Residing in a land of year-round sunshine & outdoor lifestyle, it may come as a revelation that many people here in Australia 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 (120-150nmol/L): (Oudshoorn C, et al. 2008) + (Llewellyn DJ, et al 2009).
The potential to develop autoimmune conditions such as alopecia areata, Vitilligo, psoriasis, & inflammatory bowel disease is believed to increase with Vitamin D deficiency. A Vitamin D deficiency can trigger autoimmune reactions in pre-disposed people as deficiency disorientates the immune system; attacking susceptible tissues such as the skin + the thyroid gland.
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 canreduce or eliminate thyroid antibodies by maintaining Vitamin D levels of at least 120nmol/L (as will a Gluten-free diet).
Vitamin D deficiency has an adverse effect on hair growth due to its influence on thyroid-adrenal function. There are Vitamin D receptors in the scalp; Vitamin D is essential for hair follicle maturation (maturity).
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 highly associated 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 (i.e.: >80nmol/L) compared to subjects with low or deficient levels (Robien, K., Cutler, GJ, Lazovich, D: September, 2007). A 2009 study found women with Vitamin D levels greater than 85nmol/L had a 50% LOWER RISK of being diagnosed with breast cancer than those women with levels less than 60nmol/L (Rejnmark:2009).
There are now many studies (www.vitamindcouncil.org) 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. Vitamin 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 20,000IU 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 Vitamin D Absorption + Deficiency:
- Being Female: by virtue of physiological, social and/or religious constraints women are more prone being Vitamin D deficient. Research (www.vitamindcouncil.org ) suggests one’s upper body – front + back – needs to be fully exposed and ‘un-sun screened’ to most effectively absorb/synthesise therapeutic amounts of Vitamin from sunlight. This is understandably easier for males than females – particularly where religious or cultural modesties are a factor. Most young ‘covered’ Islamic and sub-continent women who consult me are found to be severely Vitamin D deficient (<20nmol/L).
- Middle aged or older: or skin that has been heavily tanned/sun damaged when younger. Chan (2015) suggests that adults >40 will have decreased skin absorption capabilities than children or adolescents.
- 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 (termed hydroxylation). 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 (in theory) 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. Whether these studies can be extrapolated to human subjects is yet unpublished or unproven.
- Topically-applied sunscreens or blockers DO inhibit UVA/UVB and prevent Vitamin D synthesis in the skin. Sensible sunlight exposure on skin uncovered by ‘sunscreens’ or clothing is necessary to obtain Vitamin D from sunlight.
- Incorrect dosage advice: most commercial Vitamin D3 supplements give daily dosage at 1000IU/day. There are likely medico-legal reasons for this, but a 2012 study conducted at The St. George Hospital, Sydney found that Vitamin D deficient patients who were given 2000IU/day showed little or no improvement in lifting their levels – but those patients given 5000IU/day DID elevate their levels out of deficiency to ‘sufficiency’(Vitamin D Council Newsletter: 2012).
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 Australia 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. According to 2007 published guidelines for Vitamin D: <75nmol-50nmol/L is insufficient; less than 50nmol/L is deemed DEFICIENT. The revised 2016 reference range is 50-375nmol/L (Van Zanden: 2016); levels must be >100nmol/L for optimal metabolic functioning & are thyroid/adrenal hormone ‘sparing’ at upper ranges; i.e.: 150-200nmol/L (Lee: 2011).
When Vitamin D is optimised at 200nmol/L, it will ‘auto-adjust’ ionised Calcium to its ideal level of 1.25-1.26mmol/L (Van Zanden: 2016)
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).
- Caution Update: Some individuals carry slight genetic mutations (termed ‘SNiP’s) – including the nuclear Vitamin D receptors. It is also now believed Vitamin D influences THYROID receptors more than previously thought – and may alter thyroid function UP or DOWN. Of most concern are those who require small amounts of Vitamin D for their thyroid function.
Excess Vitamin D could push them in to hyperthyroidism (over-active thyroid function). WHAT Vitamin D requirements an individual needs depends on the interaction of T3, D3 and Cortisol (CC) nuclear receptors AND the balance of these hormones. The T3 receptor is considered one of (if not the most) important receptors in the body (Van Zanden: 2011).
For this (and other) reasons it’s cautious to supplement Vitamin D 5000-8000IU/day maximum initially and not be given a 50,000IU Vitamin D injection (or other mega-dose >10,000IU/day).
When first supplementing Vitamin D deficient patients, it’s now considered best practice to commence at 1000IU/day; re-testing after 3-6 months – then incrementally increase dosage as required. Some individuals may require amounts as little as 100IU/day – whilst others may need as much as 10,000-25,000IU/day for optimal thyroid functioning..,! This should be assessed by a qualified and EXPERIENCED Medical Practitioner with a sound understanding of Vitamin D interactions (Van Zanden: 2014).
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. ) Readers are advised to acquaint themselves with the latest (unpublished) study summary on Vitamin D daily dosage at my Blog (www.hairlossclinic.com.au )
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).
Recent Advance EXCLUSIVE to Anthony Pearce Trichology Clients: The use Medium Chain Triglycerides (MCT) as a base to replace current fish oil or flax seed oil bases is a most important advance in both safety & efficacy for those Clients who are Vitamin D deficient, but who also have a history of seafood or nut allergies.
Finally – when the H1N1 (Swine Flu) hysteria was dominating headlines – 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….’
*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.
Copyright Anthony Pearce 2009 (Revised August 2016); this article is dedicated to Dr. JJ Cannell MD, Director of the Vitamin D Council (USA) in recognition of his pioneering and untiring efforts in raising awareness of the importance of Vitamin D.