Category: calcium

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Low vitamin D linked to longer lifespan

A study focused on the families of people who had at least two siblings who were 89 years or older. Middle-aged children of the long-lived siblings and the life partners of the middle-aged children were included in the Leiden Longevity Study. The vitamin D levels were found to be lower in the middle-aged children than for life partners.  The life partners were used as the control group in comparison to the middle-aged children based on the idea that they would have shared similar diets and lifestyles. Vitamin D levels but not hormone D levels were mentioned. [1] The numerical lab values were not available.The middle-aged children of the families with at least two 89-91 or older siblings were found to have less cardiometabolic disease indicators such as myocardial infarction, diabetes and hypertension compared to their life partners. The group of middle-aged children of 90 year olds also had lower values for blood sugar, insulin, triglycerides and improved insulin sensitivity. [2]

Low levels of vitamin D have been associated with many diseases, however hormone D levels were not measured in most of the studies. The vitamin can be converted to the active hormone by an enzyme that is typically well controlled by the kidneys but is also made by some types of cancer cells, white blood cells and in some autoimmune conditions. Elevated hormone D levels can cause excessive loss of calcium from bone tissue and calcification of soft tissue.

Supplements of vitamin D frequently need to be taken in amounts far greater than the standard recommendation in order to raise vitamin D levels. An association with disease does not prove whether the depressed vitamin D levels are a cause or a side effect of chronic disease. Measuring both the vitamin 25(OH)D and the hormone 1, 25(2OH)D levels would be more likely to reveal whether excessive enzyme activity was causing a decrease in vitamin D levels and an increase in hormone D levels rather than there being an actual deficit of vitamin D. Chronically elevated hormone D is associated with osteoporosis and other health issues.

/Disclaimer: Information presented on this site is not intended as a substitute for medical care and should not be considered as a substitute for medical advice, diagnosis or treatment by your physician./

  1. Canadian Medical Association Journal (2012, November 5). Low vitamin D levels linked to longevity, surprising study shows. ScienceDaily. Retrieved November 11, 2012, from [http://www.sciencedaily.com­ /releases/2012/11/121105130355.htm]
  2. van Heemst D., Leiden Longevity Study, Longevity Research Background, in Dutch, [http://www.langleven.net/index.cfm?p=1B8B2369-3048-9110-624DBCCA13F65FE9]
/Disclosure – the author of this post had two grandparents who lived beyond 90 years old; and has had low to normal values for vitamin D and normal to elevated lab values for hormone D for more than five years of testing.
*January 2021 addition: Too much vitamin D seems to be problem for me – genetic over activity of the vitamin D receptor may be part of it. Transport proteins are also needed for holding a supply of vitamin D in the inactive 25-D form. Without the protein transport the body can’t keep the 25 D from converting to the 1, 25-D form which is the hormone form that can activate the Vitamin D Receptor. /

Veterans Day 2012, honoring soldiers, past and present.

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Vitamin D can be activated to hormone D within some types of cancer cells

Normal and cancerous pancreatic cells express the enzyme, 1a(OH)ase, that converts inactive vitamin D into active hormone D. [1] Asking what benefit pancreatic cancer cells might receive from converting more of the inactive vitamin into the powerful hormone D than normal pancreas cells seems like a reasonable question to consider. The excerpt below mentions some other locations that the enzyme has been found and mentions work from a different study regarding the enzyme in the diseases sarcoidosis and psoriasis. The research article the excerpt is from focuses on the use of extra vitamin 25-D or a modified form of it as a possible way to reduce proliferation of the cancer cells.

Excerpt:
“Zehnder et al. examined the distribution of 1a(OH)ase in extra renal tissues (41). They reported specific staining for 1a(OH)ase in skin (basal keratinocytes, hair follicles), lymph nodes (granulomata), colon (epithelial cells and parasympathetic ganglia), pancreas (islets), adrenal medulla, brain (cerebellum and cerebral cortex) and placenta (decidual and trophoblastic cells). They also reported over-expression of the enzyme in disease states including psoriatic skin and sarcoidosis.”  [1]

The use of extra vitamin D may not equally benefit all types of patients or possibly all types of cancer. Trials with supplements of vitamin D in live prostate cancer patients have not been found to be reliably beneficial. [2] Supplements of vitamin D and calcium have not been found to reduce fracture risk in healthy pre-menopausal women. [3] Educational materials for physicians may not include information about the risks associated with vitamin D supplements for some types of patients that are known to have risk of having low 25D values along with elevated 1,25D such as patients with sarcoidosis or cancer of the parathyroid gland.[4] [26]

Few research studies about vitamin D deficiency or effects include blood tests of both the vitamin and the hormone. The hormone form is less chemically stable and the lab test for it is more expensive than the lab test for the vitamin. Checking only the level of vitamin D  for assessing deficiency is based on the assumption that the converting enzyme is carefully controlled within the kidneys and that excess hormone D won’t build up but the enzyme is also made by some types of cancer cells and white blood cells and even within the placenta of pregnant mammals.[21] If the hormone is especially important within the placenta for growing a baby than it might also be important for growing a tumor. Including less vitamin D in the diet of prostate, breast or colon cancer patients might help more than offering more. But extra vitamin D may be helpful for other patients, and checking both lab values may help to be sure a reduced blood level of 25-D isn’t because it ‘s being converted to extra 1,25-D outside of the kidney rather than being a diet or sun deficiency.

