There are very few nutrients as crucial to our well-being as vitamin B12. The reason why this is so is that vitamin B12 is essential for cellular energy metabolism, gene transcription, and nervous system function. This vital role at the cellular level is not restricted to only some tissues and organs: it is vital for every single cell of every tissue and every organ.
For the nervous system, both for the central nervous system—our brain—and the peripheral nervous system—the spine and entire network of nerves connected to the brain and coursing through the whole body—vitamin B12 is essential in building, maintaining and repairing the myelin sheath that covers every nerve to ensure protection and proper nerve signalling. It is, in fact, the consequences of B12 deficiency on the nervous system that most often betray this very serious problem.
Everyone should supplement and maintain blood levels of B12 in the range from 600 to 2000 pg/ml in order to avoid and, if this is the case, help recover from the wide range of problems that result from B12 deficiency or insufficiency. Health care practitioners: this is the first thing you should check for every patient that comes in, independently of their age or condition.
What is vitamin B12 and how is it absorbed?
B12 or cobalamin is a large molecule whose central atom is cobalt, and around which are arranged various other compounds. To be active in the body, the cobalamin molecule must be in one of two enzyme forms: methylcobalamin or adenosylcobalamin, both of which must be in a charge state of +1. Even though cobalamin can exist in two other charge states, +2 and +3, neither of these is bio-active. Its most powerful antagonist is nitrous oxide (N2O; laughing gas), which continues to be commonly used as an anaesthetic agent during surgical operations, because it inactivates the molecule by modifying the cobalt ion from a charge state of +1 to one of either +2 or even +3.
Cobalamin is produced in the gut of animals by specific bacteria that make part of the intestinal flora. Although this can also be true for humans, we have mostly relied on animals both by eating them and products derived from them, like eggs and dairy. In animal foods, cobalamin is always bound to protein from which it needs to be separated in order to be used. This, in turn, can only be done starting in the highly acidic environment of a well functioning stomach that secretes enough hydrochloric acid, but also enough Intrinsic Factor and pepsin.
Cobalamin is carried into the duodenum—the first part of the small intestine—by salivary B12 receptors that are then broken down by pancreatic protease. This allows the free B12 to attach to Intrinsic Factor, and make its way to the ileum—the very last part of the small intestine—where it penetrates the mucosal wall for absorption. Finally, the free cobalamin latches onto the plasma transporter Protein Transcobalamin II whose function it is to carry it to the cells throughout the body. Any excess, unneeded at any given time, is carried to the liver where it is stored.
Where do we get B12?
That herbivores like sheep, goats and cows, which thrive when they eat only grass, do not suffer from B12 deficiency, but that most of us humans tend to (estimates from various large scale studies range between 40 and 80%), points to two key issues at the heart of this problem:
One, we have evolved and survived as a species over several million years by eating animals. It is believed by some that it was, in fact, the very eating of animal foods, maybe specifically bone marrow, which was, on the one hand, the only left overs after carnivore predators like lions, and then all other scavengers but predators for us like wolves and jackals had eaten all they could, and on the other, the only thing that only humans could get to by breaking apart the bones, that allowed the brain to grow in size over a relatively short evolutionary period, seting us apart from our our primate ancestors and cousins. Whatever the case may be, the organism of the human species as a whole grew accustomed and became reliant on an external supply of vitamin B12 from animal sources.
Two, it is most certainly the case that even with the healthiest, let’s even say ideal or perfect intestinal flora, as humans we will definitely have a very different flora than those of the herbivore animals we domesticated, and it will arguably always be much less capable and much less efficient at producing cobalamin from any of the plant foods we do eat. Moreover, if B12 is manufactured by some of the bacteria in our perfectly healthy colon—the large intestine, it will still not easily make it into circulation because, as we saw, absorption of cobalamin takes place in the ileum in the last part of the small intestine, which is upstream from the large intestine. The manufactured B12 would somehow have to migrate backwards from the colon to the ileum, a most likely very difficult thing to do.
The first point is supported by ample archeological, anthropological, as well as evolutionary biological evidence. In fact, it turns out that our hominid ancestors have most certainly lived for the bulk of our evolutionary history during periods of glaciation where the land over most of the Earth’s surface was covered in ice. This implies that there was a marked absence of plant life in most places on Earth, and therefore an absolute reliance on animals for survival, eating virtually only animals, which in turn also ate virtually only other animals and fish, which ate smaller fish, and on down the food chain to those feeding on sea-borne plant foods. The Inuits, who basically live on whale blubber, are the perfect example of such a scenario. But this could well have been the scenario for a lot of the humans that populated the Earth, and for a good portion of our history spanning the last 2.5 million years.
