Category Archives: calcium

Good news: Baths can be less exhausting than showers

Yes, autoimmune disease can be exhausting and it can be confusing for other people to understand because autoimmune disease may not have obvious symptoms. A person with an autoimmune disorder may suffer from severe pain or other symptoms throughout their body but not have lab tests that show obvious problems to a physician. Autoimmune antibodies are known for a few types of disorders and those can be screened for if the lab test is ordered but not all autoimmune antigens have been identified.

Magnesium deficiency may be an underlying issue though for many/most autoimmune disorders, so taking an Epsom salt bath can provide improved magnesium absorption through the skin and allow a person to sit down to wash their hair and shave their legs (if desired). No promises though, that a nap might not still be desired after the exertion of bathing while sitting, or before the exertion of blow-drying long hair.

Fibromyalgia and chronic pain problems may have autoimmune origins [3] and/or may have to do with our cell’s energy workhouses, the mitochondria, running out of their preferred energy source — magnesium. They use calcium but it can overwork them to the point of cell death. In normal physiology membrane transport systems, also called ion channels, carefully control how much calcium is allowed into the interior of mitochondria. Something called ruthenium-red (RuRed) and magnesium ions are involved in controlling the entry of calcium ions through the transport channels. [1, 2]

A deficiency of magnesium may allow excess calcium to enter the mitochondria and cause overexcitation and even lead to death of the mitochondria.

Mitochondria are actually similar to bacteria and have their own DNA that in nature always matches the mother’s mitochondria’s DNA but that is a different story.

(RuRed) – not a nutrient I didn’t know about – it’s a dye used in labs that selectively binds with some things but not others so it is used for identification purposes with unknown samples — roughly.

Disclaimer: Opinions are my own and the information is provided for educational purposes within the guidelines of fair use. While I am a Registered Dietitian this information is not intended to provide individual health guidance. Please see a health professional for individual health care purposes.

  1. http://ajpcell.physiology.org/content/287/4/C817
  2. https://www.researchgate.net/publication/20680823_Ruthenium_red_and_magnesium_ion_partially_inhibit_silver_ion-induced_release_of_calcium_from_sarcoplasmic_reticulum_of_frog_skeletal_muscles
  3. https://www.ncbi.nlm.nih.gov/pubmed/24435355

Mitochondria, P53, cancer and magnesium deficiency

Addition, 7/21/16, there is more information about mitochondria and chronic illness at this link: https://www.sott.net/article/321987-Thanks-Big-Pharma-for-the-Mitochondrial-collateral-damage, the site also has a few other articles on the topic which I haven’t read yet and the topic of magnesium doesn’t come up until you reach the comment that I added. I will have to read more about this topic. Medications that cause an imbalance in calcium and magnesium could be causing stress to the mitochondria and lead to their death and to chronic illness.

  • This article is short introducing a long video. A quote from the short text does mention nutrient deficiencies can be involved, “Nutrient deficiencies are a contributing factor to mitochondrial dysfunction. ” https://www.sott.net/article/308212-Mitochondrial-dysfunction-GMOs-Glyphosate Glyphosate  Inhibition of vitamin D metabolism could lead to magnesium and  calcium imbalance which could be stressing mitochhondria and lead to chronic illness.
  • An abstract with a link to the full text: https://www.sott.net/article/264786-Oxidative-stress-mitochondrial-damage-and-neurodegenerative-diseases
  • https://www.sott.net/article/294075-Fibromyalgia-as-a-mitochondrial-disorder
  • I haven’t watched the video or read all of the articles yet but fibromyalgia is what I had symptoms of that were bad enough to lead to my giving up wheat and gluten products initially. It simply hurt too much when I ate them. And I got better without gluten. Maybe it was the gluten or maybe my genetics with errors in the vitamin D metabolism. I will have to get back to this topic but I share the information now because pain hurts and if even one person is helped then I would be glad. *And I was a professional gourmet baker, I know how to make from scratch croissant, and French baguettes and loaf breads of many types as well as cookies and quick breads. I love wheat products but they didn’t love my body.

A comment of mine that is awaiting moderation posted on another site:

Mitochondria need lots of magnesium (and magnesium is also necessary for white blood cells to be able to perform apoptosis.) “Additionally, exposure to low Mg upregulated plasminogen activator inhibitor-1 (PAI-1) [24]. PAI-1 is considered not merely a marker of senescence, since it is both necessary and sufficient for the induction of replicative senescence downstream of p53 [27].” by D. Killilea and J. Maier, “A connection between magnesium deficiency and aging: new insights from cellular studies” Magnes Res. 2008 Jun; 21(2): 77–82. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2790427/ Please U. of Penn. researchers, look into preventing cancer by providing mitochondria with a healthy diet instead of by providing them with some sort of pharmaceutical designed to manipulate P53 — just prevent P53 from being induced by providing adequate magnesium to the cells. Thanks.

The comment is in response to this article which is about recent animal based research that suggests that a cell’s mitochondria when under stress may produce a chemical (P53) that may lead to cancer: http://scienmag.com/penn-team-finds-mitochondrial-stress-induces-cancer-related-metabolic-shifts/#comment-7188

Now I know mitochondria need a lot of magnesium so one search led to the link in the comment and ~391,000 other links, https://www.google.com/webhp?sourceid=chrome-instant&ion=1&espv=2&ie=UTF-8#q=mitochondrial+stress+P53+calcium+magnesium, including this one:

by Giorgi C., et. al., “p53 at the endoplasmic reticulum regulates apoptosis in a Ca2+-dependent manner” PNAS, Feb. 10, 2015, vol. 112, no. 6, pp 1779–1784. http://www.pnas.org/content/112/6/1779.full.pdf

Apoptosis is the method by which white blood cells are able to kill infected or malfunctioning or old cells. Calcium and magnesium are both electrically active and can both act as signals to promote different types of cellular actions. Magnesium is most active within cellular fluid and calcium entry into cells is limited in part by ion channels that are powered by magnesium. So a magnesium deficient cell can allow too much calcium to enter the cell and within the cell calcium can cause a variety of actions and can even over activate the cell to the point of cell death. (155,000 search results for “excess calcium overworks mitochondria” :   https://www.google.com/webhp?sourceid=chrome-instant&ion=1&espv=2&ie=UTF-8#q=excess%20calcium%20overworks%20mitochondria  and which includes a link about the nerve degeneration disease ALS: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2933290/  so it looks like if I want to protect myself from cancer or ALS I should not stress out my mitochondria by maintaining a good intake and internal balance of both magnesium and calcium.)

