- A recent study demonstrated that vitamin A may prevent obesity, type 2 diabetes and protect the heart.
- A second study has found that beta-carotene (pro-vitamin A, from plant foods) may actually counteract the health benefits of vitamin A functions
- Getting your vitamin A from animal sources makes more sense than ever
Vitamin A is key in the development and function of virtually all cells in the body. It is widely acknowledged as an essential vitamin with a wide range of health-maintaining functions. It has been clearly linked to the development and maintenance of healthy vision, bones, immunity and mucous membranes. Evidence suggests it may provide protection from a range of cancers, and maintain a healthy metabolism. Infections such as measles, HIV and tuberculosis are less frequent and less severe when vitamin A status is good.
Researchers from the University of Montreal have recently shown the potential of vitamin A to treat obesity and type 2 diabetes. The vitamin also provided protection from cardio-vascular complications associated with these conditions. The findings were presented on June 6, 2014 at the Annual Conference of the Canadian Nutrition Society in Saint John’s, Newfoundland.
Lead author Daniel-Constantin Manolescu reports that through experiments on obese insulin resistant mice his group have demonstrated that retinoic acid (a vitamin A metabolite) protects heart cells from apotosis (cell death) and upregulates genes that protect cardiac cells. These same genes are usually switched off in obesity and diabetes.
This work builds on their previous studies that showed that increasing levels of retinoic acid significantly decreased blood glucose, insulin resistance, body weight, and adipocyte (fat cell) size, including abdominal fat.
This happened even when identical dietary intake and physical activity were maintained between treated and non-treated animals.
This presents something of a conundrum to the calorie-in calorie-out theory of obesity: these vitamin A treated mice lost weight while consuming the same number of calories and expending the same amount on exercise as the untreated mice. How did they do this?
The researchers found that they burn more energy as heat, i.e. they have a higher basal metabolic rate. Vitamin A’s role in this process is by stimulating uncoupling protein (UCP1) in the mitochondria. Usually mitochondria convert food calories into adenosine triphosphate (ATP) – the basic energy currency of all cells in the body. However, when uncoupling proteins are raised in the mitochondria some of the calories are converted into heat instead.
So retinoic acid works on many levels to reverse the metabolic abnormalities associated with obesity and diabetes. Daniel-Constantin Manolescu goes on to say
“Our studies on animals show that retinoic acid induces normalization of blood glucose and reduction of obesity. It is an important contribution to understanding [retinoic acid’s] action on the liver, fat, muscles, and the heart, and on retinoid metabolism, energy metabolism, fatty acid oxidation, and insulin resistance. Our research identifies new metabolic effects of retinoids and may lead to anti-obesity and anti-diabetic medicines.” (my emphasis)
And there we go. Wonderful research that falls flat on its face at the last hurdle. How can research that is so clearly linked to inadequacies in the modern diet reach the conclusion that we need to create new drugs? Surely the real take home message is MAKE SURE YOU GET ENOUGH VITAMIN A IN YOUR DIET? Is that too complicated? And why wait until people are already obese or diabetic? Why not suggest increased vitamin A intake to prevent this metabolic train crash in the first place?
The best sources of vitamin A are certain animal foods: Liver, meat, eggs, milk, butter, cheese. These provide pre-formed vitamin A which is easily converted into the active retinoid forms such as that used by the researchers in the above study. Whilst plant carotenes have long been considered as nearly equivalent sources, recent research has revealed they are far less effective and in some cases actually hamper the beneficial actions of vitamin A in the body.
Recommending vitamin A in the animal form has, unfortunately, fallen out of fashion, partly because of the last half-century push to get us off traditional (high fat) animal foods, and persuade us to eat more low-fat and plant-based foods (such as soy and industrial vegetable spreads).
The other reason for the official hesitation in recommending animal sources of vitamin A is that taken in excess pre-formed vitamin A can cause toxic effects (hypervitaminosis A). However, you are unlikely to suffer from an excess if you avoid vitamin A supplements (containing retinol), and aim instead to get vitamin A directly from your diet. You can do this by regularly eating full fat milk, butter, eggs (including yolks), shellfish and organ meats.
The current recommended daily intake of vitamin A is given as 700μg (2333IU) for men, and 600μg (2000IU) for women (UK NHS guidelines). However, many nutritionists think this is unnecessarily cautious, and should be seen as a minimum to avoid deficiency. Here are some typical values from the top six animal sources:
|Preformed vitamin A||μg/100g||IU/100g||%RDA|
|Egg (equiv. 2 medium)||140||520||20%|
What you can see from the table above, is that you can achieve the guideline daily amount simply by eating 100g of liver once per week. However, if you eschew liver it becomes harder: 100g of butter or cream will suffice, but keeping that up day-after-day is not everyone’s cup of tea. You have even fewer options if you follow strict paleo principles and avoid dairy too, then your only option is to eat ten eggs every day (!!!). In practise a diet with liberal butter, cream, eggs and milk in whatever way suits you, plus liver every week or two is going to do the trick. But leave out the liver and you will need to do the sums to check you are not falling short. At the other extreme, don’t over do it and start eating 100g of liver every day.
Can consideration of human evolution shed light on how much liver we should eat? Assuming that our paleolithic ancestors did not waste good food, then they would be eating one liver per kill. In the case of, say, chicken, one liver weighs approximately 20g compared to an edible muscle mass of about 1kg. 1 kg chicken with skin, provides about 2000 calories – close to the required energy intake for a modern sedentary human – so, it is not unreasonable to consider that a highly carnivorous ancestral diet would equate to a whole chicken per day for us. Hence, it follows that an appropriate amount of liver per day would be about 20g, which, from the table above, would provide approximately 115% of the RDA of preformed vitamin A. Just right! That in turn equates to about 100-140g of chicken liver per week, or somewhat less if you are eating eggs, butter or cream. Even the overly-cautious NHS advises that liver can be eaten once per week without any risk of harm. So that’s all right then.
