it's a kind of feedback loop which becomes increasingly complex.

 

[Baz493]

I think that I may have found the base source of all of the previously mentioned issues. I was taking another look at my own gluten problems andfound that researchers now understand that the gliadin protein induces overproduction of an intestinal protein called zonulin by the intestinal lining. Zonulin causes leaky gut. https://drdavisinfinitehealth.com/2020/01/zonulin-explains-it-all/ You don't even have to have a identifiable gluten intolerance for it to happen. It has already been suggested that there may be a link between zonulin and alopecia. https://pubmed.ncbi.nlm.nih.gov/35579378/ That's likely to be due to the fact that high levels of zonulin have already been associated with atopic dermatitis, the skin condition most associated with alopecia. https://pubmed.ncbi.nlm.nih.gov/29682826/ And there is definitely a relationship between zonulin and PCOS and insulin resistance. https://pubmed.ncbi.nlm.nih.gov/25336505/ Researchers are still divided on whether it's the chicken or the egg which comes first; zinc deficiency or intestinal issues and raised zonulin levels. https://link.springer.com/article/10.1007/s10620-021-07368-6

 

[Aidan Walsh]

I think that I may have found the base source of all of the previously mentioned issues. I was taking another look at my own gluten problems andfound that researchers now understand that the gliadin protein induces overproduction of an intestinal protein called zonulin by the intestinal lining. Zonulin causes leaky gut. https://drdavisinfinitehealth.com/2020/01/zonulin-explains-it-all/ You don't even have to have a identifiable gluten intolerance for it to happen. It has already been suggested that there may be a link between zonulin and alopecia. https://pubmed.ncbi.nlm.nih.gov/35579378/ That's likely to be due to the fact that high levels of zonulin have already been associated with atopic dermatitis, the skin condition most associated with alopecia. https://pubmed.ncbi.nlm.nih.gov/29682826/ And there is definitely a relationship between zonulin and PCOS and insulin resistance. https://pubmed.ncbi.nlm.nih.gov/25336505/ Researchers are still divided on whether it's the chicken or the egg which comes first; zinc deficiency or intestinal issues and raised zonulin levels. https://link.springer.com/article/10.1007/s10620-021-07368-6

Could be also the synthetic folic acid put into flour if one has the genetic mutation passed on from Parents A1298C C677T avoiding all gluten & prepared foods & all Sugars with so many names avoid all vitamins/minerals with folic acid stop using any Doctors folic acid try using Methyl Folate with

'go slowly' on Methyl B-12 if Methyl folate is not tolerated add one daily of Folinic Acid this is not folic acid so read all the labels making sure no sugar no folic acid.

I would get my sugar from Fruits/Vegs & rule out nickel/cobalt allergies

 

[Baz493]

Could be also the synthetic folic acid put into flour if one has the genetic mutation passed on from Parents A1298C C677T avoiding all gluten & prepared foods & all Sugars with so many names avoid all vitamins/minerals with folic acid stop using any Doctors folic acid try using Methyl Folate with

'go slowly' on Methyl B-12 if Methyl folate is not tolerated add one daily of Folinic Acid this is not folic acid so read all the labels making sure no sugar no folic acid.

I would get my sugar from Fruits/Vegs & rule out nickel/cobalt allergies

Actually, I have been looking at how gluten intolerance/allergy likely relates to gliadin transformation into amyloid-like structures in the body. https://pubmed.ncbi.nlm.nih.gov/34110092/ It turns out that even people who have no allergic response to gluten can somehow experience long term health issues, around the body, as a consequence of this amyloid formation. The current line of research seems to indicate that, because amyloids tend to be identified as evidence of fungal or bacterial infection, the body has a rapid immune response to the proteins and moves a range of immune cells to the locations where they are identified. Regarding the reason that this might result in loss of hair I have been looking at how microorganisms use zinc to produce amyloids and how zinc reacts with amyloid to form toxic beta amyloid. https://www.nature.com/articles/s41598-018-23122-x Research also shows that issues with gluten, while resulting in a zinc deficiency, do not result in a similar iron deficiency. There has also been research detailing how the trypsin enzyme, such as is found in the sebum of people with alopecia, can actually exacerbate iron induced ferroptosis. Something similar occurs in the atopic dermatitis which is generally associated with alopecia.