Without also checking the blood levels of 1,25-D it is impossible to know if all patients with depressed levels of 25-D are truly deficient in hormone 1,25-D or whether they simply have depressed levels of the precursor 25-D. The website, Chronic Illness Recovery.org has more information regarding having both tests performed accurately: [6] Taking too much of either form of D regularly can lead to harmful side effects and long term bone loss and soft tissue calcification problems. [20] People with typical health responses will break down some of the excess but a large dose for months can build up to an excess. The risk is increased if there is an undiagnosed problem leading to increased conversion to 1,25-D.

If someone’s diet includes fortified breakfast cereal, toast, milk, yogurt and other fortified beverages and snack bars and the fish that are naturally good sources of vitamin D then too much supplemental vitamin D may be consumed over time without a single capsule having been taken. The average healthy person would have the enzymes needed to break down the excess but chronically ill patients may not have the enzyme that deactivates hormone D. Vitamin D is fat soluble and can be stored. That aspect of vitamin D metabolism may have been critically important to health during winter months before the fortification of foods became common.

/Disclaimer – I have tried to share my concerns regarding the possible societal and personal risks of over-fortification and over-supplementation with vitamin D. If taking excess vitamin D was truly helpful than why hasn’t it helped more people who have tried it by now? Instead supplementation has been associated with an increase in cholesterol levels. [14] Some extra vitamin D is necessary and beneficial when there is an actual deficiency of both the vitamin and the hormone but it is not helpful if the vitamin D blood levels are low because the vitamin is being converted into elevated levels of the very powerful hormone D. Psoriasis [22] and sarcoidosis are painful diseases and the most effective treatment may require avoidance of the precursors to hormone D. Topical use of 1,25-D [24] and light therapy [25] has been tested for psoriasis and found beneficial so some individuals might have a problem using dietary sources of D.

Many foods and beverages are fortified with vitamin D now and the previous fortification levels of liquid milk had already largely eliminated most problems with rickets/vitamin D deficiency during childhood. [7,8,9,10,11] I screened many patients and educated regarding the need for adequate food sources of vitamin D or sunlight for years and during that time only met one child with early signs of rickets. His legs developed normally after sardines were added to his dairy free diet (milk allergy). Now bread and breakfast cereal and other nondairy beverages are also fortified with vitamin D. He would’t need to look only to sardines for vitamin D now but he would need to read labels. Unlike milk, the fortification levels for vitamin D are not set at any consistent level in the newer fortified products. A yogurt may have 50% fortification or zero extra fortification. Food fads to sell more products can be dangerous if the fortified chemical can be stored and possibly collect to dangerous levels. Those smaller percentages of fortification from the varied sandwiches and yogurts might add up over time especially if there is an undiagnosed problem leading to conversion of the vitamin to the hormone. Oat bran is safe but vitamin D in excess is not. A list of overdose side effects of vitamin D: [5]

I do have bias against excessive fortification of the food supply with vitamin D because both myself and my significant other have chronic conditions that cause depressed lab values of vitamin D and elevated levels of hormone D. That also means that I have first hand knowledge regarding what living with the side effects of elevated hormone D is like. Rickets can cause pain but so can the elevated hormone D levels and the elevated calcium levels that increased hormone D can cause. The firsthand knowledge regarding calcium, phosphorus and vitamin D physiology helped me recognize similar symptoms when they occurred in my puppy when she was sick with Parvovirus. The canine illness is frequently deadly. She only got better when I limited foods during the recovery period that were naturally rich or fortified with vitamin D and excess calcium/phosphorus. Pathogens have learned how to use our body’s natural processes for their own benefit. Trying to fight disease while providing the pathogens with the foods that they thrive on is largely a waste of effort. (Feed a fever but starve a cold. – a somewhat true old wive’s tale.)

Taking extra CLA, an essential fatty acid, [15, 16, 17] and limiting foods rich in arachidonic acid [19] may benefit individuals who are fighting prostate and breast cancer. Similar metabolic pathways may be involved with other forms of cancer or chronic disease but not necessarily. [18] Some types of pathogens have learned how to convert nutrients that normally are stored within cellular membranes into food sources. Feeding the body and starving the cancer would make more therapeutic sense than inundating the body with chemicals that kill both the healthy and unhealthy tissue.