Another addition to look into more at some point – P53 and apoptosis has been found to be affeected by treatment with a homeopathic preparation (which would be a completely non-toxic energy based treatment. http://www.jcimjournal.com/articles/publishArticles/pdf/S2095-4964(16)60230-3.pdf

/Disclaimer: This information is provided for educational purposes within the guidelines of fair use. While I am a Registered Dietitian this information is not intended to provide individual health guidance. Please see a health professional for individual health care purposes./

Self injurious behavior in autism patients with low calcium levels

Trigger warning for people with a history of trauma, self injury or other PTSD type issues: this post is about difficult topics and was difficult for me to write and to recover from writing. It may trigger uncomfortable feelings in readers but denial of issues doesn’t help anyone learn how to modify and control the issues for an improved quality of life and/or improved level of self control and safety from self injury. Sexual assault is also a difficult topic but self injury or the urge to self-injure can happen everyday.

Interestingly, Coleman (1994) studied a group of autistic children who had low levels of calcium (i.e., hypocalcinuria). These individuals often exhibited eye-poking behavior. When given calcium supplements, the eye-poking decreased substantially. In addition, language functioning improved.” [http://www.autism.com/symptoms_self-injury]

— secondary hyperparathyroidism perhaps?

For me secondary hyperparathyroidism can cause significant mental illness symptoms including a feeling of jittery thoughts and a jittery body, with a pent up feeling of needing to pop the bubble – ‘stabby’ feelings with a desire to self injure by stabbing myself. It is extremely unpleasant feeling and at times included a feeling of wanting to pop the eyes – gouge them out. Very unpleasant is an understatement, very dangerous to self is more accurate.

Secondary hyperparathyroidism can be caused by low vitamin D or low calcium. My endocrinologist was extremely insistent that I take both vitamin D and calcium but over the years I had learned, with lab test proof, that my hormone D tends to be in the elevated end of the normal range. Irritability to an excessive level can occur at the elevated end of the range of hormone D. Lab test ranges are just based on the averages that are seen by the lab — and lab tests are usually ordered for sick people not for healthy people, so those lab test ranges are really the range of values seen in sick people not a range based on the average values seen in only healthy people.

I didn’t comply with the endocrinologist’s recommendation and found that just increasing calcium intake stabilized my level of parathyroid hormone and took away the ‘stabby’ feelings.

It is common for corticosteroid balance to be different from normal in patients with autism. [see link below] Vitamin D and hormone D are actually seco-steroids and the active hormone D acts somewhat like steroids in the body. Autism patients may be like people with obesity and many other chronic illnesses, that have been associated with low vitamin D but supplements weren’t found to be helpful for the various conditions. The problem may be more like mine where I have too much hormone D which is converted from vitamin D, and which leads to low levels of vitamin D. [http://www.preventmiscarriage.com/documents/Immunological-Considerations.pdf]

Vitamin D is carried on a transport protein that acts to keep it inactive. When free within the body the vitamin form is quickly activated to the hormone form. There are many more Vitamin D receptors throughout the body than there is usually  enough hormone D to activate them all during states of normal health.

Autism and other chronic diseases that seem to associated with low lab test levels of vitamin D may actually be reflecting a problem or deficiency in the vitamin D carrier protein rather than representing an inadequate amount of vitamin D being supplied from the diet or an inadequate amount of time spent in direct sunshine. Vitamin D is based on cholesterol and is not actually an essential vitamin in the way that other vitamins are essential because our bodies can make vitamin D from cholesterol when we get about 15 to 30 minutes of sunshine per day on our face, throat, and bare arms.

Magnesium baths help circumvent the problem elevated hormone D causes within the gastrointestinal tract — calcium is absorbed preferentially and magnesium deficiency can result which also can be a cause of significant irritability.

Providing nutrition education and individualized nutrition care in the public health sector is where I have training and experience. — ie giving away free information. Making money is not where I’ve had experience. And traveling has proven to be difficult for me with my various autoimmune and food sensitivities, but I care a lot about pain and suffering and mental anguish, in myself and others.

It is unpleasant to have to feel an urge to hurt oneself, and it is hard to control an internal explosive feeling that has nothing to do with how your childhood went — talk therapy is not much help if the problem is actually hyperparathyroidism. Multiply that internal jitteriness and explosive feeling by days, months, or years, and it is really much better to take calcium supplements and magnesium baths then to talk to a therapist about your childhood — while trying to control the urge to poke yourself in the eyes. (They don’t understand, and the endocrinologist didn’t either. Lab tests are just lab tests and mood symptoms are referred to a psychiatrist for mood stabilizing medications – in my (bad) experience.)

  • Autistic kids wash up happier in an Epsom salt bath, .
  • I describe my current Epsom salt bath routine towards the end of this post: Substance P, neuropathic pain, migraines, and the cannabinoid system,

The way “fair use for educational purposes” works is that the information is provided not for profit. I share information, which may contain excerpts from copy-righted works, in the hopes that some individuals or clinicians will find some of the information helpful, and to keep within the guidelines for fair use I don’t ask for donations or charge money for the information.

