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The Cobalamin Enigma

Cobalamin is usually found in one of two biologically active forms: methycobalamin and adocobalamin. Most prokaryotes, as well as animals, have cobalamin-dependent enzymes, whereas plants and fungi do not appear to use it.

In this chapter, we are going to further examine cobalamin’s role in our investigation of the human genome, but please bear with me, as we need to get a bit more technical at this juncture.

Cobalamin, also known as vitamin B12, is a micronutrient that is synthesized only by microorganisms yet is an essential nutrient in human metabolism. Genetic diseases of vitamin B₁₂ use constitute an important fraction of inherited newborn disease.

Vitamin B₁₂ is a large organometallic molecule, 1,300 to 1,500 daltons in size, and is the most chemically complex vitamin known. The focal point of vitamin B₁₂ is the central cobalt atom.

The fact that only prokaryotes (bacteria) have the ability to synthesize cobalamin implies that all of the vitamin B₁₂ found in algae, and indeed animals, must originally have been produced by bacteria.

Cobalamin is a structurally complex cofactor. It is usually found in one of two biologically active forms: methylcobalamin and adocobalamin, and it is the only vitamin that contains a metal atom.

Scientists consider it an ultratrace metal since it composes but 0.0029 percent of Earth’s crust.

To function as a cofactor, B₁₂ must be metabolized through a complex pathway that modifies its structure and takes it through subcellular compartments of the cell. As we shall see, this fact poses several striking problems for the theory that life began and evolved on Earth only.

As noted in the epigraph at the beginning of the chapter, “Most prokaryotes, as well as animals, have cobalamin-dependent enzymes, whereas plants and fungi do not appear to use it” (italics added). In bacteria and archaea (microorganisms similar to bacteria), these enzymes include methionine synthase, ribonucleotide reductase, glutamate, and methylmalonyl-CoA mutases.

In mammals, cobalamin is obtained through the diet and is required for methionine synthase and methylmalonyl-CoA mutase. This is because plants contain Me and Mh, whereas humans only have M.¹

The fact that this trace element is necessary for proper enzymatic function in animals yet does not exist in plants presents several enigmas. If life began and evolved on Earth, then why did “evolution” select cobalt, a rare element, to play such a pivotal role in animal metabolism?

Would not iron, which is plentifully available on Earth, have better played this key metabolic role?

The chemical element cobalt, which plays a key role in cobalamin synthesis, does not exist in a free state and is found naturally only in a chemically combined form, usually in association with nickel deposits.

It appears that cobalamin (B₁₂) is the most critical ultratrace element in the human body. One could argue that its crucial role in human metabolism strongly suggests that its association with the chromosome 2 fusion site represents a deliberate insertion. (We shall examine this shortly.)

Cobalt is the active center of the cobalamin coenzymes, the most common example of which is vitamin B₁₂. As such it is an essential trace dietary mineral for all animals. Since animals, including humans, need cobalamin to survive—it is vital to red blood cell production and nerve and brain function—it represents a curious choice to become the base for such an important metabolic role.

Bacteria in the guts of ruminant animals convert cobalt salts into vitamin B₁₂. Nonruminant herbivores produce vitamin B₁₂ from bacteria in their colons, which also synthesize the vitamin from simple cobalt salts.

However, the vitamin cannot be absorbed from their colons; therefore, nonruminants must ingest feces to obtain the nutrient. If you’ve ever wondered why your dog eats poop, there you have the real reason.

It seems a strange anomaly for natural selection to have taken this circuitous metabolic pathway. Since the majority of large animals are herbivores or ruminants, one would think that nature would have based the pathway on elements in the plant kingdom.

The rarity of cobalt in Earth’s crust and oceans and the fact that plants do not depend on it or provide it to plant-eating animals poses a challenge to Darwinian evolution.

The vitamin B₁₂ synthesized in the rumen and by bacteria in the colon is one of the most complex nonpolymeric natural products produced in nature. Then why did animals evolve such a complicated metabolism, based on an ultratrace element in short supply?

Once again, evolution is supposed to proceed by conserving energy and materials through the simplification of processes.

Animals that do not get vitamin B₁₂ from their own gastrointestinal bacteria or that of other animals must obtain the vitamin premade in other animal products in their diet, and they cannot benefit from ingesting simple cobalt salts.