Health care is not affordable if it focuses on symptoms and doesn’t tackle the underlying causes of disease./

  1.  Schwartz G, et. al., “Pancreatic cancer cells express 25-hydroxyvitamin D-1a-hydroxylase and their proliferation is inhibited by the prohormone 25-hydroxyvitamin D3,” (Carcinogenesis vol.25 no.6 pp.1015–1026, 2004) [carcin.oxfordjournals.org/content/25/6/1015.full.pdf] Excerpts: “Two samples obtained from infiltrating adenocarcinoma of the pancreas displayed robust and extensive expression of 1a(OH)ase in (Figure 2C, left two panels). High expression levels were also found in ductal breast carcinoma (Figure 2C, top right) and in a section of pediatric renal cell carcinoma (Figure 2C, bottom right). Furthermore, we found positive staining for 1a(OH)ase in the autonomic ganglia in colon and in the bile ducts of the liver (data not shown).” . . . “Our results confirm previous findings of expression of 1a(OH)ase in normal pancreas. Moreover, they demonstrate for the first time that 1a(OH)ase is also expressed in pancreatic adenocarcinoma.”  [1]
  2. Article by Mary E. Dallas, “Calcium, Vitamin D Supplements May Pose Risks for Men With Prostate Cancer,” MedlinePlus  SOURCES: Louis Potters, M.D., chair, radiation medicine, North Shore – LIJ Health System, New Hyde Park, N.Y.; Wake Forest Baptist Medical Center, news release, Aug. 7, 2012
  3. Article by Gina Kolata, “Calcium and Vitamin D Ineffective for Fractures, U.S. Preventive Services Task Force Says,” (June 12, 2012) NYTimes.com: [nytimes.com]
  4. “Physician Consideration Regarding Vitamin D,” (March 2012) MGHS, Nutrition and Medicine Committee, pdf [ww4.mgh.org] website: [ww4.mgh.org]
  5. “Cacitriol,” MedlinePlus [nlm.nih.gov/medlineplus/druginfo/meds/a682335.html]
  6. “D-Metabolites Tests” ChronicIllnessRecovery.org: [chronicillnessrecovery.org]
  7. Article by Katherine Doheny, “The Baby Won’t Take a Bow” (April 4, 1995) LATimes [articles.latimes.com] *Not too worried about rickets in 1995.
  8. Article by Janet Stobart, “Global Health Watch: Rickets showing up in some British children,” (Jan 19, 2011) LATimes: [articles.latimes.com] (*~40 children in the UK were treated for it at one hospital in 2011.) Rickets is no longer a reportable disease in the US and statistics aren’t available.
  9. Lazol JP, Cakan N, Kamat D. “10-year case review of nutritional rickets in Children’s Hospital in Michigan,” Clin Pediatr (Phila). 2008 May;47(4):379-84. Epub 2008 Jan 11.  (*96% of the cases found were breast fed infants that weren’t receiving a supplement and ethnically may have had darker skin tones.)
  10. “Top children’s surgeon says ‘poverty’ bone disease has returned in Southampton,” (Nov 12, 2010) Press Release, University Hospital Southampton: [uhs.nhs.uk] Excerpt:  “In my 22 years at Southampton General Hospital, this is a completely new occurrence in the south that has evolved over the last 12 to 24 months and we are seeing cases across the board, from areas of deprivation up to the middle classes, so there is a real need to get national attention focused on the dangers this presents.” […] “said Professor Nicholas Clarke, consultant orthopaedic surgeon at Southampton General Hospital and professor of paediatric orthopaedic surgery at the University of Southampton.”  (*So asking what changed in the one to two year time period preceding Nov. 2010 that would affect 20% of children at all income levels would seem a pertinent question rather than assuming that suddenly 20% of children were no longer receiving vitamin D fortified products and had stopped going outside. Low calcium or phosphorus can also cause rickets, not just low vitamin D. Elevated 1,25 D levels can lead to decreased bone mineralization. Twenty percent of children may have chronic inflammatory conditions that current science doesn’t recognize or test for.)
  11. Steichen JJ, Tsang RC, Greer FR, Ho M, Hug G. “Elevated serum 1,25 dihydroxyvitamin D concentrations in rickets in very low-birth-weight infants,” J Pediatr. 1981 Aug;99(2):293-8.  [ncbi.nlm.nih.gov] * 25D levels were low and 1,25 D levels were elevated. The infants were successfully treated with an increased amount of calcium and phosphorus but without a change in their vitamin D intake. The infant’s 25 D levels increased and the 1,25 D levels decreased after the change in calcium and phosphorus intake. These were premature infants, not average infants.
  12. Peter J. Malloy, J. Wesley Pike and David Feldman, “The Vitamin D Receptor and the Syndrome of Hereditary 1,25-Dihydroxyvitamin D-Resistant Rickets,” Endocrine Reviews April 1, 1999 vol. 20 no. 2 156-188 [edrv.endojournals.org/content/20/2/156.full]