 

[Aidan Walsh]

There is also a microbiome aspect. The zinc could be influencing the microbiome in some cases.

National Library of Medicine Citations for Alopecia (Hair Loss)

Chlamydia Pneumonie is involved with dandruff website on Dr. Charles Stratton's Vanderbilt University work here: www.cpnhelp.org

 

[Baz493]

While I was looking at research on topical use of algal lipids for restoration of hair I found this article on an eight year old boy, who was developing male pattern baldness, and how his physicians successfully reversed the condition. They seem to have started with a general multivitamin supplement and included fish oil, vitamin A, vitamin D3, and zinc. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7721078/ The article details steps which they took and pictures of the progress as hair was restored.

 

[Baz493]

So it turns out that the solution to everything was right in front of me the whole time. I've had a condition called nephrotic syndrome for decades. It causes the loss of blood proteins called albumin. In alopecia the albumin is generally altered in a way that I don't yet understand. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7350867/

Apparently albumin acts as the primary zinc carrier protein in the blood, transporting it from the intestine to tissues. https://pubmed.ncbi.nlm.nih.gov/19021548/ However it also seems to act as a protective, binding, agent for iron and helps to prevent the kind of oxidative stress we have discussed. https://pubmed.ncbi.nlm.nih.gov/9486090/ It binds iron so tightly that bacteria struggles to obtain any from it.

The liver produces albumin so that is the next point of call. Non alcoholid fatty liver disease and alopecia. https://onlinelibrary.wiley.com/doi/10.1111/jocd.15754 Of course, high iron content in the albumin induces kidney issues, likely explaining the cause of high albumin losses, placing greater stress on the liver to produce more albumin.

So now I'm down to where I commenced my latest investigation; the intestinal microbiome. Researchers have explored the relationship between the microbiome and hair growth for a while and have also extensively explored the connection between the microbiome and the liver but I don't know if anyone has connected the three together yet. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7996884/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9837590/ https://www.nature.com/articles/s41575-018-0011-z Proteobacteria and firmicutes seem to be the common microbiome issue in alopecia. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9837590/ Why they help to induce non-alcoholic fatty liver disease I don't know but the research shows that, as well as some other bacteria, they do.

So where this starts to get really interesting is an orchid called dendrobium. Researchers have been investigating the effects of different species polysaccharides on the liver and alopecia. https://www.sciencedirect.com/science/article/pii/S0753332222014329 https://pubmed.ncbi.nlm.nih.gov/36470987/ There are some questions about potential side effects but it does seems to be protective. Ultimately, however, this comes down to diet. An 'American style' diet increases NAFLD risk while a more plant based diet reduces it.

 

[Baz493]

It turns out that zinc deficiency gets even more complicated. The gluten protein in wheat and the glutelin protein in rice both bind cadmium so that high grain intake can result in a toxic cadmium load in our bodies. As a heavy metal this is going to cause oxidative stress. However it turns out that cadmium has at least two separate effects on relevant factors. I have already mentioned the oxidative stress with albumin but albumin also has a cadmium binding site, site B, which activates the kidneys to eliminate albumin from the body. It's an innate mechanism designed to try to detoxify the body but doctors treat it as a disease; nephrotic syndrome. Such losses of albumin will result in issues like zinc deficiency. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2974692/

However I think the more relevant of the factors is the HIZR-1 nuclear receptor. This zinc receptor is expressed most strongly in the intestines and is designed to detect high levels of zinc in order to prevent a toxic overload. Once the receptors trigger enough signaling the intestines reduce absorption of zinc. Cadmium binds to the receptors, triggering the same signaling so that zinc deficiency results. https://www.pnas.org/doi/10.1073/pnas.2022649118

 

[Baz493]