The second is hypothetical, but on firm footing given that it is indisputable that the gut flora of a herbivore will be different—substantially different—from ours, but also that we simply cannot survive for very long on greens alone as do sheep, goats, cows and all other herbivores. Furthermore, in actual fact, most humans have a dysfunctional digestive system, with heavily compromised and impaired intestinal flora. As a consequence, even those who eat adequate or even large amounts of B12-rich animal foods, usually cannot benefit from it because the cobalamin simply doesn’t make it into the bloodstream for any one of several possible impediments along the ingestion-breakdown-absorption chain.
This is not to say that our digestive flora cannot produce some B12 from plant-based foods, but the evidence shows us that it definitely cannot produce enough, whatever the reason: studies have shown that although B12 deficiency is of the order of 40% in the general omnivore population, it is 50% in vegetarians, and up to a staggering 80% in long-term vegans (see Chapter 6 of Could it be B12? and references therein).
Why is B12 deficiency such a big deal?
Well, let’s ask another question instead: What would happen if the myelin sheath that covers the nerves in our body—peripheral, spinal and brain—were to deteriorate?
Neurological symptoms would include: numbness, tingling and burning sensations in the hands, fingers, wrists, legs, feet, or truncal areas; Parkinson-like tremors and trembling; muscles weakness, paraesthesia and paralysis; pain, fatique and debility labelled as chronic fatique syndrome; shaky legs, unsteadiness; dizziness, loss of balance; weakness of extremities, clumsiness, twitching, muscle cramps, lateral and multiple sclerosis-like symptoms; visual disturbances, partial loss of vision or blindness. But the list goes on.
Psychiatric symptoms? Confusion and disorientation, memory loss, depression, suicidal tendencies, dementia, Alzheimer’s, delirium, mania, anxiety, paranoia, irritability, restlessness, manic depression, personality changes, emotional instability, apathy, indifference, inappropriate sexual behaviour, delusions, hallucinations, violent or aggressive behaviour, hysteria, schizophrenia-like symptoms, sleep disturbances, insomnia. And here again, the list goes on.
At the cellular level, every cell would be unable to adequately produce energy, be it from glucose or from fat. We can easily extrapolate and imagine what it would mean for the organism as a whole to have a lack of, or severe debility in the energy available to it at the cellular level, and this, for the trillions of cells throughout. This would have a most profound effect on everything that we do, and everything that the body does throughout the day and night.
Now consider a yet deeper level: in the nucleus of every cell, where genes are protected and cared for, a problem in the very transcription and replication of genes—these delicate operations that are necessary and vital for the continual renewal, repair and reproduction of cells—which must and do take place throughout our life, this long succession of infinitesimal instants the perception of which is almost universally absent from consciousness, but for which the timescale is, in fact, very long at the cellular level, where movements and interactions take place at phenomenal speeds. Vitamin B12 is absolutely essential for this too. And if it’s missing? Unintended, unplanned, and unwanted genetic mutations from errors in transcription. This means problems; very serious problems.
Who should be concerned about all this?
The short answer is: everyone. This means you, but also your kids as well as your parents. It means infants, toddlers, children, teenagers, young adults, mature adults, the middle aged, the elderly, and the oldest among us: absolutely everyone.
For the longer answer, it would appear to be the case that we are, or at least should be, born with a good B12 reserve, and that, as it is used over time, the amount in the body and blood slowly decreases as the reserves get used up and eventually depleted. Some consider this to be the normal state of affairs. This inevitably implies that those at greatest risk of suffering from B12 deficiency are the oldest, and also that the older we get, the greater our chances of becoming victims of the effects of this deficiency. And this is indeed what we find: practically everyone above the age of 60 is B12 deficient, and more often than not, severely deficient (serum B12 < 200 pg/ml).
It is therefore not really surprising that every single behavioural characteristic—intellectual, psychological, emotional, physiological and physical—associated with ageing and its multiple manifestations in the elderly, senior moments in all their different forms: memory problems, disorientation, inability to concentrate or even pay attention, frailty, weakness, unsteadiness, loss of balance, etc, etc, are all typical symptoms of B12 deficiency.
Could it be that all these characteristics of old age are actually the characteristics of B12 deficiency? Could it be that if we didn’t let B12 levels drop below 600 pg/ml and actively maintained them around 1000 pg/ml throughout life, that seniors would simply not manifest any of these signs of old age? Maybe. Maybe even most probably. What an entirely different world it would be: strong and healthy, energetic and vibrant, sharp and alert old people. Sounds great, doesn’t it? And hard to imagine, isn’t it? But wouldn’t that be wonderful, for everyone, and especially for the elderly themselves?
As alluded to a moment ago, we should be born with a large B12 reserve. It is of particular importance that we need to have a plentiful supply of B12 throughout our development in the womb, during infancy, and up to the 7 years of age. Why is it so important? Because our nervous system develops fastest while we are in our mother’s womb, and then during infancy and as a toddler, until it reaches maturity by the time we are about 7, and because cobalamin is essential for this development.
