Beta-lapachone - stimulator of the 'Molecule of Youth'?
If I’ve learned nothing else over the last decade, it's that that staying healthy is 100% dependent on what goes on as far downstream as you can get, specifically the body’s cellular level, and the all-important cellular mitochondria.
I’m sure every horse owner out there wants their horse to live as long a life as possible, and above all, comfortable with it, well into their senior years. So, to have affirmation that certain plant substances can profoundly affect mitochondrial health, especially in our health-wrecking polluted environment of today, is great news to hear.
Wouldn’t life be simple if we could simply chuck a spoonful of eternal life into the feedbowl? Something to not only protect our horses’ cellular matrix from life's pollutants but also create a state of healthy cellular regeneration to ensure a lovely long life for our best friend? Oh yes …
Well, there is. But first, you’ve got to indulge me because … it’s Science-Time! Introducing a science-y word - Nicotinamide adenine dinucleotide, aka NAD+ (much easier to remember). NAD+ is a coenzyme found in all living cells, and it’s a really important coenzyme because … it’s nicknamed the ‘Molecule of Youth’, and here’s why.
As a body ages, the cellular mitochondria become progressively more damaged through oxidative stresses, which naturally causes age-related decline of NAD+. Which is fair enough – the body’s aging, after all, and pretty much everything starts to decline.
Thing is, NAD+ is actually essential for fuelling two master regulators of aging – who knew there was something to regulate aging?! So now meet another science-y word for these regulators - ‘Sirtuins’, and specifically SIRT1 and SIRT3.
SIRT1 and SIRT3 are proteins that require NAD+ to function, and importantly, all three are needed to effectively trigger the formation, and optimal functioning, of new mitochondria.
So, back to that aging body where levels of NAD+ are dropping, sirtuin activity is declining as well, so we’ve got less effective cellular signaling, which leads to mitochondrial dysfunction. With me so far?
Now to the research, and a recent study has shown that a plant substance called beta-lapachone powerfully increases NAD+. Handily, beta-lapachone just happens to be a major constituent in one of my favourite herbs which I already use extensively as an effective antibacterial, i.e. for our horses afflicted with Uveitis - our EyeTonic - and wherever a hefty dose of natural antimicrobial (bacterial and virus) support is needed - our BioCARE; basically where there's bacteria, there's beta-lapachone. And where there's beta-lapachone, there's the amazing amazonian tree, Pau D'Arco (Tabebuia impeteginosa), which just happens to be a rather stunningly spectacular tree to look at as well.
*Animal testing alert - Scientists added beta-lapachone from Pau d’Arco bark into the diet of one group of mice, where it restored a high ratio of NAD+ to (get ready for another science word) NADH, a cofactor that plays a key role in the production of energy. High levels of NAD+ (relative to NAHD) are needed for DNA repair and the activation of SIRT1. With no other changes in either activity level or food, the following effects were noted, compared to the non-Pau D’Arco fed group:
As if this wasn’t good enough news, now let’s bring in White Willow (Salix alba), with another study showing its longevity effects on yeast, specifically Saccharomyces cerevisiae.
Saccharomyces cells are often used in longevity studies because they act much like mammalian cells, in that they age and die in a similar manner.
Cultivated in 2% glucose, scientists isolated six new groups of molecules that slow down the chronological aging of yeast. The most effective was extract of white willow, which was shown to increase the average lifespan of the yeast by an astonishing 475%, as well as the maximum chronological lifespan by 369%; in other words, nearly a 5-fold extension in lifespan for this yeast, which apparently makes it the most potent longevity-extending intervention ever described in scientific literature.
So what is it about white willow bark that enables it to achieve such dramatic results, and more importantly, could willow boost mitochondrial numbers?
Here’s what happens when willow bark’s ingested. The liver metabolises its major constituent – salicin – into salicylic acid (the same substance created in the body from Aspirin). Science has learned that salicylic acid may promote the production of new mitochondria in the body’s cells by turning on SIRT1, the master regulator protein we talked about earlier.
A recent study with liver cells found that salicylic acid increased the total concentration of mitochondria by up to 2-3 times, which implies that the salicin in the willow bark has mitochondrial-stimulating effects once it’s converted to salicylic acid in the liver. Result!
Equally, another potential benefit of willow bark, and very relevant to the equine diet – salicin may help control iron levels in the body, although as yet I’ve not been able to get my hands on this study.
Of course we want our horses to live a full and comfortable life, and we know that to do so largely depends on healthy, functioning mitochondria in the body’s cells, especially in those high-energy demanding organs like the heart, brain, nervous system, kidneys, liver and muscles. This is why we now include Pau D’Arco and Willow collectively in our SeniorTonic.