(Brief excerpts fit the guidelines better, the Autistic kids wash up happier post was a post from years ago, before I had learned more about fair use guideline. It contains an extensive excerpt from a much longer article, but it is very helpful information regarding some special dietary needs that are common among children with autism and which I also found helpful for improving my own diet. I have recently found that I have several genetic defects that are also commonly found in children with autism. One of them affects two important amino acids so that might be a problem that could affect my ability to make the vitamin D carrier protein – but I haven’t looked into that metabolic pathway yet.)

/Disclosure: This information is provided for educational purposes within the guidelines of fair use. While I am a Registered Dietitian this information is not intended to provide individual health guidance. Please see a health professional for individual health care purposes./

And what do osmomechanical stress, changes of temperature, chili powder, curry powder, ginger, Benicar, hormone D, steroids, and cannabinoids have in common?

// 7/1/16 addition: This post is for people suffering from Irritable Bowel Syndrome (IBS) which is not well understood, easy to diagnose or treat, and can be life threatening when more severe symptoms continue long term. The condition can continue for years or be a life long issue that flairs up at times and is less severe at other times.   http://www.news-medical.net/news/20160629/Treatment-for-IBS-proves-difficult-survey-reveals.aspx?platform=hootsuite

Dietary tips can be helpful but why some foods seem to trigger symptoms while others don’s has not been well understood either. The common factor underlying why some foods seem to be triggers for many people may be the TRP channels that are found in cells throughout the intestines and actually in most cells of most life forms. //

So what do osmo-mechanical stress, changes of temperature, chili powder, curry powder, ginger, Benicar, hormone D, steroids, and cannabinoids all have in common?

They all may be able to overstimulate Transient Receptor Potential channels (TRP channels) within the gastrointestinal system and cause severe diarrhea in susceptible individuals.

In many cases, the activation mechanism of TRP channels is unclear (Figure 1), but known activators include specific agonists such as mustard oil (TRPA1) and capsaicin (TRPV1), an increase in intracellular Ca2+ (TRPM4, 5), temperature (heat: TRPV1, 2, 3, 4, TRPM4, 5; cold: TRPM8, TRPA1), mechanical or osmotic stress (TRPV4, TRPCs?) and phospholipase C (PLC) activation. TRP channel activity can be further modulated by intracellular phosphatidylinositol phosphates, such as PI(4,5)P2 and membrane potential, but also by inflammatory mediators, cannabinoids and steroids (Nilius, 2007; Rohacs, 2007; Nilius and Voets, 2008).” [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3012403/]

The TRP channels are a large group found in many species of life from yeast, to worms, fish and mammels. The agonists/activating chemicals for many of the types of TRP channels have not all been identified as of yet. [http://molpharm.aspetjournals.org/content/75/6/1262.full]

One type of TRP channels were formerly called Vanilloid Receptors, and are now called TRPV channels. Vanilloid Receptors were known to be activated by capsaicin found in hot peppers and chili powder. And more recent or less well known research has also found that they can be activated by cannabinoids and steroids, (see the link from the excerpt above), and osmomechanical stress.

Osmo-mechanical stress might be a precursor to edema, excess fluid in the extracellular space; if an organ or cell over fills with fluid it would mechanically be adding physical pressure to the organ or cell — and instead of popping like an overfull water balloon the TRP channels open in response to the physical pressure and let the excess fluid leak out into the extracellular space or into the area surrounding the heart for example. [http://www.ncbi.nlm.nih.gov/books/NBK92821/] Fibrotic heart disease would be adding mechanical stretching stress within the heart. TRP channels are being studied for possible use in preventing fibrotic heart disease. From that research article, we are told that changes in temperature may also activate them:

The activation mechanisms of TRP channel are highly diversified. Some TRP channels appear to be constitutively active, whereas others are activated by Gq-linked receptor activation, oxidative stress, changes of temperature, or an elevation of intracellular Ca2+ [126128]. All the TRP channels appear to be regulated by PIP2 [134137] .” [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3874073/]

PIP2 = phosphoinositides = phosphatidylinositol phosphates (PIPs) = phosphorylated deriviatives of phosphatidylinositol (PI) [http://www.annualreviews.org/doi/abs/10.1146/annurev.cellbio.21.021704.102317]

PIP2 = phosphatidylinositol-4,5-bisphosphate and PI, and phospholipase C (PLC) from the first excerptare involved in cannabinoid metabolism within plasma membranes: [page 9 Kendall et. al., Behavioral Neurobiology of the Endocannabinoid System (Springer, 2009, New York)]

Steroids and hormone D function similarly. And Benicar and curcumin can function similarly to hormone D. And curcumin is a medically active extract from turmeric, a powdered spice that is a main ingredient in curry powder. Turmeric is made from the root of a plant that is biologically very similar to ginger,  which is also a root that is used as a dried spice or  may be used as a chopped vegetable in stir-fry dishes and other foods. Ginger has over 400 active phytochemicals, and one of them might be acting similarly to the curcumin — but that is speculation based on the similarity of symptoms of Irritable Bowel Syndrome that both ginger and curry powder stimulate.

Because — what else do osmomechanical stress, changes of temperature, chili powder, curry powder, ginger, Benicar, hormone D, steroids, and cannabinoids all have in common? — They all may irritate Irritable Bowel Syndrome, (IBS), for some people, along with emotional stress and other things like eating fructose in much quantity (example: from a piece of fruit or fruit juice) or gassy vegetables like cabbage and cruciferous vegetables and beans (gas would be adding mechanical pressure to those TRP channels which might be an over-active culprit in IBS patients).

The book, “Tell Me What to Eat If I Have Irritable Bowel Syndrome; Nutrition You Can Live With; Including Dozens of Healthful Mouth-Watering Recipes,” by Elaine Mager, M.P.H., R.D., includes dietary advice and other information about Irritable Bowel Syndrome (IBS). (Warning – most of the recipes contain gluten

/Disclaimer: This information is provided for educational purposes within the guidelines of fair use. While I am a Registered Dietitian this information is not intended to provide individual health guidance. Please see a health professional for individual health care purposes./

Newborn screening for autism – 3 sets of 5 potential biomarkers

I bought the research study regarding newborn screening for autism and it is exciting but was based on a small number of patients with a diagnosis of autism spectrum disorder (n=16, control group n=32).

