Hypervitaminosis D: the complications of excess Vitamin D supplementation.

The discovery, isolation and research into the fat-soluble vitamins (A + D) occurred in the first decades of the 20th century by scientists seeking to understand the causes of the centuries-old diseases: rickets, scurvy and beriberi. In the past hundred years, researchers increasingly appreciate the essential functions Vitamin D has on maintaining a healthy human body.

In hormonal-nutrient terms Vitamin D is not considered a true ‘vitamin’ because it’s endogenously synthesised from natural ultraviolet (UV) light exposure on the skin.

Once converted into its stored active form – Calcitriol (1,25 [OH] 2 D3) – Vitamin D has the chemical structure of a cholesterol derived steroid molecule, comparable to the adrenal and sex hormones.

The many complex, multi-faceted responsibilities of Vitamin D across the body are almost too innumerable to list, but some of the most crucial are:

  • Absorption and utilisation of Calcium and Phosphorus from the gut.
  • Integral to the production and balance of cells (1) which continually structure and remodel our bones.
  • Enhanced Vitamin D levels of at least 100 nmol/L is necessary for optimised thyroid-adrenal metabolic functioning (2).
  • Vitamin D is second only to Zinc as the most immunologically-calming hormone/nutrient in the body, partly due to its suppression of macrophage (white blood cell) pro-inflammatory cytokine response.
  • Sustained Vitamin D deficiency is believed to disorientate our immune defences, which can result in autoimmune attack on the body.
  • Prolonged Vitamin D deficiency increases a pre-disposed person’s risk of the following diseases:
    • Multiple Sclerosis
    • Parkinson’s Disease
    • Early Dementia and Alzheimer’s disease
    • Certain cancers
    • Osteoporosis or Paget’s disease.

With all these benefits maintaining optimal Vitamin D levels, as well as the potential disease risks to being deficient one would assume ‘more the better’ – but this is not the case.

Factors influencing Vitamin D supplementation:

Essentially there is no strict standard amount for every individual due to genetic variations in us all; some require more and some less. It’s now known Vitamin D modifies thyroid receptors to a greater degree than previously realised, and D3 can radically alter thyroid blood pathology results up or down.

Of most concern are those patients taking prescribed thyroid medication who require little daily vitamin D. If supra-therapeutic amounts are given by injection or long-term supplementation, a hyperthyroid state may be induced (Van Zanden: 2012).

 Studies have shown that on average each additional 100 IU of vitamin D3 consumed per day will raise blood vitamin D levels by 2.5 nmol/l (=1 ng/ml).(3) So unless genetic variations determine otherwise, levels should not be pressed beyond 250 nmol/L (ie: 100 ng/ml) (4).

If a young fair-skinned adult exposes their bare, non-sun screened upper torso to strong sunlight for 20-30 minutes, the skin will synthesise around 20,000 IU of non-active Vitamin D for conversion and a ready reserve of stores.

However once this 20,000 IU level is attained, physiological protective mechanisms are activated, further synthesisation is corrupted to prevent further absorption. According to Vieth (1999) there has never been a substantiated case of Vitamin D toxicity from sun exposure alone.

As is the case with iron infusions, bolus doses of Vitamin D at 25,000, 50,000, up to 600,000 IU (5) in one injection completely overrides the body’s own natural checks and balances. In susceptible individuals these are – at least temporarily – toxic amounts which can cause the person to become very unwell, and even be the cause of irreparable damage to the body.

Vitamin D (as Calcitriol) exerts an intracellular steroidal effect within cells to up or down-regulate our unique genetic codes (6).

As with other steroidal hormones, Vitamin D is bound to either its receptors or carrier proteins rather than in a ‘free’ state within the body. When hypervitaminosis D occurs however, receptors and carrier proteins become over-saturated, leading to a Vitamin D overflow which overwhelms and disorientates normal signalling processes within the cell.

One of the main disrupted signalling processes occurs in the Gut where the uptake of dietary calcium is enhanced, eventually leading to hypercalciumaemia.

The adverse effects of hypervitaminosis D:

Excess blood calcium levels (termed: hypercalciumaemia) may arise due to elevated D, which in turn further increases absorption of dietary calcium from the Gut.

Hypercalciumaemia is arguably the most serious side effect of excessive D levels due to its potential long-term health risks. Symptoms of hypercalciumaemia:

  • Vomiting, nausea, abdominal pains, loss of appetite and severe constipation (or diarrhoea).
    •  Fatigue, dizziness, confusion or altered levels of awareness, slurred speech.
    • Hearing impairment, excessive thirst and frequent urination.
    • Over time hypercalciumaemia can lead to calcium deposit, build-up and blockage of the arteries – particularly the heart, head and brain.

Excessively elevated D levels can cause skeletal bone loss by pulling Calcium out of the bones, depleting and inhibiting the action of Vitamin K2. K2’s crucial purpose is to maintain Calcium within bones and out of our blood. If a person is also Vitamin A or Magnesium deficient, bone loss may be even more severe.

Studies have found Vitamin D toxicity will give rise to moderate-severe renal dysfunction due to calcification of the renal tubules (7). The most severe complications of Vitamin D toxicity may not be apparent for months to years.

Vitamins D, A + K are fat-soluble vitamins – which in contrast to water-soluble forms cannot be easily excreted when in excess – rather they tend to build-up in the liver, other organs and body systems.

  1. Osteoblasts and osteoclasts.
  2. Vitamin D levels of minimum 100 nmol/L are necessary for optimal T3 receptor expression (Lee: 2007). D3 has a qualitative effect on T3 intra-nuclear receptors (i.e.: within the cell nucleus).
  3. Clin J Am Soc Nephrol. :2008 
  4. Genetic mutations termed ‘SNiP’s’
  5. 600,000 IU is a six-monthly deep intra-muscular injection mixed with castor oil to aid in slow release. 600,000 IU is TWENTY times more than the body will allow to be synthesised from natural UV light (Harrison: 2021).
  6. i.e.: switch the genes on or off.
  7. Kidney damage or failure (N Engl J Med: 2007)

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