Butyric acid is an unlikely contender for a newly discovered vitamin in the human species. Yet that is what we contend – apparently for the first time – here at Exploring the Bio-edge.
Here we have a substance that stinks of vomit, rotten milk, rancid butter, and the fruits of durian and ginkgo. The bacteria synthesising it include clostridia – generally associated with botulism, tetanus, gas gangrene and colitis. If there’s anything good about clostridia, in most people’s minds, it’s that one of their toxins can be useful cosmetically as Botox.
Also making it hard to conceive of butyric acid as a vitamin – which we tentatively label ‘vitamin M’ – is its usual description as a fatty acid. After all, no other vitamin is a fatty acid. Furthermore, butyric acid is saturated, unlike those fatty acids that have held the nutritional limelight for decades. So how could a component of fat, let alone a saturated one, possibly amount to a newly discovered vitamin?
Well, this calls for lateral thinking – partly because this vitamin has produced no symptoms of extreme deficiency analogous with scurvy or rickets, and partly because pharmaceutical companies have done little research on a substance which can’t be patented anyway. Based on converging lines of indirect evidence, we’ve come to suspect that many seemingly well-fed people are subclinically deficient in butyric acid today, contributing to various degenerative diseases.
Experiments with the domestic rat and domestic pig have shown that butyric acid reduces inflammation and boosts the immune system, induces apoptosis and controls cancer, helps stabilise blood sugar and regulate carbohydrate metabolism, helps satiation, helps heal nerve damage after stroke, acts as an antioxidant, and supplies energy to the colon while regulating the permeability of the intestinal wall and preventing constipation. How many other functions remain undiscovered?
Sufficiency in our ‘vitamin M’ may have come naturally for humans tens of thousands of years ago but poses a potential problem today.
Prior to the evolution of Homo and the advent of cooking, our primate ancestors would have acquired most of their butyric acid by way of microbial mutualism in the gut. In this process, various bacteria – including beneficial clostridia – in the colon and caecum ferment plant fibre anaerobically to produce butyric acid. As long as the colon retained a healthy fermentation based on periodic consumption of plenty of plant fibre, our requirements for butyric acid were met.
So, how could deficiency in ‘vitamin M’ have arisen? Our hypothesis goes as follows.
There are essentially only three sources of butyric acid in the nutrition of adult humans: fermentation of fibre in the human colon, external fermentation of various foods according to traditional culture, and the butterfat of ruminants. It’s important to realise that no fresh foods available to humans contain butyric acid except for butterfat and the specialised arillate fruit called durian.
Cooking, which may have been ubiquitous among humans from the start, converts the softest fibres into digestible starch. This conversion enhances the extraction of food energy at the expense of butyric acid, because it reduces the substrates for beneficial fermentation. Later, in the industrial age, eating too much sugar may have exacerbated this imbalance because insulin and blood-borne butyric acid act in antagonistic ways. Although the advent of antibiotics in the last century was particularly deleterious in razing the microbial community in the colon – allowing detrimental bacteria and unicellular fungi to prevail – it is the prevalence of lactose in the modern diet that may be even more pernicious as regards butyric acid. This is because milk sugar produces unhealthy, gassy colonic fermentations that yield negligible butyric acid and at the same time hypothetically disrupt the activities of the bacteria that do produce ’vitamin M’.
Our hunting and gathering ancestors evidently discovered, soon enough, that diverse external ferments, of both plant fibre and animal matter, could be used to supplement the vital factor that we now identify as butyric acid, alias ‘vitamin M’. These traditions were modified with the domestication of plants, producing diverse products such as kimchi in Korea. However, all these ferments have lost favour in the industrial world, even as our reluctance to chew has minimised our intake of fibre.
