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Vitamin D Levels in Elders

• SCREENING FOR VITAMIN D
• Vitamin D Levels Seem, Generally, Unwarranted
• Vitamin D deficiency
• Vitamin D Screening and Supplementation
• vitamin D deficiency occurs at >> 20 ng/mL.

SCREENING FOR VITAMIN D

JL Brown, 24 Apr 2009 12:58 PM EST

Competing interests: None declared

Should we know the vitamin D levels of elderly patients? Who will pay for this screening?

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Vitamin D Levels Seem, Generally, Unwarranted

E Chamberlain MD, 26 Apr 2009 1:54 PM EST

Competing interests: None declared

Seems we should assume a degree of Vitamin D deficiency (relative or absolute) and forego routine primary screening and simply advise Vitamin D supplementation (400 to 800 IU) for anyone with or at risk for osteoporosis.

If, after addressing various osteoporosis preventive/ treatment factors, bone density is not responding, then 25-OH Vitamin D levels could be warranted. One caveat is that if we are addressing screening in the younger population and not checking bone density until much later in life (at say, age 60 or 65), then unsuspected failure to respond to simple Vitamin D supplementation would go unnoticed for years or decades. But it seems best to, instead of routine screening-- once or repeatedly-- to screen by, say, medical or social/ ethnic history, to determine who is at particular risk to fail to respond to simple supplementation.

Initial (and repeated) levels could be in order in selected populations-- but, again, levels seem less valuable in primary screening, as the treatment would remain the same, with or without levels. And, even though Vitamin D is a fat-soluble vitamin, it would require mega-doses to overdose, so the safety of standard treatment without levels is negligible in the general population and probably even in every population.

According to the ACP, among elderly patients who sustain osteoporotic hip fractures, 30- 50% have low blood levels of Vitamin D. With that population prevalence, testing seems unnecessary and unwise for what is generally a readily treatable deficiency.

Again according to the ACP, Vitamin D deficiency is common when dietary intake is insufficient and when exposure to sunlight is limited and may have become more common in recent years because of the increased use of high SPF sunscreen. Older adults are at particular risk of developing Vitamin D deficiency because aging skin does not synthesize Vitamin D as efficiently and because the kidney does not convert Vitamin D to its active form as readily. The American Academy of Dermatology stated around November of 2008 as best I recall that we should stop telling patients to attempt to attain or maintain their Vitamin D levels via sun exposure. None-the-less, again according to the ACP (as of late 2008 and I'm not aware that they have echoed the Academy of Dermatology's statement), in general, 10-15 minutes of sun exposure to the face, arms, hands, or back without sunscreen two or more times per week usually produces adequate Vitamin D. Sunscreen can be applied after this initial exposure, although in northern latitudes this amount of exposure could be too little. The amount of Vitamin D synthesized in the skin by UV light is affected by season, latitude, cloud cover, pollution, skin pigmentation, and by the use of sunscreen with an SPF of 8 or greater.

Special groups at increased risk for Vitamin D deficiency include those with fat malabsorption. Such patients, it seems to me, fall into the special selected population category and warrant additional attention, beyond that of usual primary screening.

In addition, according to the ACP, wide inter-laboratory variation in Vitamin D testing has been noted, so test results should be interpreted with caution. This seems, then, like another reason not to test in primary screening.

Dietary sources of Vitamin D include vitamin D fortified milk, fortified cereals, cheese, egg yolks, and certain fish (salmon, tuna, mackerel, sardines), . But supplementation seems more reliable, appropriate, and practical than attempting to estimate dietary intake, except, again, in select cases, but not in primary screening.

(The only other recommendation I have is that everyone move to Sun Diego, but that's just my personal preference.)

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Vitamin D deficiency

Ann I. Pollock, 26 Apr 2009 1:54 PM EST

Competing interests: None declared

The patient should be responsible for screening test. If they have insurance that assists them, great. If not, they have the right to pay for their own preventive health care, or they can opt out and not be screened.

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Vitamin D Screening and Supplementation

Sandra E Murphy, Primary Care Clinic, 29 May 2009 2:23 PM EST

Competing interests: None declared

Frankly supplementation with 400-800IU Vit D3 is useless. If there is even a suspicion of deficiency, 4000IU and higher are the only reasonable ways to influence serum 25-OH Vit D status. Enormous quantities of cholecalciferol are rapidly made in the skin if: the sun is high in the sky (midday and the summer season), your skin is not covered by clothes or sunblock, you stay in the sun until your skin just begins to turn pink (not red), and you are not behind glass. Professor Michael Holick of Boston University School of Medicine has shown that in Caucasians 10,000 and 50,000 units of cholecalciferol is made within 30 minutes of sun bathing and believes a reasonable average of all the studies is 20,000 units. As we have all been sunbathing (with baby oil in my teens!) without any toxicity (PTH interference, LFT abnormalities, hypercalcemia) it is unreasonable to assume oral Vit D3 supplementation in physiological doses is toxic and also irresponsible to continue recommending far less than needed to correct the deficiency.

