Vitamin D – the Re-discovered Key to Illness Prevention

Residing in a land of year-round sunshine & outdoor lifestyle, it may come as a revelation that many people here in Dubai and UAE are Vitamin D (25(OH) D) deficient. Vitamin D (as Cholecalciferol) is synthesized from sunlight when our bare skin is exposed. In a further conversion cascade involving enzymes from the liver & kidneys, the active & most potent form of Vitamin D – termed Calcitriol – is produced & stored in the liver & to a lesser extent, the tissues of the body.

Although commonly referred to as a ‘vitamin’, Calcitriol is a biological response-modifying steroid hormone – and now understood to be one of the most influential steroid hormones in the body. 25(OH) D has emerged as the 2nd most important nutrient (after iron) in healthy body functioning.

Vitamin D is essential for the active absorption of Calcium & Phosphorus from the gut. It then regulates their utilisation within the body. Vitamin D is integral to the production & balance of cells that constantly remodel our bones – these cells are known as osteoclasts & osteoblasts. Vitamin D also helps prevent Calcium and some other minerals from being excreted via the kidneys.

Vitamin D deficiency is known to be associated in osteoporosis, impaired immunity, diabetes, high blood pressure, ‘stroke’, heart disease, liver disease, depression + other disturbance of mood, body muscle mass wasting, gum disease, & certain forms of cancer.

Sutherland et al (1992) postulates Vitamin D deficiency is linked to the neuro-degeneration of Alzheimer’s disease. Two recent studies found cognition and mental clarity of dementia patients improved when 25(OH) D levels were optimized (200nmol/L): (Oudshoorn C, et al. 2008) + (Llewellyn DJ, et al 2009).

The potential to develop autoimmune conditions such as alopecia areata, vitiligo, psoriasis, & inflammatory bowel disease is believed to increase with Vitamin D deficiency. Asthma exacerbation in children may be increased by 70% when the child is 25(OH) D deficient: Low vitamin D linked to asthma exacerbations.

Autoimmune Thyroiditis patients can reduce or eliminate thyroid antibodies by maintaining Vitamin D levels of at least 125nmol/L (as will a Gluten-free diet).

Collectively known as a T-Helper 1 cytokine-mediated inflammatory disorder – the symptoms & prognosis of these diseases may be significantly improved with Vitamin D supplementation (up to 12,500 IU per day). Physiological doses of Vitamin D alter gene response, and appear to suppress Macrophage (white blood cell) pro-inflammatory cytokine response.

Multiple Sclerosis (MS) is a degenerative disorder of the Central Nervous System where ‘demyelination’ of nerve fibres within the brain + spinal cord occurs. Epidemiological studies increasingly indicate a correlation between 25(OH) D levels and the course of the disease. An open study by Kimball et al (2007) found direct evidence that Vitamin D supplementation (up to 10,000IU/day) helps treat MS. Incredibly – the number of neurological lesions per patient in the treatment group decreased; and they experienced fewer summer exacerbations of their MS. Ward, KA, et al: (2009) found Vitamin D is highlyassociated with neuromuscular performance in athletic competition.

An 8 year study of over 34,000 women found there is an 11% reduction for risk of breast cancer when women have ‘normal’ levels of 25(OH) D compared to subjects with low or deficient levels (Robien, K., Cutler, GJ, Lazovich, D: September, 2007).

There are now many studies ( which demonstrate that an optimal Vitamin D status during pregnancy is essential for both maternal well-being and in-utero development of the child. There is also a growing awareness of the link between gestational Vitamin D deficiency in the pregnant mother and autism in her still-unborn child: Canadian Paediatric Society. Vitamin D supplementation: Recommendations for Canadian mothers and infants. Paediatr Child Health 2007;12(7):583-9 + Cannell JJ.  Autism and Vitamin D. Med Hypotheses 2008;70(4):750-9.

An earlier paper by Cannell et al (2006) proposed a convincing correlation between Vitamin D supplementation & an increased resistance to seasonal epidemic influenza.

The mortality rate of 25(OH) D replete males with biopsy-confirmed prostate cancer is decreased by up to SIX times over 25(OH) D deficient males with same stage prostate cancer (Tretli, S. et al: 2009).

‘Statin’ drugs deplete the body of Co-enzyme Q10; causing debilitating myositis and myalgia in some patients. 25(OH) D supplementation to levels >125nmol/L reversed these conditions in 92% of patients (Ahmed, W. et al: 2009)

If we totally avoid the sun, our bodies require around 4,000 International Units (IU) i.e. 100 micrograms of Vitamin D per day. Approximately 20-30 minutes of strong sunlight on bare, non-sun screened skin will produce approximately 20,000 IU of 25(H) D – providing a ready reserve of stores. Once these levels are achieved, the skin combines with ultra-violet light to limit Vitamin D production; corrupting excess Cholecalciferol so it cannot be further converted. According to Vieth (1999) there has never been a substantiated case of Vitamin D toxicity from sun exposure alone.