Final post on this subject. I was able to put together that male pattern baldness should actually be classified in the category of connective tissue diseases due to the hair loss fitting the pattern of the underlying galea aponeurotica. The cadmium, and other heavy metals, can induce increased expression of matrix metalloproteins, enzymes which break down collagen. https://pubmed.ncbi.nlm.nih.gov/26514923/ https://www.sciencedirect.com/science/article/abs/pii/S0300483X05000971 Normal metalloprotein activity is zinc dependent but cadmium often mimics zinc. This includes binding to metallotheionein, a metalloprotein essential for wound healing and hair growth. https://pubmed.ncbi.nlm.nih.gov/2056197/ https://www.nature.com/articles/s41467-023-38588-1 https://www.sciencedirect.com/science/article/abs/pii/B9780080268255500140 Collagen is the main constituent of connective tissues, such as the galea aponeurotica. Trypsin, as I have previously discussed as involved in hair loss, activates MMP-2 and MMP-9. Due to the presence of collagen in both the underlying bone and the skin above these result in damage to both regions. It means that this is an extremely complex disease state which isn't isolated to the scalp and that hair loss is only an early symptom. At normal levels metalloproteins are essential to hair growth but excessive levels can be a problem. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3138469/

 

[Baz493]

Just a quick update, though important. I finally worked out the primary mechanism behind my own hair loss, relating to gluten allergy. Because cadmium binds to grains and allergy exacerbates the absorption of the heavy metal this led to significant levels binding to the albumin protein in my blood. Albumin is the primary protein for carrying zinc, and other metals, in the bloodstream. When cadmium binds to it the kidneys begin to eliminate it in urine. In people with allergy related albumin loss in urine, albuminuria, this is called minimal change disease. It is a condition which can be identified by foaming of urine when it lands in water. Because albumin carries zinc, and other essential minerals, to tissues the loss is central to skin conditions and hair loss. I now realise that I began losing my hair just two or three years after the albuminuria commenced. Another name for albumin loss is nephrotic syndrome, a condition which is now recognised by some specialists as relating to hair loss. Cadmium is bioaccumulative in the body. In the kidneys it has a half life between 6 and 38 years and in the liver 4 to 19 years and these are body organs of elimination. https://www.atsdr.cdc.gov/csem/cadmium/Biological-Fate.html

 

[Baz493]

For anyone still reading this thread I have been putting together some useful information recently, regarding cadmium toxicity in the body. It doesn't just mimic zinc in the body. Ferritin and transferrin are blood proteins which transport iron around our bodies. Cadmium binds to them, locking out the iron and triggering loss of them in the urine. In muscle cells cadmium has been found to mimic calcium, so reducing muscle contraction. It also turns out that cadmium impairs vitamin A metabolism in the body, probably because that metabolism requires zinc related factors. When you look at the metabolites of vitamin A, retinoids, and their effects throughout the body you really get a sense of why we lose our hair. Retinoids are needed for maintaining a healthy liver, healthy kidneys, healthy blood vessels, healthy skin, and healthy hair. Ingested artificial retinoic acid, all-trans retinoic acid/tretinoin, actually induces hair loss yet has proven to have some topical benefit for hair growth. Retinoids affect the function of the renin-angiotensin system. So impaired vitamin A metabolism is likely to be the underlying factor for renin-angiotensin involvement in alopecia. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4198813/ The same factors seem to be involved in people who experience hair loss as a result of covid.

 

[Baz493]

The connection between cadmium, vitamin A metabolism, and alopecia seems to be in how cadmium alters gene expression. In the section on results in this article it is detailed how upregulation of gene's affecting synthesis of retinoic acid is upregulated in alopecia while downregulation of gene's affecting degradation of retinoic acid is downregulated. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3546144/ The gene's affecting degradation of retinoic acid are the CYP26 gene's. They regulate production of three cytochrome P450 enzymes which break down retinoic acid. Although other factors can cause the same reduced levels of retinol binding protein 4 mentioned in the article cadmium is one of the factors which can be involved through loss in urine. https://www.sciencedirect.com/science/article/abs/pii/B9780128000946000030 Retinol binding protein 4 is the blood transporter for vitamin A, in the form of retinol, so deficiency means reduced delivery of vitamin A/retinoic acid to tissues. This article details cadmium's effects on downregulation of the cytochrome P450 enzymes as well as similar upregulation of gene's affecting synthesis of retinoic acid as were detailed in the article on alopecia. https://www.jbc.org/article/S0021-9258(20)30580-9/fulltext I do make note of the difference between the article in alopecia describing upregulation of Aldh1a3 and the article on cadmium's description of upregulation of Aldh1a1 and Aldh1a2 and do not yet have an answer to the discrepancy.

