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Just The Tip Of The Iceberg – More Bad News About Vitamin D How easy it is to poison yourself with synthetics.

Vitamin D is a hormone precursor.

I only recommend cod liver oil, regular whole fat mammal milk with naturally occurring amounts of Vitamin D and other natural sources, including daily sunlight.

It doesn’t take high amounts of Vitamin D to be effective, even on cloudy days. This gauge of effectiveness can easily be found in large study groups directly comparing cod liver oil with synthetic D3 for health benefit. You can also learn that seasonal decline, malnutrition or detoxification events (meaning hair loss, skin issues, rashes, arthritic conditions, poor carb digestion issues etc.) do not occur in animals in early nutrition studies that extend beyond 365 days; meaning there is no association between less sunlight/season and autoimmune diseases. There is such a thing as Vitamin D resistance and without oleic acid and sulfate for accelerated clearance it can bio accumulate and become toxic. With those substances it can be a highly effective macrophage activating factor transport mechanism for GC Protein or VDBP (Vitamin D Binding Protein). The addition of sugar to fish oils can also lead to rancidity so the benefits of fish oil or any healthy oil can quickly become a non benefit with the addition of some sugars. Early malnutrition studies that relied on butter quickly determined this. If you want to see how easy it is to mis-use Vitamin D you can visit the library to see how D metabolites were researched as use for birth control methods. Most would be surprised to learn that D3 is a rodent poison. High dose D3 in those who aren’t proficient in metabolizing is the equivalent to rodent poisoning in humans. Early malnutrition studies did not use synthetic D vitamins but relied on natural sources and milk was initially fortified with cod liver oil. I know of severe lesion formation with D3 intoxication. I also know of extremely high levels of D2 (ergosterol) in those who did not supplement with either synthetic form of D. With some synthetic vitamins the effects aren’t so bad as they are easily excreted, not so with synthetic D’s or Vitamin A. Some have little problems with synthetic D3 or D2, some have severe problems, I say why take the chance when there are virtually no problems from natural sources and there is only benefit. The only synthetic vitamins I recommend as needed are sodium ascorbate (C) and pantothenic acid. Sodium ascorbate and whole fat mammal milk is an excellent and fast detoxifier of nearly all toxins with no need to determine the specific toxin. No synthetic vitamin is equal to how they are made and synthesized from friendly organisms via a healthy gut.

I suspect most forms of D fortification in cereals began with the effort to prevent product loss from rodents and this fortification was quickly branded as a health benefit. Later it was observed that the rodents lived longer consuming the box rather than the cereal. Whole fat mammal milk today only contains naturally occurring amounts of the vitamin.

Merck

Cholecalciferol (vitamin D3) is used both as a dietary supplement and a rodenticide. It appears to be toxic at a much lower dose when consumed in a bait form than when ingested as a technical grade agent. Most rodenticide baits contain 0.075% cholecalciferol. Incidence of vitamin D3 toxicosis in animals is relatively less than that of anticoagulant and bromethalin toxicosis. Relay toxicosis from vitamin D3 has not been documented. One international unit (1 IU) of vitamin D3 in nutritional supplement is equivalent to 0.025 mcg of cholecalciferol.

Cholecalciferol toxicosis is characterized by hyperphosphatemia and hypercalcemia, leading to renal failure, cardiac abnormalities, hypertension, CNS depression, anorexia, vomiting, diarrhea, and lethargy. The increased calcium and phosphorus can lead to calcification of soft tissue, notably the highly vascular areas of kidneys and lungs, as well as within the walls of the great blood vessels.

Clinical signs generally develop within 18–36 hr of ingestion; initial signs can include depression, anorexia, polyuria, and polydipsia. The serum phosphorus more commonly rises first, at ~12–24 hr after ingestion, with serum calcium levels rising within another 12–24 hr. Nausea, vomiting, hematemesis, and depression are common as the clinical signs progress. It is important to obtain a baseline biochemistry profile as early as possible after the exposure, so that each animal can be monitored based on individual values.

Ingestion of vitamin D3 at >0.1 mg/kg may require decontamination (induction of emesis and administration of activated charcoal) and monitoring of serum calcium, phosphorus, and renal values. Emesis can be induced within 2 hr of exposure with 3% hydrogen peroxide or apomorphine in dogs and xylazine in cats. Activated charcoal at 1–2 g/kg is an appropriate initial dose for decontamination, and a second half dose after ~6–8 hr may be helpful. In addition, use of cholestyramine, a bile acid sequestrant, may be useful to decrease the body burden of vitamin D3 that undergoes enterohepatic recirculation with bile acids. However, the efficacy of cholestyramine to reduce vitamin D3 levels in dogs has not been determined. The recommended dosage is 0.3–0.5 g/kg, dissolved in liquid and administered orally every 6–8 hr for 3–5 days, depending on the initial dose of cholecalciferol ingested. Premature initiation of calciuresis (see below) may disrupt normal calcium-phosphorus metabolism, triggering osteoclasts to move additional calcium into the blood stream, artificially increasing serum calcium and phosphorus levels and mimicking vitamin D3 toxicosis.

Once the biochemical values begin to increase, there are two approaches to management. The first is to promote calciuresis by administering normal (0.9%) saline at 2–3 times normal rates. Furosemide at 2.5–4.5 mg/kg, PO, every 6–8 hr promotes calcium excretion but can also increase fluid loss (so hydration status should be monitored). Prednisolone at 1–3 mg/kg, PO, bid-tid, can reduce bone resorption as well as decrease calcium absorption from the intestine. Treatment with a phosphate binder (aluminum hydroxide 30–90 mg/kg, PO, in divided doses) to decrease phosphorus absorption and feeding a diet low in calcium should also be considered.

The preferred treatment for persistent significant hypercalcemia is pamidronate, an injectable bisphosphonate that inhibits osteoclastic bone resorption. It is administered at 1.3–2 mg/kg via slow IV infusion in saline over 2 hr. After administration, as the calcium and phosphorus levels start to decrease, supportive therapies (furosemide, prednisolone) should be tapered. A repeat dose may be required if significant hypercalcemia redevelops.

In the past, use of salmon calcitonin (administered at 4–6 IU/kg, SC, every 2–3 hr) has been suggested to decrease calcium and phosphorus levels, but this treatment is no longer used commonly. The two major disadvantages are that some animals may become refractory to calcitonin, and that once this therapy is instituted the use of pamidronate is not helpful.

Calcium and phosphorus levels should be monitored and treated until they return to baseline. Treatment may have to be continued for days or weeks because of the lipophilic nature of vitamin D3. Renal function should be monitored, and other clinical signs treated as needed.