  1. Newborn screening for autism: in search of candidate biomarkers. [http://www.ncbi.nlm.nih.gov/pubmed/23547820 ]

The research study evaluated the newborn umbilical cord blood for 90 biomarkers (various types of lab tests), 76 biomarkers were found to have consistant data available for all study subjects,  and three sets of five biomarkers were found to be consistently increased or decreased in the infants who were diagnosed with autism later in life compared to the infants in the control group (the research study only used patients with an autism diagnosis who had been screened and diagnosed by the same physician in order to reduce risk of inconsistent diagnostic standards in the experimental group (n=16).

The three sets of five biomarkers need to be tested with a larger group of children with autism diagnoses to see if the results can be repeated. Feasibly to save money on lab tests all newborns might be screened with the set of five most predictive lab tests and the infants who are positive for those five might then be screened for the second set of five tests or all ten of the other biomarkers. The fifteen biomarkers include calcitonin (increased) and Thyroid Stimulating Hormone (TSH, decreased). Low TSH levels can cause increased calcitonin levels which causes reduced blood calcium levels. Elevated blood levels of calcium may cause an increase in calcitonin and having adequate levels of hormone 1, 25 D may be necessary for keeping calcitonin levels within a normal range. [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC442503/]

Vitamin D was not one of the 90 lab tests that were included in this research study, however the sibling study performed in Sweden suggested that low vitamin D at birth is involved but that other factors are also involved because all of the children born to Somalian refugees were found to have low vitamin D so that lab value would not be helpful as a screening test. 2) Swedish Study Suggests Low Vitamin D at Birth May Increase Autism Risk [https://www.autismspeaks.org/science/science-news/swedish-study-suggests-low-vitamin-d-birth-may-increase-autism-risk]

Alpha feto-protein (AFP) is one of the fifteen biomarkers found to be predictive for autism later in life. Levels of AFP have been found to be increased in both the mothers of infants who develop autism later in life and in the infants who develop autism later in life. Buy the research study to find out the other twelve – feasibly a concerned parent (with money and a cooperative physician) might be able to have their newborn’s blood screened for the fifteen biomarkers on their own initiative, right away, rather than waiting for the mainstream medical industry to do further research studies.

— The fact that autism was unknown in Somalia suggests that it is unlikely to be a naturally occurring condition and that it is unlikely to be caused by a lack of anti-autism medicine or by the lack of an anti-autism vaccination, so waiting for the for-profit medical industry to devise a for-profit strategy to prevent autism seems like it might take awhile. Concerned parents should have a right to seek effective care for their children and for themselves.

Autism seems to be a condition that occurs prenatally which leaves the newborn infant with metabolic differences but who otherwise appears normal and then, depending on nutritional and environmental conditions, at around age two to four the child’s development shifts towards symptoms of autism. The goal of newborn screening would be to identify which infants are most at risk for that later shift towards autism so that they might be able to be given additional care in order to prevent the damaging autoimmune like changes to the child’s brain. A few different genetic defects that affect nutrient needs may be involved so a newborn who is identified as high risk for developing autism symptoms later in life might then benefit from being screened for genetic defects in the methylation cycle, or with the vitamin D binding protein, or with hemoglobin metabolism. Infants identified as more at risk for autism later in life may also benefit from being screened for hypothyroidism, iodine deficiency, or an excess of bromide, chloride and fluoride.

In summary, for now, this is complicated but very exciting — we have the information we need in order to help women prevent autism before conception and to help identify which newborns may be more at risk for developing autism symptoms later in life so that we can help give the infants the additional nutritional and environmental support that might help them prevent the longterm autoimmune like brain damage from ever occurring.

Older individuals who already have autism diagnoses may also be helped by additional nutritional and environmental support (reduce their exposure to pollutants and foods or foods additives that their unique metabolism can’t digest as well as average) but a “cure” for the changes that already occurred in the brain may not be possible for children and adults who have already been diagnosed with an autism spectrum disorder. Individualized nutritional support might help reduce negative symptoms and improve quality of life for patients who already have an autism diagnosis.

/Disclosure: This information is provided for educational purposes within the guidelines of fair use. While I am a Registered Dietitian this information is not intended to provide individual health guidance. Please see a health professional for individual health care purposes./

Calcium and vitamin D supplements and prostate cancer; IOM and NIH reports

Use of calcium supplements has been already been associated with an increased risk of prostate cancer for men for many years in a National Institute of Health (NIH) an Institute of Medicine (IOM)report, (see page 6 and see excerpt later in this post)(and prostate cancer is also mentioned in a 1997 report on page 144, and from page 142 a summary statement about some groups of people who may be more at risk from excessive calcium intake:

Subpopulations known to be particularly susceptible to the toxic effects of calcium include individuals with renal failure, those using thiazide diuretics (Whiting and Wood, 1997), and those with low intakes of minerals that interact with calcium (for example, iron, magnesium, zinc).”)

from: Dietary Reference Intakes for Calcium, Phosphorus, Magnesium, Vitamin D, and Fluoride, Jan 1, 1997 [http://iom.nationalacademies.org/Reports/1997/Dietary-Reference-Intakes-for-Calcium-Phosphorus-Magnesium-Vitamin-D-and-Fluoride.aspx]

If you are a person who is already seeing health professionals about prostate cancer risks and you haven’t been told that excess calcium has been associated with an increased risk of prostate cancer then maybe it’s time to ask why not? The following webpage does suggest men may be better to use calcium rich foods instead of supplements, however prostate cancer risk is not mentioned: MayoClinic.

While I was looking for the Institute of Medicine report I found a more recent National Institute of Health update on vitamin D levels and prostate cancer which shows on an apparent U-shaped trend for risk of prostate cancer and vitamin D levels.