The complication, however, a point of crucial importance, is that only B12 consumed by the pregnant mother at first, the breast-feeding mother afterwards, and finally by the toddler can be used to ensure an optimal development and building of a healthy brain and nervous system. Even if the mother had good B12 levels before, during and following pregnancy, only fresh B12 can be used in the developing child. So, if she doesn’t consume much or any during this critical period, the unborn child and infant will have only a meagre or non-existent supply of cobalamin, and consequently, impaired—often severely—brain and nervous system development.
This is a very serious matter. In fact, for many infants, it is a matter of life or death. Or just barely less dramatic but maybe even worse in some respects, it can make the difference between a normally healthy brain and nervous system, and permanent developmental disability, both physical and intellectual, right down to a full or partial vegetative state for a whole lifetime.
All of this shows why B12 deficiency tends to be not only transmitted, but to worsen in severity from one generation to the next, with all the negative consequences that come with it, but most notably those that affect the brain and all cognitive functions. Terribly sad and unfortunate as it is, numerous studies and reports on the babies of vegetarian but especially vegan and macrobiotic mothers have shown very serious neurological problems, developmental delays as severe as stunted brain growth and death, but also that even mild deficiencies in infancy are associated with seriously impaired cognitive performance in adolescence and adulthood. I cannot stress this enough: B12 deficiency is really very serious.
Now, between the oldest and the youngest there is everyone else. If we are born with an excellent B12 status, then we are lucky and likely to be able to make it to old age without any apparent problems in this regard. If we are born B12-deficient, then we are most certainly likely to suffer from it greatly, and this, much sooner than later. And if we are born with anything in between, an intermediately good or bad B12 status, then problems will appear later in life, or sooner, depending on many other factors, but most importantly on how much cobalamin we consume, and how well it is absorbed. Consequently, manifestations of cobalamin deficiency can appear at the age of a few months or a few years; as a child or teenager; as a young adult or person in their prime; near retirement or in old age; or it may also never become apparent. Unfortunately, this condition is continuously growing in importance, the people it affects growing in number, and the reported cases growing in severity.
Unfortunately, and extremely sadly for way too many people whose bodies, minds and lives are destroyed by an undiagnosed deficiency, B12 is not something that doctors routinely check or know much about. Most of them believe that it will appear in the total blood count (TBC) panel either as enlarged (megaloblastic anaemia) or fewer red blood cells (pernicious anaemia). But by the time you get there, you have been suffering the ravages of B12 deficiency for a while already, and have thus almost certainly also already suffered permanent neurological damage. So, for your sake, don’t wait for your doctor to notice this. Instead, teach them about it. You will be doing them and their patients an immense favour.
Closing with the good news
It is really easy to prevent and avoid becoming cobalamin deficient, but also to correct a deficiency that exists or even one that has persisted for several years or decades, no matter if you eat animal products or not, want to or not, think that you should or not. We must, very simply, check our B12 status regularly by measuring three markers—serum B12, plasma homocysteine (Hcy), and urinary methyl-malonic acid (MMA)—and make sure to supplement in order to raise and maintain B12 levels in the range between 600 and 2000 pg/ml, with concentrations of Hcy and MMA as low as possible. Pregnant and nursing mothers should maintain levels above 1000 pg/ml to ensure healthy nervous system development in their children.
(Both Hcy and MMA are toxic byproducts of protein metabolism that must be converted to benign and/or useable forms, the animo acid methionine, for example, by the action of B6, folic acid (B9) and especially B12. Here is a good information-dense compilation of B12/Hcy/MMA publications, and transcript of an interview with John Dommisse, a psychiatrist and B12 expert, who published the above quoted serum B12 range as optimal in this authoritative paper cited in Could it be B12? where I read about it.)
Supplementation should be with methylcobalamin—not cyanocobalamin—and should be as aggressive as needed depending on the result of the assessment. In cases where B12 levels are below 200 pg/ml, we should request methylcobalamin injections to be administered daily for 5-6 days, and then weekly until B12 reaches 2000 pg/ml. It should be maintained there at least until Hcy and urinary MMA have dropped significantly, and then monitored and maintained around 1000 pg/ml.
For anything else between 200 and 600 pg/ml and/or elevated Hcy or MMA, methylcobalamin patches are an effective way to get B12 levels up. In addition, oral supplementation, although the least effective of the three, still works surprisingly well compared to other supplements, and obviously cannot possibly hurt; it can only help. I recommend doing both patches and oral supplements until levels are around 1000 pg/ml, and then maintaining them with either one.
Finally, and very important to know is that you cannot overdose on methylcobalamin B12: not one negative physiological side effect has been reported or is known from methylcobalamin supplementation. You cannot do yourself or anyone any harm by taking B12 as methylcobalamin in large quantities for a long time; you can only do yourself and others harm by allowing a deficiency, as mild as it may be, to develop or linger. This applies to everyone.
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