 

[Baz493]

Everything broken down into a simple equation is that zinc is essential for vitamin A metabolism. https://pubmed.ncbi.nlm.nih.gov/9701158/ The breakdown of vitamin A into retinoids, most specifically various types of retinoic acid, influences multiple factors in both the skin, sebaceous glands, and hair growth cycle. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3237781/ By triggering production/release of serine protease enzymes, which damage both skin and hair, retinoic acid and retinoids are indirectly responsible for enzymatic breakdown of hair. Although extreme deficiency or excess of retinoids can trigger hair loss over all of the body a moderate deficiency or excess can lead to patchy loss of hair or male pattern baldness. Fibroblasts are a significant portion of cells in the fibrous tissue of the galea aponeurotica which underlies the pattern of male pattern baldness. Retinoids affect the fibroblasts in a range of ways including production of collagen so also lead to thinning of the scalp in the area of the galea aponeurotica. https://www.sciencedirect.com/science/article/abs/pii/S019096228670248X As dietary and environmental cadmium can mimic zinc, iron, and calcium, it is capable of altering the entire process of vitamin A metabolism and levels of retinoids. It does so partially through upregulation of genes affecting retinoic acid production and downregulation of genes affecting retinoic acid degradation.

 

[Baz493]

I kept pushing the line of reasoning and now have a pretty good idea of the last pieces of the puzzle. Because vitamin A is being rapidly converted into retinoids, as well as being used in conversion of cholesterol to 3 alpha androstanediol/dihydrotestosterone, the body can develop low levels of it. Vitamin A is essential for iron metabolism in the body. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8835033/ So a deficiency of vitamin A, resulting from its rapid conversion, means that iron deficiency is likely to occur. Copper is also required for iron metabolism but, without the vitamin A, the body can't use it and stores it in the liver. Increased vitamin A levels, therefore, decrease copper levels in the liver because the body is using it for iron metabolism. Of course iron is essential for hair growth and iron deficiency, resulting from poor iron metabolism rather than lack of iron in the diet, bad enough to cause dermatitis is going to eventually cause hair loss.

Without the vitamin A and copper that doesn't happen no matter how much iron doctors tell us to take. The higher the levels of copper in the liver the more likely we are to have non-alcoholic fatty liver disease (NAFLD). https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9929538/ Having NAFLD makes alopecia much more likely. https://www.dermatologytimes.com/vi...opecia-universalis-and-patchy-alopecia-areata and https://onlinelibrary.wiley.com/doi/full/10.1111/jocd.15754
Regarding people with thyroid related issues I would suggest the role of vitamin A deficiency, likely resulting from rapid conversion of vitamin A to retinoids. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9592814/ and https://academic.oup.com/endo/article/147/3/1438/2501298?login=false So that you know, some types of retinoic acid fall into the category of the rexinoids mentioned in that last article, in terms of their involvement in triggering hypothyroidism.

 

[Aidan Walsh]

I am trying to get my head around this Alopecia, not everyone has this with ME/CFS EDS Hair loss, countless take fish oils, multi vitamins minerals & most stop them as they become bothersome. There are a few good Groups on Copper on Facebook & one is dead against any blood tests for copper saying they are useless they do not believe in ranges or toxicity they mention vitamin A as well they take this & iron.

There is an interesting paper I read & not all have a kidney that is enlarged but my left one is & so was hers she was a 21 year old Medical student she became sick she tested positive for the latent TB form & negative on the other one. She was treated but her illness did not go away. She had an untrasound they said her kidney was enlarged & it took her more years to have the proper venous scans.

They kept telling her that her kidney was fine but it was not her kidney it was the vein one inch higher above she was finally diagnosed with Nutcracker Syndrome but she underwent the first of its kind in the UK an auto-transportation surgery.

