Is science on the cusp of changing the future of disease prevention via a deeper understanding of an individual’s biology at a molecular level?
Is science on the cusp of changing the future of disease prevention via a deeper understanding of an individual’s biology at a molecular level?
Imagine a world where we live to 130, 150 or 500 years old. Anti-aging pioneer, Dr. Aubrey de Grey, joins us to share his confidence in how technology will dramatically extend human lifespan. He joins our host, Heather Sandison, ND, to look at aging as a problem to be solved. In this episode, Dr. Aubrey de Grey offers hope to people looking for cutting-edge therapies to live longer.
In September-October 2018, a 3-week sample of Qualia Life (formerly called Eternus) was sent to volunteers. Volunteers were selected to include a mix of people who were and were not currently taking Qualia Mind. No information was given on what product was intended to do, ingredients contained in the product, or expected responses. Instructions were to take 8 capsules with breakfast 5 days a week, with 2 off days, for 3 weeks. All participants were asked to complete a survey questionnaire after 5 days, 2 weeks, and 3 weeks. Seventy-one persons completed the 3 weeks of supplementation and provided responses to the survey.
In 1958, Jack Preiss and Philip Handler published a scientific paper describing how NAD+ was made from niacin in three steps.(1) This pathway was later named the Preiss-Handler pathway after the co-discoverers. It describes the enzyme steps needed to convert niacin into the NAD+ molecule.
In this article, we’re going to introduce an indirect way of supporting NAD+. Rather than making more, this article will be teaching you about using less. Using less requires downregulating a protein called cluster of differentiation 38 (CD38 for short). When CD38 is not as active, less NAD+ is used by it. The result is higher NAD+ levels and greater NAD+ availability for important healthy aging uses.
The NAD+ form of the molecule is required for certain cellular signaling reactions that change the way cells behave. Unlike redox, where the molecule is conserved, the NAD+ molecule is broken apart or “consumed” when used for signaling. It’s these NAD+ consumption uses that have been a main reason for the resurgence of scientific interest in strategies to boost NAD+.
L-tryptophan is an essential amino acid. This means the body cannot synthesize it: it must be obtained from the diet. It’s been known for decades that L-tryptophan has niacin equivalent activity in the body (i.e., we can make NAD+ molecules from it). L-tryptophan is unique because it’s the only way to build NAD+ that doesn’t start from vitamin B3. It does this by a de novo synthesis pathway, which creates a niacin molecule through a series of biological reactions. So, L-tryptophan’s inclusion would seem to be a natural fit in a formulation that wants to support boosting NAD+.
The salvage pathway is used to produce NAD+ from nicotinamide molecules. Whether the source of the nicotinamide is vitamin B3 (as niacinamide), newer nicotinamides (e.g., nicotinamide riboside [NR], nicotinamide mononucleotide [NMN]), or molecules in food that get broken down during digestion into nicotinamide, the salvage pathway turns them into NAD+ in our tissues.
Most organisms have several alternatives for producing the NAD+ molecule. In humans, there are three major NAD+ biosynthesis pathways: the De Novo Pathway, starting from the essential amino acid L-tryptophan; the Preiss-Handler pathway, using niacin (nicotinic acid); and the Salvage Pathway from niacinamide (nicotinamide). In this article, we’ll be covering the De Novo Pathway.