  13. “Vitamin D3 1,25-Dihydroxyvitamin D, Interpretation” Medscape [emedicine.medscape.com] Excerpt: “In granulomatous disease such as lymphoproliferative disorders, sarcoidosis, tuberculosis, and inflammatory bowel disease, 1α-hydroxylase enzyme activity was found in macrophages as the extrarenal source of 1,25(OH)2 D. When 1α-hydroxylase is activated, it converts 25(OH)D to 1,25(OH)2 D, just as what occurs under physiologic conditions in the kidneys.[12] However, unlike the kidney, the 1α-hydroxylase in the macrophages in granulomatous diseases is not controlled by the usual physiologic regulators.”
  14. “Vitamin D Supplements Won’t Help Cholesterol Levels: Study,” (Sept 4, 2012) MedlinePlus: [nlm.nih.gov] SOURCES: Manish Ponda, M.D., M.S., assistant professor, clinical investigation, Laboratory of Biochemical Genetics and Metabolism, Rockefeller University, New York City; Michael Holick, M.D., professor, medicine, physiology and biophysics, Boston University School of Medicine; Sept. 4, 2012, Arteriosclerosis, Thrombosis and Vascular Biology (* Vitamin D in normal metabolism is made from cholesterol and excess amounts of it are converted back into cholesterol so those who don’t need extra vitamin/hormone D are buying and taking a supplement of a slightly different form of cholesterol. Taking supplemental cholesterol is not a typical recommendation for anyone.)
  15. What Doctors Don’t Tell You (vol 13, issue 5): “CLA fatty acids may combat prostate cancer,” healthy.net: [healthy.net]
  16. Song HJ, et. al., “Conjugated linoleic acid inhibits proliferation and modulates protein kinase C isoforms in human prostate cancer cells,” Nutr Cancer. 2004;49(1):100-8  [ncbi.nlm.nih.gov]
  17. Ochoa JJ, et. al., “Conjugated linoleic acids (CLAs) decrease prostate cancer cell proliferation: different molecular mechanisms for cis-9, trans-11 and trans-10, cis-12 isomers,” Carcinogenesis (2004) 25 (7): 1185-1191. [carcin.oxfordjournals.org]
  18. Field CJ, Schley PD, “Evidence for potential mechanisms for the effect of conjugated linoleic acid on tumor metabolism and immune function: lessons from n 3 fatty acids,” Am J Clin Nutr 2004;79:1190S–8S, Full text pdf: [ajcn.nutrition.org]
  19. A previous article of mine, “Prostate and Breast Cancer and omega 6s and 3s,” (May 16, 2012) Gingerjens: [gingerjens.blogspot.com]
  20. “Hypervitaminosis D, Symptoms and presentation” Wikipedia [en.wikipedia.org]
  21. Chapter author, Daniel D Bickle, “Extrarenal Synthesis of 1,25-Dihydroxyvitamin D and Its Health Implications,” Vitamin D: Physiology, Molecular Biology, and Clinical Applications , Nutrition and Health 2010, pp 277-295, Ed. Michael F. Holick [link.springer.com]
  22. Article by John Gever, “Low Vitamin D Plus Hypertension May Worsen Cardiovascular Risks,” (Jan. 7, 2008) MedPageToday: [medpagetoday.com]  Excerpt: “Dr. Wang and colleagues could not rule out the possibility that vitamin D deficiency is not causative. “Unmeasured characteristics associated with vitamin D deficiency could account for the increased cardiovascular risk,” they acknowledged. They pointed out that “an alternate explanation for the present findings is that vitamin D deficiency is a marker of chronic nonspecific illness rather than a direct contributor to disease pathogenesis.” ” (* Depressed levels of vitamin D that are associated with elevated levels of hormone D would lead to increased wasting of magnesium and hypertension is a primary symptom of magnesium deficiency. Other aspects of cardiovascular disease are also related to magnesium deficiency.)
  23. Morimoto S, et. al., “Inverse relation between severity of psoriasis and serum 1,25-dihydroxy- vitamin D level,” J Dermatol Sci. 1990 Jul;1(4):277-82.  [ncbi.nlm.nih.gov]
  24. Kowalzick L, “Clinical experience with topical calcitriol, (1,25-dihydroxy-vitamin D3) in psoriasis” Br J Dermatol. 2001 Apr;144 Suppl 58:21-5. [ncbi.nlm.nih.gov]
  25. Amra Osmančević, “Vitamin D Status in Psoriasis Patients Treated with UVB Phototherapy,”  (2009, Sahlgrenska University Hospital, Institute of Clinical Sciences at Sahlgrnska Academy)[gupea.ub.gu.se/bitstream/2077/19041/1/gupea_2077_19041_1.pdf ]
  26. “The parathyroid glands and vitamin D,” Chapter Five in Endocrinology: An Integrated Approach. Nussey S, Whitehead S.Oxford: BIOS Scientific Publishers; 2001. [ncbi.nlm.nih.gov/books]
Biochemistry and physiology are complicated and one answer is not going to work for every patient.