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vitamin D deficiency occurs at >> 20 ng/mL.

D P Poulter, 15 Jun 2009 4:28 PM EST

Competing interests: None declared

It is unlikely any single study is going to provide adequately comprehensive information on this subject to manage dosing members of the public. Consider:

1) the many very significant Vitamin D benefits that only begin at much higher doses / much higher serum 25(OH)D levels, such as reduced risk of cancer, diabetes, falls, fractures and MS clearly shown in the chart

• titled Disease Incidence Prevention by Serum 25(OH)D Level

• at http://www.grassrootshealth.org/_download/disease_incidence_prev_chart_101608.pdf

• by CF Garland and CA Baggerly

• summarizing peer reviewed and published epidemiology.

2) at the ">75ng/ml" = ">187.5 nmol/Litre" 0,25 hydroxy D blood serum levels associated with the highest score of “neuromuscular performance, independent living and surviving”, based on analysis of the Longitudinal Aging Study - Amsterdam (LASA). Ref 1) Wicherts et al. JBMR. 2005; 2) Visser et al. (AJCN; 2006; 84:616–22); both summarized graphically in slide show in: http://www.grassrootshealth.org/_download/Heaney%20GrasssrootsHealth.pdf

3) the lesser co-benefits of higher 0,25 hydroxy D:

• increased immunity

(for flu’s and virus’s, may not occur until high plasma 0.25 hydroxy D )

• increased muscle strength,

• increased positive mood,

• reduced risk of periodontal disease,

• reduced risk of asthma progressing into COPD

• reduced muscle pain and recovery times after exercise

• reduced propensity to burn in the sun,

• reduced risk of mothering a child suffering from autism,

• for infants reduced risk of autism

• reduced rate of DNA damage and decline as we age

• reduced propensity to suffer incontinence as we age

4) nutrition is a symphony not a solo performance, and so appropriate levels of co-nutrients must be present for maximum benefit; such are:

• Vitamin K2-MKx, where x>6, and

• adequate but not excessive co-nutrients

{calcium, magnesium, boron, silicon, vitamin A and vitamin E}. There is evidence for example that vitamin A in excess of the body's daily requirement, as may be found in cod liver oil, liver, and many multi- vitamins nullifies many of the benefits of vitamin D, by interfering with its receptor. Along the same line the 2008 Cochrane review found supplementing with vitamins A, C and/or E, contra-indicated, but getting such nutrition from diet, presumably with appropriate co-nutrients lost in the production of vitamin pills, presumably was best.

5) DRUG INTERACTION WARNING:

Cytochrome P450 enzymes are responsible for both the initial metabolism and subsequent catabolism of vitamin D. Therefore, drugs dependent on cytochrome P450 enzymes – and there are many – may effect vitamin D metabolism. What clinically relevant interactions cytochrome P450 metabolised substances – including cardiac drugs, erythromycins, psychotropics and even grapefruit juice – have on the metabolism of vitamin D is an area awaiting further research. Patients on such drugs should have frequent 25(OH)D level checks when being treated for vitamin D deficiency. Of the research done on drug/vitamin D interactions, anticonvulsants [Valsamis H, Arora S, Labban B, Mcfarlane S. Antiepileptic drugs and bone metabolism. Nutr Metab (London) 2006;3:36-47.], corticosteroids, cimetidine, antituberculosis agents, theophylline and orlistat may lower 25(OH)D levels, whereas thiazide diuretics increase 25(OH)D levels [Epstein S, Schneider AE. Drug and hormone effects on vitamin D metabolism. In: Vitamin D. Feldman D, Pike JW, Glorieux FH, editors. San Diego: Elsevier; 2005. p. 1253-91]. CONTRA-INDICATIONS that might be shown with a 1,25 di-hydroxy D test.

High 1,25 dihydroxyvitamin-D, is present when there is excess parathryoid hormone or when there are Th1 diseases such as sarcoidosis, Lyme disease, chronic fatigue syndrome, fibromyalgia, lupus and rheumatoid arthritis (among others) when various species of Cell Wall Deficient (CWD) bacteria infect white blood cells, which respond by producing 1,25 dihydroxyvitamin-D. (Normally the kidneys are the principal blood serum source of 1,25 dihydroxy vitamin-D.) Treatment of such diseases requires lowering 0,25 hydroxy and/or 1,25 dihydroxy vitamin D levels. For a detailed literature based review of Vitamin D safety issue reference: http://www.westonaprice.org/basicnutrition/vitamin-d-safety.html http://esciencenews.com/articles/2009/04/08/vitamin.d.may.exacerbate.autoimmune.disease Deficiency in vitamin D has been widely regarded as contributing to autoimmune disease, but a review by Trevor Marshall of Murdoch University, Western Australia, appearing in Autoimmunity Reviews explains that low levels of vitamin D in patients with autoimmune disease may be a result rather than a cause of disease and that supplementing with vitamin D may actually exacerbate autoimmune disease. By deactivating the Vitamin D nuclear receptor (VDR) and subsequently the immune response, 25-D lowers the inflammation caused by many of these bacteria but allows them to spread more easily in the long-run. They outline how long-term harm caused by high levels of 25-D has been missed because the bacteria implicated in autoimmune disease grow very slowly. For example, a higher incidence in brain lesions, allergies, and atopy in response to vitamin D supplementation have been noted only after decades of supplementation with the secosteroid.