Having low levels of vitamin D and having elevated levels of vitamin D was associated with risk of prostate cancer in men, however the trend was only apparent when patient’s data was grouped by quartiles rather than by the three currently accepted categories of vitamin D sufficiency. Quartiles divide the data into five groups. If the U-shaped trend was more apparent for the 20% of patients with the lowest levels of vitamin D and for the 20% with the most elevated levels of vitamin D then the lab values of those groups of patients must not have overlapped very closely with the range of lab values that are included in any of the three established categories of vitamin D sufficiency: “(concentrations less than 50 nmol/L being considered deficient, 50–75 nmol/L insufficient, and 75–125 nmol/L considered sufficient).” — which suggests to me that those currently accepted ranges of vitamin D sufficiency do not actually provide any information that is useful for assessing or counseling men about their risk of prostate cancer.

We would need to go to the original research study and see what the lab values were for the patients who fell in the lowest and highest quartiles — the 20% with the lowest values and the 20% with the highest lab values for vitamin D — in order to have some idea of how low or how elevated the lab values were for the men who had an increased risk of prostate cancer. The lowest 20% might have had values that were lower than 50 nmol/L (below 20-30 nmol/L is considered deficient) and the most elevated 20% may or may not have had values below or above 75 nmol/L — but we have no idea without going back to the original research article.

  • Excerpt from Vitamin D and Calcium: A Systematic Review of Health Outcomes (Update).:
  • Prostate Cancer

    “In the current report, four new nested case-control studies (two rated A, two rated B) and one new prospective cohort study (rated B) found no association between baseline serum 25(OH)D concentrations and risk for prostate cancer. Two new nested case-control studies (both rated B) observed a trend between higher serum vitamin D concentrations and increasing risk for prostate cancer. In one study this increase was seen only among men whose sera were sampled in summer or autumn; in the other study, this trend was observed only when participants were divided by quartiles of 25(OH)D concentration, but not when they were divided by categories of vitamin D sufficiency (concentrations less than 50 nmol/L being considered deficient, 50–75 nmol/L insufficient, and 75–125 nmol/L considered sufficient).”

    “In the original report, 12 nested case-control studies (3 rated B, 9 C) evaluated the association of baseline serum 25(OH)D concentrations and prostate cancer risk. No eligible RCTs were identified. Eight of the nested case-control studies found no statistically significant dose-response relationship between serum 25(OH)D concentrations and the risk of prostate cancer. One C-rated study found a significant association between lower baseline serum 25(OH)D concentrations (<30 compared with >55 nmol/L) and higher risk of prostate cancer. Another C-rated study suggested the possibility of a U-shaped association between baseline serum 25(OH)D concentrations and the risk of prostate cancer (i.e., lower and higher serum 25(OH)D concentrations were associated with an increased risk of prostate cancer compared with that of the in between reference level).”

  • Evidence Reports/Technology Assessments, No. 217.
    Newberry SJ, Chung M, Shekelle PG, et al.
    Rockville (MD): Agency for Healthcare Research and Quality (US); 2014 Sep. [http://www.ncbi.nlm.nih.gov/books/NBK253544/]
  • Dietary reference intakes for calcium and vitamin D / Committee to Review Dietary Reference Intakes for Vitamin D and Calcium, Food and Nutrition Board ; A. Catharine Ross … [et al.], editors. Copyright 2011 by the National Academy of Sciences — ISBN 978-0-309-16395-8 (pdf) [http://www.nap.edu/read/13050/chapter/2#5] Excerpt, Box S-3: Potential Indicators of Adverse Outcomes for Excess Intake of Calcium and Vitamin D (page 6):

BOX S-3: Potential Indicators of Adverse Outcomes for Excess Intake of Calcium and Vitamin D (page 6)

Calcium

Vitamin D

  • Intoxication and related hypercalcemia and hypercalciuria

  • Serum calcium

  • Measures in infants: retarded growth, hypercalcemia

  • Emerging evidence for all-cause mortality, cancer, cardiovascular risk, falls and fractures

So excess calcium and excess vitamin D are both officially associated with increased risk of prostate cancer or with “emerging evidence for cancer” in general.

From some old notes, [8]: 12. [ncbi.nlm.nih] Carcinogenesis. 2011 Jun;32(6):822-8. Epub 2011 Mar 10. Enhanced formation of 5-oxo-6,8,11,14-eicosatetraenoic acid by cancer cells in response to oxidative stress, docosahexaenoic acid and neutrophil-derived 5-hydroxy-6,8,11,14-eicosatetraenoic acid. Grant GE, Rubino S, Gravel S, Wang X, Patel P, Rokach J, Powell WS.

“Stimulation of neutrophils with arachidonic acid and calcium ionophore in the presence of PC3 cells led to a large and selective increase in 5-oxo-ETE synthesis compared with controls in which PC3 cell 5-oxo-ETE synthesis was selectively blocked by pretreatment with NEM. The ability of prostate tumor cells to synthesize 5-oxo-ETE may contribute to tumor cell proliferation as well as the influx of inflammatory cells, which may further induce cell proliferation through the release of cytokines. 5-Oxo-ETE may be an attractive target in cancer therapy.”

***Did anyone besides me notice that they stimulated those cancer cells with calcium? Might simply not over stimulating cancer with excess calcium be an attractive target for cancer therapy? and cheap? – less calcium intake – more health output? /speculation/

/Disclosure: This information is provided for educational purposes within the guidelines of fair use. Information is not a substitute for individual health guidance. Please see a health professional for individual health care purposes./

Calciphylaxis, molecular mimicry and egg white albumin; an experiment, n = 1

Calciphylaxis is a rare type of wound that is associated with hyperparathyroidism and is most commonly seen in patients who are receiving kidney dialysis due to end stage renal disease. The condition is also associated with an eight times increased risk of morbidity (death) compared to patients who don’t have calciphylaxis.

