Vitamins
Boosting Mitochondrial Health with Folate, B12, and B6
B vitamins play a key role in maintaining healthy mitochondria and preventing age-related diseases.
Vitamins
B vitamins play a key role in maintaining healthy mitochondria and preventing age-related diseases.
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There's some sensational news. Well, what do I mean by "news"? edubily readers have known this for years:
Mitochondrial function can play an important role in serious diseases
We're talking about cardiovascular disease, neurodegeneration, and more. It shouldn't be surprising, because: Many—perhaps all—diseases share a common denominator: dysfunction in the cell's energy metabolism. In other words: tiny cellular power plants, the mitochondria, stop working properly.
The technical term for this is mitochondrial dysfunction. With advancing age, this affects virtually all of us. Starting around age 35, roughly half the population shows signs of it. You can see this because roughly half of adults in Western nations have mild, moderate, or severe insulin resistance.
Those in the know understand this: insulin resistance is almost certainly a sign of mitochondrial dysfunction in our largest energy consumer—the muscles. Conversely, we've long known that many "traditional peoples" don't suffer from our civilization diseases. That's partly because they maintain fit mitochondria throughout their lives. Our book explores this exact topic.
In any case, what you read above was actually a headline from an article in a scientific magazine discussing a study just published in the prestigious journal Science. It's groundbreaking, as it identifies a key reason why mitochondria, especially with advancing age, stop working properly.
Let's take a look:
Earlier studies showed that both SAM and cellular energy levels decline during aging. Our study suggests a connection between these two pathways, showing that low SAM levels can affect mitochondrial energy production.
Our findings indicate that mitochondrial function is sensitive to one-carbon cycle activity and benefits from adequate SAM levels.
OK, that sounds complicated. It's about something called methylation. Those familiar with it understand: methylation of, for example, target genes plays a crucial role in maintaining cell health. Methylation happens with the ultimate methyl donor SAM (S-Adenosylmethionine)—and that's what we're discussing here.
To keep producing enough SAM, we need adequate amounts of the amino acid methionine. But that's not all: the one-carbon cycle mentioned above (English: one-carbon metabolism) essentially consists of the folate and methionine cycles. The folate cycle, in turn, is fed by B12, B6, and folate.
For good methylation, we need at minimum adequate amounts of:
Back to the study: researchers found that this methylation plays a crucial role in maintaining mitochondrial health. Why? The authors explain:
Ouch. Simply because methylation isn't happening properly. By the way: how well you methylate can even be partially read from blood tests. If methylation isn't working right, a "waste product" builds up in the blood—so-called homocysteine. Unfortunately, it's a vascular toxin. So methylation deficiency doesn't just cause mitochondrial dysfunction—it also damages your blood vessels.
Since the one-carbon cycle depends strictly on, for example, methionine and B12 supply (as mentioned), studies from especially the 2000s repeatedly showed that vegans often unfortunately have too-high homocysteine levels. It's reasonable to assume that better awareness has led to better B12 supplementation among vegans today.
Still, this is relevant for everyone. Studies repeatedly show that a large portion of the population has elevated homocysteine levels and therefore almost certainly poor methylation. The consequences have been described extensively here. By the way, this is exactly why we recommend a good multivitamin. The especially bioavailable B12, B6, and folate forms in it provide nearly optimal amounts of these compounds for everyone.
"Our study has provided evidence that some modifications can be modulated through diet, but we need to investigate further whether we can change the pathological process for the better," says Anna Wredenberg. "So far we've only looked at protein modifications, but other molecules can also be modified by intra-mitochondrial SAM. We need to investigate these modifications to better understand the role it plays."
So there. More investigation needed. In the meantime, let's take action and make sure we get adequate amounts of the compounds mentioned here.