I don’t have all the answers or full access to the expensive research articles and journal subscriptions but I do have different questions. If the medical industry only asks the same questions then we will never learn how to cure or prevent chronic disease. One of the earliest symptoms of magnesium deficiency is hypertension and elevated 1,25 D levels lead to increased wasting of stored magnesium and decreased intestinal absorption of magnesium. Identifying individuals who have undiagnosed hypertension in order to stabilize them on pharmaceuticals will not be cheap or effective if the person’s hypertension was caused by magnesium deficiency. Magnesium is very inexpensive and hasn’t been known to cause side effects when added to foods or beverages. Adequate magnesium is essential for apoptosis and apoptosis is used by white blood cells to protect us from infected or precancerous cells.

True vitamin/hormone D deficiency can also be a cause for hypertension. It would be good to know for sure whether a depressed 25D level was signalling a metabolic pathway malfunction leading to elevated 1,25-D or a true combined vitamin/hormone D deficiency.

We don’t know what we don’t know. Learning requires being open to the idea that previous answers or theories might be wrong or might be wrong for some cases. Accurately testing 1,25 dihydroxy D levels in addition to 25-D would tell us whether the epidemic of low vitamin D levels is actually an epidemic of depressed vitamin D levels and elevated hormone D rather than an epidemic of actual deficiency.  Or, even better, it would tell us which patients are part of the epidemic of chronic illness and which actually are low in vitamin and hormone D and would benefit from modifying their diet or starting to use a supplement.

Edited 9/28/12 8:50pm EST,  edit-10/1/12

/The Short Disclaimer: Information presented on this site is not intended as a substitute for medical care and should not be considered as a substitute for medical advice, diagnosis or treatment by your physician./

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Calcium sparklets, TRPV channels and vanilla

     Calcium sparklets are not a good thing, not in excess at least. This is just a few interesting articles that have TRPV channels in common. The calcium channels cause problems in a variety of ways for some people. Identifying who is at risk for problems with fluid balance could help prevent the chronic degenerative changes that can result from electrolyte imbalance. (This post led to parts of this webpage: effectivecare.info/G3. Relaxation & Stress)
     I was amused when the search term ‘sparklets’ turned up something pertinent to my field of interest. TRPV channels and vanilloid receptors with overactive calcium flow can increase pain and other types of muscle and nerve signals.

Calcium sparklets are not a type of chewing gum. They are a sudden increase in flow of calcium through certain calcium channels in vascular tissue. A specific chemical trigger called protein kinase Calpha (PKCalpha) was found to signal L type calcium channels into increased calcium flow [3]. The sparklets occurred in diabetic vascular tissue following high blood sugar levels [2]. A cooperative action taking place with as few as three calcium channels needing to be open for maximal vasodilation to occur [1].
TRPV4 are a type of vanilloid receptor. Loss of function due to genetic difference has been associated with hyponatremia, low sodium blood levels. [6]

“TRPV4 is activated by hypotonicity in vitro, and perturbations of even a few mOsmol/kg H2O were sufficient to achieve this effect (5–7); such exquisite sensitivity closely parallels the in vivo mechanism whereby a change of only a few mOsmol/kg H2O influences release of arginine vasopressin. In rodents, TRPV4 is expressed in the blood–brain barrier-deficient central osmosensing nuclei (5, 35), and targeted deletion of the TRPV4 gene gives rise to aberrant osmoregulation in murine models (20, 21).” [6]

     Time to bake something with vanilla. The above paragraph’s reference to a blood-brain barrier deficiency having a genetic component suggests that susceptibility to headaches also could have a genetic component. The change in osmoregulation means that membranes could be more resistant to fluid and particles crossing or more open and barrierless (and  prone to get migraines). The problem could combine a deficiency in ability to transport needed nutrients into the cell with an increase in leakiness of important things out of or into the cell. The lack of nutrients like magnesium would further reduce the calcium channel blocking potential of the cell.
     So is vanilla something that some people genetically need more of? good question. And the bigger bell ringing loud was the risk of hyponatremia means that a low salt diet could lead to even lower levels of sodium in the blood.
     TRPV receptors have to do with pain control as well as flow of fluid and electrolytes (osmoregulation). Vanillin receptors can have a calming effect on the body and sooth pain. Baked goods with vanilla have a little extra besides love soothing the body. (So does hot pepper though – capsaicin).
 

Magnesium flow through the proton gates that the TRPV group of receptors control is what helps reduce  pain (when there is enough magnesium) and what causes pain signals when there isn’t enough to protect the cell interior from calcium entry. Calcium signals overwork, which leads to pain.
Calcium channel blocker medications are trying to close the gates and keep the calcium out – magnesium would be super delighted to do that if enough were being absorbed from the intestines (too full of calcium and active hormone D3).

