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Finnish (Finland) research shows that yes, Vitamin A toxicity, acute and chronic, is absolutely possible from eating liver

There's a minor YouTube celebrity and liver-consuming-Carnivore-diet advocate who claims that Poison/"Vitamin A" toxicity, aka hypervitaminosis A, isn't really possible from eating liver.  This is untrue both in his personal results, as well as in the scientific literature is and fairly easy to demonstrate.

First, to use an extreme example, a form of hysteria/schizophrenia in the Inuit people--who are known to eat many rich food sources of Poison/"Vitamin A"--that has the specific name "pibloktoq" or "piblokto" is associated with hypervitaminosis A in the literature:

Pibloktoq (hysteria) and Inuit nutrition: possible implication of hypervitaminosis A.

The hysterical reaction among Eskimo peoples known as pibloktoq, one of a group of aberrant behaviors occurring among Arctic and Circumarctic societies termed 'arctic hysterias', has been explained by a variety of theories: ecological, nutritional, biological-physiological, psychological-psychoanalytic, social structural and cultural. This study hypothesizes the possible implication of vitamin intoxication, namely, hypervitaminosis A, in the etiology of some cases of pibloktoq. Its biocultural approach implicates elements of several explanatory classes, which are not mutually exclusive. Experimental and clinical studies of nonhumans and humans reveal somatic and behavioral effects of hypervitaminosis A which closely parallel many of the symptoms reported for Western patients diagnosed as hysterical and Inuit sufferers of pibloktoq. Eskimo nutrition provides abundant sources of vitamin A and lays the probable basis in some individuals for hypervitaminosis A through ingestion of livers, kidneys, and fat of arctic fish and mammals, where the vitamin often is stored in poisonous quantities. Possible connections between pibloktoq and hypervitamonosis A are explored. A multifactorial framework may yield a more compelling model of some cases of pibloktoq than those that are mainly unicausal, since, among other things, the disturbance has been reported for males and females, adults and children, and dogs.

Note that nowhere above were any supplements or synthetic forms of Poison/"Vitamin A" mentioned.  Thus, it is/was all naturally sourced.  Ergo, natural sources of Poison/"Vitamin A" are NOT harmless, and anyone who reads the literature (and more on my blog-forum here) will see this.  I'm going to assume that there was no cod liver oil being consumed either.  They were eating "livers, kidneys, and fat of arctic fish and mammals" as the likely cause of their Poison/"Vitamin A" issues.

So, if we have established that "natural", animal tissue-based hypervitaminosis A can occur WITHOUT any synthetic sources and/or concentrated supplement forms of Poison/"Vitamin A", then always remembering that "the poison is in the dose", we can then assume that other sources of Poison/"Vitamin A" (beef liver, for example) can also cause this problem if they are consumed in large enough amounts.  Natural, food-based sources of Poison/"Vitamin A" can absolutely still cause hypervitaminosis A!

On the polar bear liver causing schizophrenia note, has science ever linked Poison/"Vitamin A" as the CAUSE of schizophrenia?  See below! One tip...whenever you see "retinoid dysregulation" mentioned in a study, you should know that the authors are doing their best to not say "Vitamin A toxicity" or "hypervitaminosis A", because that would show what the real problem is.

Three independent lines of evidence suggest retinoids as causal to schizophrenia

Retinoid dysregulation may be an important factor in the etiology of schizophrenia. This hypothesis is supported by three independent lines of evidence that triangulate on retinoid involvement in schizophrenia: (i) congenital anomalies similar to those caused by retinoid dysfunction are found in schizophrenics and their relatives; (ii) those loci that have been suggestively linked to schizophrenia are also the loci of the genes of the retinoid cascade (convergent loci); and (iii) the transcriptional activation of the dopamine D2 receptor and numerous schizophrenia candidate genes is regulated by retinoic acid. These findings suggest a close causal relationship between retinoids and the underlying pathophysiological defects in schizophrenia.