HEAVY METALS / HEAT & LIGHT INSTABILITY CAUTION:

Moon J - "The role of vitamin D in toxic metal absorption: A review" J Am Col Nutr 13 (6): 559-564 (1994)

"Vitamin D increases intestinal calcium and phosphate absorption. Not so well known, however, is that vitamin D stimulates the co-absorption of other essential minerals like magnesium, iron, and zinc; toxic metals including lead, cadmium, aluminum, and cobalt; and radioactive isotopes such as strontium and cesium. Vitamin D may contribute to the pathologies induced by toxic metals by increasing their absorption and retention. Reciprocally, lead, cadmium, aluminum, and strontium interfere with normal vitamin D metabolism by blocking renal synthesis of 1,25-dihydroxyvitamin D. This is the first review of the role of the vitamin D endocrine system in metal toxicology."

Moon JC - "A brief history of vitamin D toxicity" J Appl Nutr 49 (1- 2):18-31 (1997) "Vitamin D is very unstable both to light and to heat."

6) TAILORING DOSES

• Vitamins D & K should be taken with fat to ensure proper absorption.

• Vitamin D, Adults should begin at 4,000-5,000 IU/day, and then after 3 months and testing verifies no toxicity, then likely more (as recommended by the not-for-profit web sites set up by leading vitamin D researchers at www.vitamindcouncil.org and http://www.grassrootshealth.net/ ). (See sites for children doses. If a subject patient is not going to get tested, continuing such a dose for more than 4-5 months may expose the patient to unnecessary risk.)

• supply appropriate co-nutrients:

• calcium and magnesium, typically from diet, with supplements not likely to produce net benefit beyond doses of 700mg of calcium and 300mg of magnesium. Just because calcium is in a food, does not mean that the body will achieve net absorption. Such is the case with dairy and spinach. Spinach is frequently high in oxalates that inhibit calcium absorption.

• trace boron and silicon as from eldanté cooked broccoli

• vitamin K2-MKx, where x>6, (and not frozen in the presence of moisture)

- if male or female as in natto, (Japanese rice straw fermented cooked soyabean) or a daily K2 supplement with 100 mcg with K2-mk7.

- if female >45 mcg as in fermented (not processed) higher fat hard cheese, like 70g Norwegian Jarlsberg, 150g Swiss Emmental E-1, or 112g Edam

http://www.medkb.com/Uwe/Forum.aspx/cardiology/12411/Edam-cheese-is- heart-healthy Matti Narkia - 21 Feb 2009 14:16 GMT reports that at http://www.medkb.com/Uwe/Forum.aspx/cardiology/12411/Edam-cheese-is-heart- healthy, the Finnish doctoral thesis by Terhi Koivu-Tikkanen: DETERMINATION OF PHYLLOQUINONE AND MENAQUINONES IN FOODS BY HPLC found Edam cheese as the the best food source of long-chain vitamin K2 forms in Finland. It reported that in Edam-type cheese, the concentration of vitamin K, which was almost the sum of MK-8 (~100 ng/g) and MK-9 (~300 ng/g), was 494 ng/g. According to their results, the vitamin K concentrations in Emmental samples ranged from 80 to 90 ng/g.

the Japanese study "Quantitative measurement of tetrahydromenaquinone -9 in cheese fermented by propionibacteria" by Hojo K, Watanabe R, Mori T, Taketomo N. in the J Dairy Sci. 2007 Sep;90(9):4078-83. PMID: 17699024 doi:10.3168/jds.2006-892 at http://jds.fass.org/cgi/content/full/90/9/4078 found

• 652 ng/g MK-9 + 84 ng/g MK-4 in Norwegian Jarlsberg cheese, and

• 314 ng/g MK-9 and 81 ng/g MK-4 in Swiss Emmental E-1 cheese,

which makes these cheeses at least as good sources of long-chain vitamin K2 forms as Finnish Edam cheese.

Vitamin D without adequate vitamin K2 can result in atherosclerosis, (hardening of the arteries). Vitamin K2 removes calcium from soft tissues and puts it back on the bone. Vitamin K2-MKx, where x<6, has short half lives in the body, requiring much larger doses, and hourly dosing to maintain adequate dosing.

• do not yoyo Vitamin D dosing. When the body detects declining stores, it begins rationing reducing benefits, to ensure it has adequate stores for the more critical body functions.

7) Additional information and references are available complements of vitamin D researchers at www.vitamindcouncil.org

8) I have no accreditation, and the above references may not be vetted by the publisher, so it is appropriate for the reader to do the so, before acting on this my reader feedback remark.

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