     A study on the use of magnesium with opioid pain killers demonstrated the power of magnesium’s effect on for helping reduce diabetic pain. Diabetics normally do not find pain relief from opioids but when magnesium was given in advance the pain killer worked – and the pain killing effect continued for three days after the opioid medication effect would have worn off. The research discussion seemed to focus on using 30 mg with IVs of  morphine or other opioid and didn’t not address the fact that the 300 mg dose had reduced pain on its own, without opioid medication. [18]
 
  • by Sonkusare SK et al, Elementary Ca2+ signals through endothelial TRPV4 channels regulate vascular function. Science. 2012 May 4;336(6081):597-601. [ncbi.nlm.nih.gov/pubmed/22556255]
  • Calcium and diabetic vascular dysfunction, Focus on “Elevated Ca2+sparklet activity during acute hyperglycemia and diabetes in cerebral arterial smooth muscle cells,  by Katherine M. Dunn, KM and Mark T. Nelson (11/11/09 Am J Physiol Cell PhysiolFebruary 1, 2010 vol. 298 no. 2 C203-C205) “This report is also the first to describe a molecular mechanism by which hyperglycemia produces increased [Ca2+]i in VSM and suggests that this mechanism of Ca2+ sparklet activation may be uniquely initiated by hyperglycemia.”    [ajpcell.physiology.free article]
  • Article by Amberg GC et al “Calcium sparklets regulate local and global calcium in murine arterial smooth muscle” J Physiol. 2007 Feb 15;579(Pt 1):187-201. Epub 2006 Dec 7. [Free article]
  • The first three are from a search for ‘sparkles’ in pubmed, no sparkles-but autosuggester came up with ‘calcium sparklet’ and the whole list looks interesting: [ncbi.nlm.nih.gov/pubmed?term=calcium%20sparklet]-Truth can be stranger than fiction.

4. A different search ‘magnesium deficiency hyperglycemia‘ provided a summary worth reading :  Magnesium and Potassium in Lone Atrial Fibrillation, by Patrick Chambers, MD, pdf file: [afibbers.org/resources/PCmagnesium.pdf] *** this needs to be added to the IoM 1997 report on magnesium. Lefthandedness section near the bottom notes an increase calcium flow across cell membranes in left handers. A genetic difference that can lead to an increase in the isoprenoid pathway and inhibition of Na/K pumps in the membranes is suggested to occur in some left handed people. The difference can lead to an increased need for magnesium.

5. Reminder – vascular calcification is somewhat reversible and a simple way to start is to add less by limiting the amount of calcium taken in daily. Two servings a day of calcium rich foods is adequate for most people; there is also calcium in smaller amounts in many other foods too. Calcification of Soft Tissue, hardening organs and softening bones (post, 8/19/11 )

6. A loss-of-function nonsynonymous polymorphism in the osmoregulatory TRPV4 gene is associated with human hyponatremia, by Wei Tian, et al [pnas.org/content/early/2009/08/03/0904084106.full.pdf]

7. Physiology and Pharmacology of the Vanilloid Receptor, by Angel Messeguer, Rose Planells-Cases, and Anton Ferrer-Montiel (Curr. Neuropharmacol., 2006 January: 4(1) : 1-15) [link]

Excerpt:  In addition to the contribution of the vanilloid receptor as a target of the neurogenic inflammation underlying different diseases, TRPV1 is gaining interest for the treatment of neuropathic, postoperative and chronic pain and, recently, for the therapy of epithelial disorders. Thus, for instance, topical capsaicin or resiniferotoxin have been used in postherpetic neuralgia, diabetic neuropathy, postmastectomy pain and arthritis [64,103]. Recently, TRPV1 has been clearly validated as a key target for management of chronic pain in bone cancer [42]. As a result, the development of specific TRPV1 antagonists is a central focus of current drug discovery

***antagonist equals block – the vanilloid receptors are also involved in soothing – feed and educate the receptors because they all serve multiple purposes. Pain has a purpose – to signal that something is wrong. Masking pain with antagonists that deaden a function – to signal a problem – was a very disappointing climax to that paragraph. TRPV1 receptors and all the rest of the gang are very exciting – let’s not waste more money and time inventing synthetic antagonists to a message system that is very intertwined in controlling gates and flow of substance. the pain is there for a reason – starvation – lack of building blocks – lack of function.

8. More on vanilla from “Confessions of a Cardamom Addict” blogspot – blog part one–  –blog part two – ***These cover the history, processing, environmental concerns, major botanical varieties.

18(vit D bib.). [ncbi.nlm.nih.gov/pubmed/20081245] Magdalena Bujalska, Helena Makulska-Nowak, Stanis³aw W. Gumuka Magnesium ions and opioid agonistsin vincristine-induced neuropathy , Department of Pharmacodynamics, Medical University of Warsaw, Krakowskie Przedmieoecie 26/28, PL 00-927 Warszawa, Poland

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. Thanks.