That includes predators as well as human beings.

As noted, in the wild, ingestion of feces is common among monogastric animals. Many of the B vitamins, including B12, are synthesized as a result of bacterial fermentation in the large intestine, but B₁₂ is excreted because it must be bound by an intrinsic factor produced in the stomach before it can be absorbed.

Studies have shown that when ruminants, such as cattle, are on a cobalt-deficient diet, there is a gradual loss of appetite, weight loss, muscle wasting, depraved appetite, anemia, and eventually death.² The animals appear as if they have been starved, the visible mucous membranes are blanched, and the skin is pale and fragile. Very similar symptoms occur in people with B₁₂ deficiency.

Cobalt deprivation in ruminants leads to a vitamin B₁₂ deficiency that can be corrected with cobalt supplementation because these animals have the right gut bacteria to break the salts down.

However, human beings and monogastric animals lack this ability. We have to eat animal products or take B₁₂ supplements.

The underlying mystery: Why did the cobalt pathway occur in the most primitive organisms and then skip the higher plants, to reappear again in complex animals?

Equally as enigmatic: Why are there so many animal species that require cobalamin to trigger needed enzymes, yet their gastrointestinal systems are ill-equipped to obtain it?

Just as baffling is the fact that some sea algae have what is called cobalamin acquisition protein 1 (CBA1). This is a special protein that these species of sea algae use to grab cobalamin (B12) from the ocean water and ingest it, similar to the way a sponge soaks up fluids.

The next question: Why do animals, including humans, lack this lifesaving mechanism, which confers an obvious survival advantage? If evolution originally took place on Earth, as is assumed by evolutionists, and this mechanism developed in the earliest microorganisms, why was it not passed on to animals? This supports the theory of panspermia and exoplanet origins for life on Earth.

Instead of a simple pathway based on a readily available element, we find a byzantine pathway based on a rare element. It seems clear that sea algae got it right by grabbing vitamin B12, latching onto it, and escorting it through their digestive systems.

That way, they never had to risk suffering from B₁₂ deficiency. We do have that risk.

Common side effects of B₁₂ deficiency in humans include peripheral sensory neuropathy causing symptoms such as numbness, tingling, burning, and complete lack of sensation; chronic fatigue; anemia; low red blood cell count; and digestive disorders, to name the most prevalent.

It would seem that natural selection has monogastric animals skating on thin ice. Research has estimated that approximately 39 percent of the human population is vitamin B₁₂ deficient. Many people over age fifty lose the ability to absorb B₁₂ from foods.

This would indicate that B₁₂ deficiency may have acted as a factor that limited life spans in human history. In fact, it will do so more in the future as our soils become more depleted. Although the average level of cobalt in soils is 8 parts per million, there are soils with as little as 0.1 parts per million and others with as much as 70 parts per million.

Because the cofactors such as B₁₂ are complicated to synthesize and required in trace amounts only, it is possible that there is a selective advantage in dispensing with the need to produce them.

However, such mutations or gene inactivation can only have occurred if there was a reliable external supply of the cofactors in the environment. But there is no evidence to suggest that Earth ever provided a reliable, sufficient source of cobalamin.

As we saw above, cobalamin is an ultratrace element in short supply. In addition, only very minuscule amounts of this vitamin were ever present in natural waters.

David W. Menzel and Jane P. Spaeth reported that moderate diatom blooms occurred in the Sargasso Sea when cobalamin concentrations were at their highest, and several other studies have shown a link between algal productivity and vitamin B₁₂ concentrations.

Taken together, the foregoing suggests that the cobalamin metabolic pathway is more likely to have evolved on a cobalt-rich planet. I have other reasons to suspect that this may, in fact, have been the case.

CONCLUSION

The crucial role that the trace mineral cobalamin plays in human metabolism is anomalous. Why natural selection would create a complex pathway that depends on a difficult to obtain substance that is often in short supply does not fit the Darwinian model.

It suggests that the origin of this B₁₂ dependency was not Earth but a cobalamin-rich planet. As various researchers have suggested, the most primitive life-forms seemed to have arrived on Earth fully formed. These early organisms already had the ability to synthetize cobalamin and molybdenum.