In the one YouTube video I watched from this person, he admitted to getting insomnia if he himself ate too much liver or took too much Vitamin D.  An excess of either/both of these compounds (one is a toxin, the other is a hormone) will cause hypercalcemia, and hypercalcemia is associated with insomnia in the scientific literature.  Lucky for this person, his diet is extremely low in calcium...if and when he ingests more calcium, all that stored Poison/"Vitamin A" and Hormone D in his body will rapidly cause him major symptoms due to the effects of Poison/"Vitamin A" and Hormone D on increasing blood calcium.  Apparently he doesn't tolerate dairy at all, and has said as much in other videos.  Dairy is high in calcium. Avoiding nearly all calcium will prevent hypercalcemia for a while...until the known osteoporosis-causing effect of Poison/"Vitamin A" starts taking all the calcium from the bones (yes, this happens). To be clear that excess Poison/"Vitamin A" causes hypercalcemia:

Hypervitaminosis A is prevalent in children with CKD and contributes to hypercalcemia

Serum retinoid levels significantly predict hypercalcemia.

Do you see the connection? Vitamin A, Vitamin D, calcium, insomnia.  It's right there.  There are no coincidences.

Did you know that the Finnish Board of Health in 1990 advised ALL pregnant women and children to avoid all liver-related products? Why would they do such a thing if they didn't have evidence?

An update from Finland on this very same topic, from 2008:

Intake of vitamin A from liver foods among Finnish 1-, 3- and 6-year old children - a quantitative risk assessment

Before we jump in, how many other whole foods do you know of that need "quantitative risk assessments"?  Not too many, I'd gather!

Liver is a good source of vitamin A and many other nutrients. In addition to many beneficial effects, liver consumption also has some potential risks. One of them is that liver contains vitamin A in retinoid form, which can be toxic if ingested in large amounts on a continued basis.

In order to prevent excessive intake of vitamin A, liver-based foods have not been recommended for children under the age of one year since 1990. With toddlers, it has been advised that the consumption of liver-based foods (ground liver patties, liver steak, liver stew, liver casserole), liver sausage and liver pâté should be restricted to a couple of meals per month. To reevaluate current recommendations, the Finnish Food Safety Authority, Evira has undertaken a risk assessment of retinoid intake from liver foods among Finnish children. The objectives of the risk assessment were to estimate the relevance of retinoid exposure from liver products among Finnish 1-, 3- and 6-year-old children and to assess whether children’s consumption of liver foods still needs to be restricted.

Note that this is a RE-evaluation.  They're checking to see if what they found back then still holds true today.  SPOILER:  Liver still causes hypervitaminosis A.

The risk assessment was based on liver food consumption data (DIPP Nutrition Study), recipe information and analysis results of vitamin A (retinoids). To estimate intake by consumption of both non-liver and liver sources of vitamin A, Monte Carlo simulations were performed. The impact of liver consumption on the intake of vitamin A was estimated separately for single meal and daily long term average consumption. The simulation model results were compared with intake recommendations and upper intake limits. The models were also applied to estimate safe combinations of portion size and eating frequency for liver foods and their combinations.

Based on risk assessment, the following conclusions were made:

  1. Although consumption of liver foods helps to fulfil some children’s daily vitamin A needs, there is a risk of intolerably high retinoid intake among other children.
  2. Among children, the proportion of true eaters of liver foods is very probably higher than can be seen on the basis of 3-day food records.
  3. When considering safe long term consumption of liver foods, in addition to portion size, eating frequency is an important factor. One-year-old children can eat safely liver sausage or pâté and 3- and 6-year-old children all liver foods as long as they do not do it too often. The safe portion size and eating frequency depends on the age group and type of liver food. In general, liver sausage or pâté can be eaten more often than liver casserole, liver sauce and liver patties.

Going by that first sentence, are you going to bet that your child is in the "some" category, or the "other" category?  If you take that bet, you'll probably only find out that you lost once your child is toxic with Poison/"Vitamin A".

Vitamin A toxicity in humans may be generally categorized as either acute or chronic. Acute toxicity occurs within hours or at most a day or two after a very large intake. Chronic toxicity occurs when lesser amounts that are not acutely toxic are consumed for several weeks, months, or years. Biological indicators of toxicity include high serum retinol concentrations, production of toxic metabolites, high vitamin A concentrations in the liver and liver damage (Allen & Haskell 2002).
[...]

Chronic toxicity
Onset of chronic toxicity is dependent on the dose and the length of exposure. According to Olson (1987), toxic doses are at least 10 times higher than the RDA (1-3 year olds: > 230 μg RE/kg body weight) and usually cannot be obtained from foods except by the chronic ingestion of significant amounts of liver. For children, daily intakes of 450 μg/kg body weight have reportedly led to toxicity (Bendich et al. 1989; Hathcock et al. 1990; Coghlan & Cranswick 2001; Penniston and Tanumihardjo 2006).

