My feelings about salivary telomere testing

I want to address salivary telomere testing directly. A company called TeloMe offered a salivary based telomere test and the marketing was getting traction in some health and longevity circles. The pitch sounded reasonable. Spit in a tube, learn your biological age, take action. The problem is that the underlying science does not support that pitch, and I think people are spending money on something that cannot deliver what is being promised.

Here is what I think you need to know before paying for any telomere test.

Saliva is not blood

The comparison to 23andMe genetic testing, which has been the entry point for a lot of consumer biology testing, is misleading. 23andMe measures genes. Genes are long, generally tens to hundreds of thousands of base pairs each, which makes them tolerant of the kind of DNA degradation that happens in saliva samples. Even when a sample is partially degraded, you can still read the variants you are looking for.

Telomeres are different. The average newborn telomere is around 10,000 base pairs. The average middle aged adult sits closer to 6,800 base pairs. These are short sequences in genomic terms, and they are far more vulnerable to misinterpretation when the sample DNA is partially degraded. Most consumers handling a salivary test kit are not forensic scientists. The collection, transport, and storage conditions degrade the sample to varying degrees. The measurement noise that introduces is not small.

Saliva also misses the white blood cell compartment that blood based telomere testing measures. If you care about immune senescence, which is one of the most clinically meaningful telomere related markers, salivary cells tell you nothing about it. Period.

Average length is not the useful number

Even if salivary measurement were technically clean, the metric most consumer telomere tests report is average telomere length. This is not the biologically meaningful number. Biological age and disease risk are driven by the percentage of critically short telomeres, not by the average.

I have seen multiple cases where two individuals had nearly identical average telomere lengths but radically different percentages of critically short telomeres. The clinical pictures were also radically different. An average length test would have called them equivalent. They were not.

The high resolution test that actually delivers this metric is the HT Q FISH assay developed in Maria Blasco’s lab. Run twice, a year apart, you can detect meaningful change. Average length tests, especially run from saliva, do not have the precision or reproducibility to do this.

The calorie restriction sidebar

The TeloMe marketing included claims that calorie restriction reliably extends life, presented as established science. This was already shaky when the marketing went out, and it has aged worse since. Calorie restriction extends life in some invertebrate models. The effect attenuates dramatically as you move up the mammalian ladder. The flagship monkey study at the National Institute on Aging did not show the lifespan extension predicted by the early mouse work. The recent reanalysis comparing the National Institute on Aging cohort to the Wisconsin cohort highlighted the role of the control diet quality, which had largely been ignored.

Maria Blasco’s lab has also tested calorie restriction directly against telomerase activation in mice. Calorie restriction did not extend lifespan in either wild type or telomerized mice in that work. Telomerase activation did. The cleaner conclusion is that telomerase intervention is currently the only broadly applicable approach to extending lifespan across mammalian species. Calorie restriction is a more specific intervention with narrower applicability than the popular framing suggests.

The mitochondrial theory of aging

The other framing in some consumer test marketing positions mitochondrial decline as the master driver of aging. This is also weaker than it sounds. The mitochondrial theory has been around since the 1950s and never fully delivered. The simplest counter argument is that primary mitochondrial diseases do not present with accelerated aging. Telomere disorders, the telomeropathies, do present with accelerated aging. The work of Joao Passos, Ron DePinho, and others over the last few years has clarified that short telomere length appears to control much of what we observe as mitochondrial decline, rather than the reverse. Mitochondria have too few of their own genes to plausibly orchestrate aging by themselves.

What to actually do

If you want telomere testing that will give you a number you can act on, the price points and the technologies vary significantly. As a general rule:

• Spit kits with low price points and average telomere length output are entertainment, not data. Save the money.
• Blood based percent critically short telomere tests from established labs are the higher cost option and are the only category I would currently spend my own money on for clinical decision making.
• Two tests run a year apart are much more useful than a single test. The trajectory tells you what the absolute value cannot.

And if you want to actually act on telomere maintenance, the only compound with human safety and efficacy data is TA-65. The rest of the supplement world has thrown the word telomere on bottles, but as of today, TA-65 is the one with the receipts.

Dr. Maria Blasco, one of the most accomplished telomere scientists working today, has stated publicly that there are food supplements, including TA-65, that activate telomerase and contribute to natural rejuvenation and life extension without driving cancer. That is a meaningful endorsement from a serious source.

— Doc