They did not want do this so she told the Team she would go to the USA or France so they gave in & said we will do this. She felt well in the post-op recovery room she knew this was why she was so ill & she recovered but several months later she developed Stenosis of a renal vein & had to undergo another Surgery.

There are other tests she did Gold standard ones urine collections she wrote about on her Published paper. Patient/Medical Student/GP/Author Dr. Tamara Keith She is now a partner GP in Cambridgeshire. They told me I had a Dromedary Hump a large lop sided kidney like a single Camel hump on ultrasound but never did the venous venography testing she underwent. She is also on Twitter...

 

[Baz493]

I think that the best place for me to respond to that question is by mentioning a documentary called White coat rebels. Sorry if I can't provide a link but the one's I know about are considered commercial websites so wouldn't be appropriate to post. One of the experts in the doco states that one of the primary attributes which universities tend to look for in choosing medical students is their level of obedience, rather than intellect or commitment to helping patients. Medical associations keep a tight rein on their union members and, as the doco mentions, senior members of the associations tend to have significant pharmaceutical company connections and don't want the membership going around curing patients, since we are seen as cash cows. When you begin looking at the medical research which is available online you find a massive difference in quality between the highly skilled researchers and the one's who are only funded because of their connections. The best research is around twenty or thirty, if not more, years ahead of standard medical practice because doctors simply aren't allowed to refer to the research in their practices. They actually have to sign a commitment to avoid even speaking about subjects not approved by their medical associations. So you shouldn't be too surprised if standards of medical care aren't particularly high.

As my own standard of medical care, throughout my life, has been particularly substandard I have become increasingly better at trying to understand what is happening in disease. What I have found in looking at medical research is that you get groups of diseases which all share common causal factors so one person's chronic fatigue may relate to one set of diseases while another person's will relate to a completely different set. While I am fairly limited to knowledge of medical research on the subject of just a handful of diseases I have looked at what you are asking because of my own nephrotic syndrome. Firstly you have to understand that copper holds the distinction of being both a heavy metal and an essential nutrient (in small doses). Quite simply, you don't want to have high levels of copper in your body and probably get enough from your diet to cover your needs, though it never hurts to have the occasional food containing high levels. https://www.eatforhealth.gov.au/nutrient-reference-values/nutrients/copper Doctors always go on about taking iron for deficiencies but I have watched people grow old quickly from such advice. Iron is used in some explosive recipes because of the high oxygen content and flammability it has and this is the same reason that it is a cause of oxidative stress in the body. You can have high levels of it in your blood, causing oxidative stress, and yet still have symptoms of deficiency because your body isn't using it efficiently.

Anyway, because the kidneys and liver are our bodies organs for detoxification it means that almost all of the toxins and heavy metals we are exposed to are going to pass through them at some point. https://www.eatforhealth.gov.au/nutrient-reference-values/nutrients/copper Medical research connects my own nephrotic syndrome more with cadmium and organic solvents than with other factors. Because of my exposure to engineered silica nanoparticles in my last job I honestly thought that might relate but they seem more likely to damage the kidneys. https://www.news-medical.net/news/20220829/Inhaling-silica-nanoparticles-can-damage-the-kidneys.aspx I'm sorry to have to tell you that doctors can make up all kinds of excuses to deny patients medical investigations as they have in my own case. I have had specialists describe my local hospitals denials of investigations as suspicious, given all of the facts in my case. In Australia doctors protect their peers at the expense of their patients so one doctors screw up will lead to other doctors refusing the investigations which are likely to expose those mistakes. As for vitamin A and iron metabolism here are a few articles to consider. https://pubmed.ncbi.nlm.nih.gov/27551308/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3847738/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8835033/ Although a number of other nutrients are required for iron metabolism it is essential to have vitamin A as well but some of our bodies will quickly convert it into retinoids before it can be used in iron metabolism. Since cadmium, which disrupts many processes in our bodies (including increasing conversion of vitamin A to retinoids), is bioaccumulative the older we get the worse its effects on our health.