At what point can preformed vitamin A become toxic?
The Linus Pauling Institute states that signs of toxicity are associated with long-term consumption of vitamin A in excess of ten times the RDA (i.e. 8,000 to 10,000 μg/day or 25,000 to 33,000 IU/day). A 1991 paper examining cases of vitamin A toxicity found “The smallest continuous daily consumption leading to cirrhosis was 25,000 IU per day during 6 years, whereas higher daily doses (greater than or equal to 100,000 IU daily) taken during 2½ years resulted in similar histological lesions.”
Pretty well all cases of vitamin A toxicity arise from taking mega-doses of retinol-containing supplements, or where arctic explorers ate husky dog or polar bear livers, which are much higher in vitamin A than farm animal livers. Normal dietary sources of pre-formed vitamin A are simply not associated with toxicity.
Many factors affect the health benefits and toxic threshold of vitamin A. For example, zinc and iron act synergistically with vitamin A, and deficiencies in these vitamins can interfere with vitamin A function. Also, vitamin D and K2 work synergistically with vitamin A, enhancing its effects and reducing the toxicity at higher doses. Ensuring you gain adequate amounts of these vitamins from your food will help you maximise the benefits from dietary vitamin A. For an in-depth exploration of this subject, I would recommend a careful read of the vitamin A articles on the Weston A Price Foundation site here, and their article on liver consumption here.
Many plant foods contain vitamin A precursors, called carotenes. The most well-known one is beta-carotene, associated with orange coloured vegetables such as carrot, squash and sweet potatoes.
Dietary carotenes are cleaved in the gut by enzymes to make a range of compounds that can be converted into retinoids. However, there are some important issues that should give us pause for thought before relying on carotenes as our main source of vitamin A.
Firstly, there is little evidence that our evolutionary ancestors ate significant quantities of food sources of carotenes. As discussed above, most of their vitamin A came from animal sources.
Secondly, carotenes have a low conversion efficiency in humans. According to the Linus Pauling Institute you need to ingest approximately twelve times as much beta-carotene as preformed vitamin A to gain the same benefit. Furthermore, there is a great deal of variability from person to person, with many people failing to convert beta carotene to any detectable quantity of vitamin A at all (see this paper).
Beta carotene can actually counter vitamin A function in the body
Worryingly, a 2012 study by Ohio State University demonstrated that the digestive breakdown of carotenes produces a range of fragments that instead of being turned into retinols and activating the normal vitamin A receptors throughout the body, become vitamin A antagonists (see graphic).
This means that although they bind to the vitamin A receptors, they do not activate them. Once attached they prevent vitamin A from binding and hence block the effect of vitamin A signalling, effectively reducing the vitamin A status of the person consuming them.
The lead author of the study said:
“These materials definitely have anti-vitamin-A properties, and they could basically disrupt or at least affect the whole body metabolism and action of
These findings shed light on a puzzle that has confused scientists since the 1990’s. The CARET trial used high dose supplemental beta-carotene in an attempt to reduce incidence of lung cancer among a highly susceptible population: smokers and asbestos workers. It was well understood that vitamin A has potential anti-cancer properties, so researchers were very surprised, when the beta-carotene supplemented group had a much higher incidence of cancer. So bad was the effect that the trial had to be halted on ethical grounds.
So not only are plant sources of pro-vitamin A (carotenes) poorly absorbed and poorly converted – making them an unreliable source at best – it now appears that they actively work against the benefits that improved vitamin A status should bring.
Finally, vitamin A is one of the fat soluble vitamins, along with D, E and K2. Consequently to properly absorb it you must consume it with adequate fat. Again the animal sources of vitamin A are superior as they invariably contain the required fat to ensure upwards of 70% absorption. Plant sources of beta-carotene such as carrots, sweet potatoes and squashes are naturally very low in fat, meaning that absorption rates can fall close to zero unless eaten with plenty of added fat.
The evidence from an evolutionary perspective is that mankind has relied on animal sources of vitamin A for hundreds of thousands of years. The idea that plant sources of carotenes are superior do not stack up, and evidence is mounting that they are at best a poor substitute and may actually be, at least to some degree, an anti-nutrient.
Take home message
- Ensure you are eating sufficient preformed vitamin A from quality animal products (liver, kidneys, eggs, milk, butter, cream) to achieve at least your RDA.
- Eating liver once per week is a great way to gain plenty of vitamin A along with many other valuable nutrients.
- Don’t try to get your vitamin A by eating an excess of beta-carotene containing foods (carrots, sweet potatoes, squash etc) as they may actually reduce our vitamin A function.
Footnote: GM and beta carotene
Proponents of genetic engineering have long been trumpeting projects to bio-engineer staple crops in developing countries to fight vitamin A deficiencies, which are the leading cause of blindness worldwide. Projects such as the development of ‘golden rice’ in Asia, ‘golden maize’ in South America and cassava in Africa are trumpeted as the moral side of GM. However, the research on beta carotene discussed above is flagging up a possible problem with this brave new worldview.
“A concern is that if you engineer these crops to have unusually high levels of beta-carotene, they might also have high levels of these [vitamin A antagonist] compounds,” said a researcher from Ohio State University.