The term calciphylaxis came to my attention this year when I found out that I had an elevated parathyroid hormone level. See the following posts for more information about calciphylaxis and about other symptoms associated with elevated parathyroid hormone:

  1. Secondary hyperparathyroidism, calcium deficiency and irritability
  2. Elevated parathyroid hormone (PTH) and 1-25-D, calcium deficiency and calciphylaxis‘Calciphylaxis is more of a risk with end stage renal disease but it has also been found in people who had normal vitamin D levels and normal kidney health. And “high dose vitamin D administration is capable of inducing STC (soft tissue calcification) and calciphylaxis in murine models. [56, 57] In an attempt to reestablish normal calcium-phosphate homeostasis, ESRD patients receive vitamin D analogs that could theoretically increase their risk of calciphylaxis if hyperphosphatemia and hypercalcemia ensued. [58, 59]” [3]

    “Experimental sensitizing events and agents included nephrectomy and exposure to parathyroid hormone (PTH) and vitamin D. Substances used as challengers included egg albumin and metallic salts. Calciphylaxis was the end result.4  – from a 1962 study, abstract is free. [4.5]’

  3. Secondary hyperparathyroidism and calciphylaxis symptoms; an update with lab values
  4. Calciphylaxis may be caused by several different nutrient issues

Antibodies against chemicals that are a normal part of the human body can develop in autoimmune disease. The term molecular mimicry refers to the autoimmune antibodies that may be manufactured by overactive white blood cells in response to a large foreign protein allergens that may have made it through ‘leaky’ intestinal walls into the blood stream.  See: Robert S. Fujinami, et. al., Molecular Mimicry, Bystander Activation, or Viral Persistence: Infections and Autoimmune Disease, Clin Microbiol Rev. 2006 Jan; 19(1): 80–94.

To skip to the point, egg white albumin is very similar to the albumin found in human blood. It is an essential protein within plasma and it helps maintain fluid balance between the blood plasma and extracellular fluid (too much extracellular fluid would be noticeable as edema – puffy ankles from excess fluid collecting outside of the cells and blood vessels.

After finding the research about egg white albumin on September 24, I eliminated egg white from my diet. My symptoms did get better fairly rapidly but I had tried a few strategies at the same time so it wasn’t clear whether stopping egg white had been necessary for the symptoms to improve or whether the other strategies I had tried may have been adequate on their own — so after feeling better for a couple weeks I decided to retry egg white to see if eliminating them had been an unnecessary strategy. Sadly I found that the day after trying egg white albumin again (in the form of baked chocolate chip cookies) my skin sores returned. I stopped eating egg white again. The sores aren’t as bad as they had been in September but calciphylaxis sores are termed necrotic wounds and necrosis means death and dead tissue in wounds can lead to gangrene and septic bloodsteam infections.

Open sores with oozing plasma that sticks to fabric is unpleasant and painful as well as being associated with an eight times increased risk of morbidity (which means death of the patient).

So I don’t have proof that my body set up autoimmune antibodies to albumin but I would rather stop eating egg white than continue having oozing sores – that is my choice, it is my body and I should have a right to take care of it to the best of my own ability rather than having to follow mainstream medical advice about a condition that is not well understood but is associated with an increased risk of death.

For more information about albumin antibodies and autoimmune disease see:

  • Rodríguez-Juan C, et. al., Increased levels of bovine serum albumin antibodies in patients with type 1 diabetes and celiac disease-related antibodies., J Pediatr Gastroenterol Nutr. 2003 Aug;37(2):132-5.
  • Excerpt from Abstract: “Although 46% of patients with autoimmune thyroiditis had positive results, the level detected (22.1 +/- 8.7 AU) was significantly lower than that recorded in patients with type 1 diabetes who had celiac disease antibodies (P = 0.04) and celiac patients (P = 0.04). Healthy volunteers showed no antibodies against bovine serum albumin.”  “Thirty-one percent of patients with diabetes yielded a positive result…” End stage renal disease is actually a significant risk for people with autoimmune Type 1 Diabetes because diabetes can cause an increased load on the kidneys from excess blood sugar and increased leaking of protein into the urine. Thirty-one percent of them might benefit from avoiding beef (bovine) or egg white albumin – but more research would probably be necessary before an ‘evidence-based’ recommendation could be made – except Rodriquez- Juan C, et al, did get a nice start on the project.

 

/Disclosure: This information is provided for educational purposes within the guidelines of fair use. While I am a Registered Dietitian this information is not intended to provide individual health guidance. Please see a health professional for individual health care purposes./

Magnesium deficiency can cause irritability, anxiety, and chronic degeneration

Inspirational quote: “Whenever I have a problem I sing, then I realize that my voice is a lot worse than my problem.” (and I feel better about my problem).

And then I take an Epsom salt bath to help treat irritability and the muscle cramps that can result from a magnesium deficiency. Some people may be more at risk for chronic magnesium deficiency due to intestinal malabsorption of the nutrient. Calcium may be preferentially absorbed within the intestines instead of magnesium.

Magnesium deficiency may affect levels of the brain neurotransmitter, acetylcholine, which may cause mood changes if it is not in balance with other more calming neurotransmitters. [Neurotransmitters and mood] The supplement choline is a precursor for acetylcholine and some users have noticed depressive affects with use of a high dose. [Acetylcholine and mood]

Taking the calcium supplements seemed to help reduce the elevated parathyroid hormone level but more recently they have seemed to cause a very rapid increase in muscle cramps and severe irritability. A magnesium bath every morning helped my mood change from rage to feeling like singing. It was kind of incredible to have my mood change so rapidly for reasons that were actually physical events — first I felt extremely angry shortly after swallowing a 100 mg calcium supplement and then I felt joyful after soaking in a bathtub for twenty minutes (soaking forty minutes or more can actually be dangerous because too elevated magnesium blood levels can cause an extreme slowing of the heart rate — don’t try that at home).