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The Arthritis Foundation, Juvenile RA and minocycline

Close-mindedness can be hard on oneself, other people and for the planet.

[arthritistoday.org/magazine]

I got irate last night reading a free magazine but I kept going and found some helpful information and even reinforcement of my recommendation for use of antibiotics for an autoimmune condition. The complimentary magazine that arrived was, Arthritis Today, Advice from the Experts You Trust, which is published by the Arthritis Foundation. Their motto is, “Take Control, We can help”. The cover story is about a medically disabled 26 year old veteran, Mike Jackson, whose photo makes me think cannabinoid deficit not ibuprofen deficit – although ibuprofen does help reduce breakdown of endogenous cannabinoids. He suffered through ten years of military service with osteoarthritis and was given cortisone shots and ibuprofen and later on shoulder surgeries.

I would have given him green leafy vegetables and nutmeg, beans, nuts and seeds, and ibuprofen. The magazine does have an article about cooking with quinoa for gluten avoidance and four recipes that use cocoa powder.

The gluten article mentions that only an estimated 5% of people with celiac disease have been diagnosed. There is a lab test for aiding in diagnosis. Primary symptoms include bloating, digestive pain and constipation is frequently an issue. Joint pain has also been found to be a symptom because the overactive white blood cells from the intestines can travel and cause problems elsewhere in the body.
/Speculation/ Celiac disease may be an autoimm

Another nutrition article discusses portion control when using healthy fats or foods that are rich sources like walnuts (1/4 cup sv size) or avocado (one sixth of an avocado sv size). “Go to ArthritisToday.org/MA12 to learn more about the differences between good and bad fats.” I went – I don’t agree with the article’s grouping of all saturated fats as equally “bad” as trans fats. That is a very brief article with a brief list of a few foods and a few risks or benefits. The portion control article was more accurate.

Article on glucosamine was helpful about which chemical form may provide more relief. A 2005 Cochrane Review of trials regarding effectiveness of the supplements found that glucosamine sulfate (GS) trials had more consistantly positive results than trials that used glucosamine hydrochloride (GH). That makes perfect sense to me, although the article mentions that “Oliver Grundmann, PhD, . . .  says it isn’t clear why the two have different effects.” Our average diet is lower in sulfur containing foods than chloride or chloride containing additives. Chloride can interfere with the thyroid gland in a way similar to bromide and fluoride. So thanks for complimentary magazine – I have early symptoms of osteoarthritis but I don’t think it was ever added as an official diagnosis yet as I have been actively fighting the degeneration for over a decade with the regular use of magnesium, glucosamine, and Methylsulfonylmethane (MSM) among other things. Veterinarians use MSM regularly.[arthritis-msm-supplements.com/msm_for_horses_dmso.htm]

This quote fills me with wrath:

“Even if methotrexate leads to ‘clinical remission’ (defined here as no more than three swollen joints) in RA, a new study shows the joints might still be eroding.” – Shahreen Abedin,     Source: Annals of the Rheumatic Diseases, Nov. 7, 2011

The suggestion is to add more DMARD’s in addition to the methotrexate and if there are any slow healing wounds then the article next to it suggests that following the aggressive immune suppressants with skin-graft surgery would make that wound healing problem go away. Reminder – DMARD is a fancy acronym meaing we are using some chemotherapy drugs in an off label use – not for cancer. And the article on the next page encourages parents to use an aggressive mixtures of the immune suppressing drugs in their young children with a diagnosis of Juvenile Rheumatoid Arthritis.

“Disease-modifying antirheumatic drugs (DMARDs), as the name suggest, are drugs designed to modify the course of rheumatic diseases.” (Gee, vasculitis is part of the group of diagnoses that DMARDs are recommended for. and Minocycline is actually on the list with the note that it is not currently approved for arthritis by the FDA.) Article, “What you need to know about DMARDs”

Why is Benicar plus antibiotics and avoiding excess vitamin D, calcium and free glutamates such a horrible treatment suggestion compared to drugs that make one’s hair fall out. Should four year olds be bald – no.

Two young girls diagnosed with Rheumatoid Arthritis were 2012 Arthritis Walk National Honorees along with Mike Jackson. Unlike osteoarthritis which I think has to do with a genetic susceptibility to problems with disruption of nerve and muscle signals that result in the degeneration over time, Rheumatoid Arthritis has been proven to be related to cell wall deficient bacteria by research scientist, Lida Mattman. I posted links and a little more about her work, 2/17/2012: [https://transcendingsquare.com/2012/02/17/cell-wall-deficient-pathogens-l-forms/]

[lymebook.com/cell-wall-deficient-forms-mattman]

An excerpt that I posted within that article:

“Dr. Hoekstra’s mentor, Lida Holmes Mattman, Ph.D., also of Wayne State (now professor emeritus of biology), confirmed the causal role of P. acnes in a laboratory experiment. Dr. Mattman extracted the bacteria from the synovial fluid (which lubricates joints) of human arthritis patients, and injected it into chicken embryos. The chicks then exhibited symptoms of rheumatoid arthritis. When she treated the chicks with antibiotics known to disable P. acnes, the disease disappeared.”