Common Reasons for Poor 25(OH) D Absorption + Deficiency:

  • Genetic tendency to be low in Vitamin D or the body may synthesise/convert it more slowly.
  • Gut/Biliary dysfunction resulting in fat malabsorption (termed Steatorrea)
  • Oral 25(OH) D supplements are best absorbed in the presence of a fatty-acid protein meal, and so are generally poorly absorbed by practicing Vegans or Vegetarians. These individuals require regular sun exposure or Vitamin D injections to prevent deficiency.
  • Darker skinned people such as full-blood Aborigines, Pacific Islanders,
  • Sub-Continent* or African immigrants need five to ten times longer exposure to synthesise the same amounts of Vitamin D that a fair skinned person would produce in 20-30 minutes. Because of this, dark-skinned folk are at greater risk of Vitamin D deficiency when removed from their traditional environment.
  • Disorders of the liver may impair Cholecalciferol conversion (termedhydroxylation). Patients with non-alcoholic fatty liver disease often have marked 25 (OH) D deficiencies (Targher, G. et al: 2007).
  • Medication-induced deficiency: taking Phenytoin Sodium (Dilantin) in long-term anti-convulsant therapy.
  • Air pollution in large urban cities reduces solar UVB wavelengths of light from which Vitamin D is synthesised.
  • Bathing/showering too soon after sunlight exposure can wash away the 25(OH) D being produced ON the skin’s surface (Holick, MF et al: 1980). In their rat skin studies, Gaylor et al (1964) found sebum – natural skin oil produced by sebaceous glands – retained > 70%.of 25(OH) D’s precursor: 7-dehydrocholesterol.

Dietary sources of Vitamin D are egg yolk; ‘oily’ fish such as salmon & sardines, cod liver oil**, Vitamin D fortified bread & cereals, or milk. Be mindful though a standard glass of milk will provide about 100 IU of Vitamin D only, so in Dubai sensible sunlight exposure and/or supplementation in the colder months is the most effective means to maintain optimal Vitamin D levels.

The nutritional co-factors essential to activate 25(OH) D are Magnesium, Potassium, Zinc and the trace element Boron. All of these nutrients can be found in fresh spinach.

Assessing Vitamin D levels is achieved via blood pathology for 25-OH Vitamin D. New reference ranges (NEJM 357:3 July19th 2007) are 50-200 nmol/L. Levels less than 75nmol/L is considered Vitamin D insufficiency, whilst levels less than 50nmol/L is deemed ‘deficient’.

Vitamin D, Oestradiol (E2) and Thyroid hormone belong to a class of steroid hormones termed ‘C-ERB’. As such they are structurally similar, closely related and posses the capacity to influence the other’s expression:

  • Triiodothyronine (T3) thyroid hormone receptor expression is enhanced when 25 (OH) D is sustained above 100nmol/L (Lee: 2007).
  • Vitamin D is Thyroid + Cortisol hormone ‘sparing’ when 25(OH) D levels are maintained at 150-200nmol/l. Our bodies operate more efficiently with less demand for Thyroid + Cortisol hormone.

If we totally avoid sunlight exposure our bodies require an average 4,000IU Vitamin D per day, so a minimum supplementation of 5,000IU per day is recommended by the Vitamin D Council to maintain stores and avoid deficiency. Integrative Medical Practitioners may prescribe up to 12,500IU to patients with severe or intractable deficiency.

Vitamin D can be toxic when large amounts (i.e. >50,000 IU) is supplemented for prolonged periods of time.

Vitamin D supplementation should be prescribed by an experienced Health Practitioner after Vitamin D blood levels are established. Vitamin D3 – known as Cholecalciferol – is the only form of Vitamin D supplement that should be taken, as it’s the one naturally-occurring form for our bodies. All other forms of Vitamin D are metabolic or chemical alterations. Ergocalciferol is plant-derived Vitamin D2 – and is approximately 100 times LESS efficacious than Vitamin D3 (Lee: 2007).

Finally – in the current climate of H1N1 (Swine Flu) hysteria – an interesting ‘side effect’ of Vitamin D: those of us with replete 25(OH) D levels would be very unlikely to generate an immune response from ‘Flu vaccine inoculation. Two Russian studies found hi-range Vitamin D levels de-activate immune response which the vaccine is attempting to generate (Shadrin, AS. et al: 1977 + Zykov, MP, Sosunov, AV: 1987). It’s as if the body is saying ‘with high Vitamin D levels I don’t need this.’

This article is dedicated to Dr. JJ Cannell MD, Director of the Vitamin D Council. His tireless crusade to re-establish the importance of Vitamin D in long-term health is yet to be fully appreciated by some areas of orthodox medicine + public health regulators.

*Goswami, R. et al (2009) found the average 25 (OH) D levels among Indian people was only 17.5nmol/L!! This is severe Vitamin D deficiency.

**Supplementing Cod Liver Oil to correct Vitamin D deficiency is NOT desirable because of the high Vitamin A content found in Cod Liver Oil.

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