I haven’t had a psychiatrist tell me about the risks of magnesium deficiency to the mood or the benefits of an Epsom salt bath for the mood but I can hope, I can share information, and I can enjoy the benefits of Epsom salt baths while I wait. Eventually maybe psychiatry will recognize that the brain is connected to the body and that it is built out of nutrients, not out of pharmaceuticals.

Not surprising: People Reward Angry Men But Punish Angry Women, Study Suggests. Magnesium is effective and inexpensive and proton pump inhibitors are dangerous but patent protected. Get angry because the advice being sold as healthcare at an expensive profit may be causing harm over time. [PPIs and fracture risk, C difficile risk, FDA warning]

There may also be a gender bias regarding creativity, and provision of pain medication. There is also gender inequality in autoimmune disease — the majority of sufferers are female and the length of time between first onset of symptoms and diagnosis can be many years or even decades. Fifty million Americans are estimated to be suffering from some type of autoimmune disease (AD) and 75% of them are estimated to be female for reasons that are not clear at this time. [AARDA, Autoimmune disease in women]

“AARDA-conducted studies reveal a lack of trust in prescribing physicians, very likely fostered by the fact that the average AD patient may see more than four doctors in as many years before receiving a correct diagnosis. Also, more than 40 percent of AD patient report they have been told they were “too concerned about their health” or that they were hypochondriacs.”   –AARDA Launches “3-Second Adherence” Public Service Campaign.

I have been told that my physical symptoms are all psychosomatic so often that I really have no desire to go back  to anyone claiming to provide evidence based medicine. The evidence suggests to me that fifty million people are at risk from a system that doesn’t know what causes their condition or how to help them but who at the same time are willing to make random expensive guesses because after all they are just gambling with the patient’s time, money and long term health not their own.

Maybe eventually more health professionals will succumb to autoimmune illness themselves and then they will be more motivated to find more effective treatments that actually work on the underlying problems of nutrient deficiencies and metabolic imbalances. The body needs to be well nourished in order to make sialic acid for white blood cells to be able to properly identify damaged or improperly labeled cells such as the improperly labeled autoimmune antibodies and then to destroy the defective cells with a magnesium fueled enzymatic death (apoptosis).

I can hope, and I can share, and I can continue to try to take care of my own health.

/Disclosure: This information is provided for educational purposes within the guidelines of fair use. While I am a Registered Dietitian this information is not intended to provide individual health guidance. Please see a health professional for individual health care purposes./

 

Calciphylaxis may be caused by several different nutrient issues

Calciphylaxis usually includes an imbalance of calcium and phosphate and a deficiency of protein C may also be involved. Protein C deficiency may be caused by genetic or acquired reasons. Protein C is involved in blood clotting. Vascular and soft tissue calcification frequently is also present in patients with calciphylaxis symptoms. The mineral content of the calciphylaxis sores has been found to resemble the mineral balance of bone.

Imbalance in vitamin D and hormone D metabolism might affect magnesium levels in some unusual cases and may promote intestinal malabsorption of magnesium. However elevated magnesium is more typically found in patients who have calciphylaxis as a side effect of dialysis in end stage renal disease. The kidney disease causes an abnormal lack of hormone D because the kidneys in normal health are the only place where vitamin D is activated into the hormone D form.

These are copies of links that I was reading and Tweeted last night:

  1. Mineral substance of bone tissue and of experimental cutaneous calcinosis in rats: chemical analysis and ESR study.
  2. Calciphylaxis assoc w cholangiocarcinoma… /heparin & vit K didn’t help/ Thrombosis & protein C deficiency involved/
  3. Retrospective analysis of tissue plasminogen activator as an adjuvant treatment for calciphylaxis. /Ca P homeostasis/
  4. Calciphylaxis… “the reported median survival time is 2.6 months after diagnosis,”
  5. Aggressive calciphylaxis in end-stage renal disease… /assoc w vascular & soft tissue calcification/
  6. Calciphylaxis is a cutaneous process without involvement of internal organs… /assoc w vascular calcification/
  7. Net-like pattern of calcification on plain soft-tissue radiographs in patients with calciphylaxis. – PubMed – NCBI
  8. Is calciphylaxis best treated surgically or medically? – PubMed – NCBI
  9. Calciphylaxis in a morbidly obese woman w RA presenting w severe weight loss & vit D def. /pamidronate & D tx worked/
  10. Calciphylaxis in the absence of end-stage renal disease. – PubMed – NCBI /low vit D but tx surgery/
  11. The surgical management of renal hyperparathyroidism. – PubMed – NCBI
  12. Secondary hyperparathyroidism in children with chronic renal failure: pathogenesis and treatment. – PubMed – NCBI
  13. Vitamin D, parathyroid hormone, and acroosteolysis in systemic sclerosis. /low 25D w 2ndary hyperPTH in sunny climate

  14. Bone metabolism in celiac disease. – /following gluten free diet for 6 mo normalized 25D, calcium & PTH levels/

  15. Hypomagnesemia. Suppression of secondary hyperparathyroidism in chronic renal failure. – PubMed – NCBI

  16. Magnesium deficiency: possible role in osteoporosis associated with gluten-sensitive enteropathy. – PubMed – NCBI
  17. Recent data on magnesium & osteoporosis. “Mg def in post-menopausal osteoporosis, prob caused by Mg malabsorption.”
  18. [The significance of magnesium in medicine. (II) Disturbances of Mg metabolism & their treatment (author’s transl)].
  19. Metabolic disorders of cattle. /pellagra discussed, zinc, B6 Cu Mg def, malabsorption, iron overload can deplete B3/

Why do I care? because even though my symptoms are unusual I feel that I still deserve individualized health care. As a dietitian I was taught to look up information about any unusual diagnoses that patients might have and to provide individualized guidance if available or provide background information to help patients be able to make more informed choices about their treatment plan.