Original Source: Lida H. Mattman, Ph.D., Cell Wall Deficient Forms–Stealth Pathogens, 2nd Edition, CRC Press (1993), CRC Press, 2000 Corporate Blvd. N.W., Boca Raton, FL 33431. I found the excerpt posted within a Lyme’s disease article: [shoptown.com/Dean/ALS2Lyme.htm] [4]

I knew a preschool child with juvenile rheumatoid arthritis whose mother was curious about the possibility of alternative treatments but she was never able to talk her Medicaid doctor into trying antibiotics instead of methotrexate. She did find moderate use of vitamin D and calcium foods and increased magnesium foods helpful for reducing the number of bad days her child experienced. I don’t know how they are doing now. I don’t think Minocycline would help an adult with osteoarthritis but it would be likely to help the two little girls with Juvenile RA more than Methotrexate would in the long run. Immune suppression will not support the healthy white blood cell’s ability to find the cells that have been colonized by the cell wall deficient forms of the Propioni acnes bacterium.

In the case of rheumatoid arthritis, a hallmark of conventional medical treatment is the use of steroids, which can provide symptomatic relief, but no cure. The danger here, cautions Dr. Hoekstra, is that such drugs “give a free and clear run to the bacteria involved (Propioni bacterium acnes). If such a patient is ever to subdue this microorganism, they must have a competent immune system, and to have this, they must be off the steroids.”[link #4]

Gluten intolerance and celiac disease can have overactive white blood cells causing damage in the joints and  in osteoarthritis damage to joints results over time. Genetic differences may be triggering more food allergen recognition in white blood cells in sensitive people. So elimination diets can help identify which foods are better to limit for life and to consider as treats. Over use of the trigger foods can increase coagulation of the allergen protein clumps in joints and inflammation damage occurs over time.

The girls with Juvenile RA on the other hand may be sensitive briefly during disease flair up when there are too many white blood cells for other reasons (P. acnes) and they start reacting to more foods and other external allergens but get rid of the infection and the food sensitivities would gradually go away as the intestines healed and the number of white blood cells returned to a normal number. So avoiding gluten or other flair up foods while treating the underlying cell wall deficient bacterial infection might eventually lead to fewer flair ups with less severe symptoms and the treats might become a normal food to use again.

Some people can be gluten intolerant genetically and some can be gluten intolerant while having sensitive digestive problems for other reasons. Just like lactose intolerance some people have it for life and some only have it after a digestive sickness.

Juvenile RA means one is born with problems. I was never able to breathe well and was covered with eczema blotches during my infancy. Born with problems from birth will really reduce life expectancy when methotrexate is chosen, but even with generally good control the later degeneration is somewhat inevitable as the CWD bacteria continue to parasitize preferred organs and tissue types. Based on the life cycle of the T. cruzi and T. brucei in a chronically infected human then 20 years plus 15 years is the expected timeline for early cardiac or CNS symptoms to start appearing. The spirochetes of syphilis have been linked to megalomania / obsessive compulsive tendencies in the later stages of the disease. At age 45 almost 46 I am actually doing pretty well if my mother’s Rocky Mountain Spotted Fever was lingering in her system.

This is not a pleasant thought but wouldn’t treatment options for a 2 and 4 year old that didn’t involve eventual hair loss be a prettier thought?

So as defined earlier the goal of therapy with DMARDs is to achieve ‘clinical remission’ or to get the pain narrowed down to only three swollen joints – or fewer – but not necessarily all the way to zero. And so swollen painful areas are considered a normal part of clinical remission and, worse, the irreversible degeneration was found to be ongoing even during this wonderful state of ‘clinical remission’.

A potential side effect of many of the immune suppressing drugs is osteoporosis.

I enjoyed the article with tips for packing for a major move with less pain (more organized = less work = less pain) near the end of the magazine – I think I will enroll in the Arthritis Foundation and continue getting their magazine. I do have one toe with loss of range of movement where an old injury had occurred.

Update: After examining both feet, the broken toe actually isn’t that different from the other foot’s toe now. Early calcification is reversible with a change in diet and hormonal balance.

Their motto “Take Control, the Arthritis Foundation can help.” I did find some helpful info, recipes and other tips that will assist me in my continued battle to control my chronic degenerative condition. First impressions can close a mind, going back for a second look can open doorways and minds. I don’t have to agree with everything to find value in some things.

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. Thanks.