Turning again to the dairy industry: it is only within the last few thousand years that various ruminants have been selectively bred to produce milk prolifically. Although overall a problematic food for adults, milk is – if simply processed – a potentially valuable source of our ‘vitamin M’. Butyric acid is hardly recorded in the milk of hoofed mammals other than true ruminants, but occurs in bovine milk at an ample concentration. The misfortune is that it is associated with the lipid component of dairy products, which tends nowadays to be shunned as part of a general – if largely misguided – fear of saturated fats. And the lactose in milk tends to be indigestible even to beneficial bacteria such as lactobacilli, fouling the colonic fermentation system and diminishing the production of butyric acid that could otherwise be absorbed via the colon.
On the basis of this information, our rationale in proposing the existence of a ‘vitamin M’ in humans is as follows:
The concentrations of butyric acid in relevant foods and the human body are, as for other vitamins such as ascorbic acid, small.
Unlike the domestic pig, the human species cannot synthesise butyric acid in our own cells, depending for it on absorption from the gut.
With only four atoms of carbon, the molecule of butyric acid is far smaller than those of the essential fatty acids. Accordingly there is no evidence that butyric acid acts as a fatty acid in the human body, although it is known to do so in true ruminants.
Butyric acid is probably an essential catalyst for various metabolic functions, although it does not participate directly in either anabolic or catabolic reactions in the way other fatty acids do.
Studies of other omnivorous mammals suggest that deficiency – often subclinical – of butyric acid is partly responsible for a wide range of human ailments including cancers, immune dysfunction, depression, irritable bowel/leaky gut, osteoporosis, cardiovascular disease, and maladies of carbohydrate metabolism including diabetes and obesity.
We go on to hypothesise that a deficiency of ‘vitamin M’ has frequently arisen in humans for the following reasons:
Most consumers of dairy products prefer de-fatted products from which most of the butyric acid has been removed.
Most consumers of dairy products (including yoghurt) suffer from maldigestion/intolerance of lactose, in which the microbial environment in the colon is disrupted and the endosymbiotic production of butyric acid diminished.
Most people in developed countries tend to avoid the raw fibre required for this production of butyric acid by various beneficial bacteria in the colon.
Abuse of antibiotics – taken directly by humans, or fed to livestock, or used to treat bovine mastitis – further compromises the microbial community in the human colon.
Most people have abandoned the traditional fermentations, e.g. kombucha, that formerly supplemented butyric acid. Even the cheese industry sets out to reduce concentrations of butyric acid except in certain types (e.g. parmesan).
Excessive consumption of linoleic acid and other unsaturated fats/oils, refined from the seeds of annual dicotyledonous crops, hypothetically antagonises butyric acid, increasing the requirement for ‘vitamin M’.
We hypothesise that the medical industry has overlooked the existence of ‘vitamin M’ because:
Butyric acid smells of vomit and body odour and is produced partly by clostridia, both of which misleadingly imply toxicity.
Butyric acid cannot be patented, which means that pharmaceutical companies have sponsored few investigations.
Butyric acid does not qualify as a vitamin for most species of livestock, which produce it in abundance in foregut fermentation or are capable of synthesising it in their own cells.
Certain functions of butyric acid may not have been clearly distinguished from those of vitamin D (which is really a photosynthesised steroid hormone), given the possibility that butyric acid catalyses the conversion of cholesterol to the active hormonal molecule, calcitriol.
Butyric acid functions in foregut-fermenting mammals as a saturated fatty acid rather than a vitamin, and the physiological distinction between ruminants and primates has not been fully realised.
Saturated fatty acids have suffered from a false association with cardiovascular and other diseases, and polyunsaturated fatty acids (particularly linolenic acid, alias omega-3) have instead dominated public and medical thinking.
So here’s a provocative thought from the Bio-edge: let’s adopt a working hypothesis that butyric acid is a vitamin. In the meantime, if readers suspect any deficiency, please remember that the only widely accepted food containing ‘vitamin M’ without fermentation is butterfat. So, regardless of biological nuances, the solution may be as simple as following the healthy example of the French – and using butter freely.
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