I also care because I think women deserve individualized healthcare even if we may get emotional or moody. Physical and mental illness symptoms can be related to underlying issues and simply medicating a symptom not only fails to address the underlying issue but it also fails to look for an underlying issue which can be life threatening if care is delayed in acute situations:

Whether male or female in a for-profit health industry being your own patient advocate or hiring a professional patient advocate may be life saving when navigating the increasingly complex health care system.

See the previous post for my own patient struggles with symptoms of hyperparathyroidism and calciphylaxis like sores: Secondary hyperparathyroidism and calciphylaxis symptoms; an update with lab values

/Disclosure: This information is provided for educational purposes within the guidelines of fair use. While I am a Registered Dietitian this information is not intended to provide individual health guidance. Please see a health professional for individual health care purposes./

Secondary hyperparathyroidism and calciphylaxis symptoms; an update with lab values

Last month I described some health difficulties that I had been experiencing for quite awhile. Lab tests that had been drawn earlier in the summer suggested that the problem might be secondary hyperparathyroidism and I also had been having a number of odd symptoms including calciphylaxis that can be associated with secondary hyperparathyroidism but is a more common in end stage renal disease (ESRD) particularly for patients on dialysis who were also receiving calcium supplements (and calciphylaxis is associated with eight times increased morbidity in ESRD). In the second post I reported that I was already feeling much better on the treatment plan that I had developed for myself.

I started taking 300-500 mg calcium per day based on the theory that the symptoms were related to calcium deficiency secondary hyperparathyroidism. I also increased my protein intake except for eliminating egg white and tree nuts from my diet – as a precaution in case I had developed autoimmune sensitivity to those protein sources which I had been eating more regularly than other foods during a time when I wasn’t eating enough overall. A steroid skin cream containing Triamcinolon 0.5% applied twice a day helped the calciphylaxis like skin sores heal. And I started taking 40 mg Benicar/olmesartan per day in an attempt to modify the low vitamin 25 D and vitamin 1, 25 D > 42 pg/mL. Levels of vitamin 1, 25 D above 42 pg/mL signals the bones to release calcium and phosphorus and can increase risks of osteoporosis and soft tissue calcification. [1, 2: MPKB- Science behind olmesartan (Benicar).]

  1. Secondary hyperparathyroidism, calcium deficiency and irritability, 
  2. Elevated parathyroid hormone (PTH) and 1-25-D, calcium deficiency and calciphylaxis, 

The 6/15/15 lab values:

  • Parathyroid hormone level – PTH Intact – 154.1 pg/mL — normal range: [15.0-75.0]
  • Calcium – 8.8 mg/dL — normal range: [8.4-10.2]
  • Phosphorus was not ordered but would probably be good to check.
  • Vitamin D, 25 – 10.9 ng/mL — normal is considered: [30.0-100.0]
  • Vitamin D 1, 25 – 55 pg/mL — normal is considered: [18-72] (the active hormone D)

The 10/12/2015 lab values:

  • Parathyroid hormone level — PTH Intact — 66.1 pg/mL — normal range: [15.0-75.0]
  • Calcium — 9.3 mg/dL — normal range: [8.4-10.2]
  • Serum Phosporus — 3.6 mg/dL — normal range: [2.5-4.5]
  • Vitamin D, 25 — 18.4 ng/mL — normal range: [30.0-100.0]
  • Vitamin D 1, 25 — 36  pg/mL — normal range: [18-72] (the active hormone D)

So I started taking calcium supplements and 40 mg of Benicar on September 23 and on October 12 my parathyroid hormone level is back within the normal range. My active 1, 25 D is below the osteoporosis inducing level of 42 pg/mL and my inactive vitamin 25 D level increased from 10.9 to 18.4 ng/mL — even though I am not taking vitamin D supplements but I do get more than fifteen minutes of sunshine most days of the week. My calcium level is still within the normal range but it went up from near the low end of the range to closer to the middle, from 8.8 to 9.3 mg/dL.

During the last couple days the calcium supplements have been causing me to have increased muscle cramps and irritable mood and I found that soaking in Epsom salt tub or footbath helped reduce the muscle cramps and bad mood. So the balance between magnesium and calcium intake is important and intestinal malabsorption of magnesium may be part of the underlying problem.

Overall I’m feeling much better than I was in early September before I started taking the calcium supplements. I had been having a racing heartbeat on very little exertion (like tachycardia) and for a long time I had been having an internal jittery-ness that felt like a bottled up pressure that needed a release valve or pinprick to pop the overfull bubble. The painful skin sores had been a fairly new and very unpleasant development. So yippee I have skin again! And I can walk downstairs without having to pause to let my heart rate slowdown.

I still have autoimmune thyroid antibodies but my thyroid hormone and thyroid stimulating hormone levels are within normal range — 10/12/2015 lab values:

  • Serum Thyroglobulin AB — 41 IU/mL — normal range: [0-40]
  • Serum Thyroid Peroxidase AB — 301 IU/mL — normal range: [0-34]
  • T3 Free Serum — 4.09 pg/mL — normal range: [2.77-5.27]
  • T4 Free Serum — 1.14 ng/dL — normal range: [0.65-1.86]
  • Serum Thyroid Stimulating Hormone — 1.20 mIU/L — normal range: [0.46-4.68]

To prevent autoimmune hyperthyroid symptoms I have been avoiding foods containing gluten and iodine sources since receiving the diagnosis in 2013. The gluten protein molecule contains a section called gliadin that is chemically similar to the thyroid hormone. The chemical similarity between gliadin and the thyroid hormone may allow autoimmune thyroid antibodies to develop in susceptible individuals, so avoiding gluten in the diet may be helping reduce or prevent the production of the autoimmune thyroid antibodies.

–The bad news – my endocrinologist still wants me to take a vitamin D supplement for my low vitamin D. [previous post: Whether to be compliant or to be healthy seems like an easy question to answer

/Disclosure: This information is provided for educational purposes within the guidelines of fair use. While I am a Registered Dietitian this information is not intended to provide individual health guidance. Please see a health professional for individual health care purposes./