I want to do the math on this one.  So 450 micrograms (mcg) per kilogram of bodyweight (BW) of retinol equivalents (RE) has reportedly caused toxicity in children.  I'm going to convert this for myself and my non-metric system folks too.

Let's say we have a theoretical 11 kg child (~25 pounds).

11 kg bodyweight * (450 mcg RE per day/kg bodyweight) = 4950 RE = 16,500 IU, converted using 1 IU RE is 0.3 mcg RE.

For you to visualize:  "1 oz. meat = size of a matchbox; 3 oz. meat = size of a deck of cards"

A quick Google of "vitamin A content of liver" spit out the easy answer of 15,297 IU in 3 ounces of liver. Close enough, I'd say.

So, a daily consumption of liver that is only the size of a matchbox in an 11kg/25lb child can potentially cause chronic long-term hypervitaminosis A.  I do believe that other problems that researchers didn't connect to hypervitaminosis A were likely happening and just not recognized or thought to be significant.

What if I told you that the Weston A. Price Foundation (WAPF) has a "Liver-Based Formula" recipe for nursing BABIES on their website that has 2 ounces of liver in it, along with a teaspoon of cod liver oil?  What if the mother was herself already eating a high Poison/"Vitamin A" diet like the WAPF advocates heavily?  Poison/"Vitamin A" absolutely goes into the breastmilk. This is a recipe for disaster.

In the meta-analysis of Myhre et al. (2003), chronic toxicity was reported with daily doses of 190-18 800 and 70-4600 μg RE/kg body weight in children aged 0-2 (n=50) and 3-16 (n=39) years, respectively. Chronic hypervitaminosis was concluded to be induced after daily doses of 2 000 μg RE/kg in oil-based preparations for many months or years (Myhre 2003). In contrast, doses as low as 200 μg RE/kg in emulsified/water-miscible and solid preparations for only a few weeks seemed to cause chronic hypervitaminosis A (Myhre et al. 2003).

Tolerance to excess vitamin A intake has also been seen to vary between individuals. In one case study, two boys were given chicken liver that supplied about 690 μg/day vitamin A and various supplements that supplied another 135 to 750 μg/day. One boy developed toxicity symptoms at the age of 2 years, and the other one at the age of 6 years. An older sister who had been treated similarly remained completely healthy (Carpenter et al. 1978; FNB 2001).

Onset of Poison/"Vitamin A" toxicity varies among individuals, you say?  Even within the same family, you say?  How can one know whether they have a high tolerance or a low tolerance, unless they poison themselves to find out?  Is it possible that this minor YouTube celebrity is simply one of the "lucky" ones that has a higher tolerance (and/or detox capacity) for Poison/"Vitamin A" and will simply take longer to see the coming negative effects?  I'd say this is probably what is going on here, folks.

Conclusions
This risk assessment showed that long term liver consumption may expose children to retinoid intakes higher than what is considered safe. The amount of vitamin A obtained from liver-based retinoids, seems to remain below the safe intake from a single portion. With long-term consumption of liver foods however, there is a risk of exceeding upper tolerable intake levels. However, in long term consumption moderate portions of liver foods are still safe as long as they are not consumed too often. The safe portion size and eating frequency depend on the age group and type of liver food. When considering the total daily vitamin A intake from the nutritional point of view, liver consumption has a positive effect. However, the benefits of eating liver can probably be substituted by a well-balanced diet with plenty of vegetables and a reasonable amount of meat without the risk of an excess intake of retinoids.

From the data, we can surmise that:

  • Different forms of Poison/"Vitamin A" will cause toxicity at different rates.
  • Some people tolerate/detox Poison/"Vitamin A" better than others.
  • In children, it is possible to cause Poison/"Vitamin A" toxicity with as little as 2-3 bites of liver on average, daily.
  • Liver is dangerous in excess and this is known to be true, hence the "risk assessment" being necessary.

There are other YouTube celebrities out there that I hear about who are absolutely poisoning themselves to early deaths with massive excesses of Poison/"Vitamin A".  There are also several recent minor nutritional celebrity deaths associated with fermented cod liver oil and a high Poison/"Vitamin A" diet.  The proof will be in the pudding, just wait and watch.  As Hanz and Franz used to say, "Hear me now and believe me later!"

Dr. Garrett Smith, the "Nutrition Detective"
Licensed Naturopathic Physician (NMD) in Arizona
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