Week 28 of Changing to a youthful phenotype with broccoli sprouts

Did a little math to end this 28th week of eating a clinically relevant weight of microwaved broccoli sprouts every day:

  • I changed the title of weekly updates after Week 7 as a result of A rejuvenation therapy and sulforaphane. Numbers used from its study: “Rats were injected four times on alternate days for 8 days.”
  • Study numbers in Part 2 of Rejuvenation therapy and sulforaphane regarding the new human-rat relative biological age epigenetic clock: “The maximum lifespan for rats and humans were set to 3.8 years and 122.5 years, respectively.” I’m at a similar percentage of species maximum lifespan as were the study’s treated subjects.
  • A human-equivalent multiplication factor that can be applied to a rat post-development time period is 122.5 / 3.8 = 32.2. An 8-day rat treatment period ≈ 258 human days, and 258 / 7 ≈ 37 weeks.

To paraphrase the study’s lead laboratory researcher’s An environmental signaling paradigm of aging paper, aging is a programmed series of life stages. A body clock reset described there and subsequently experimentally tested changed 30 measurements to earlier life stages.

A reset may not require more than what I’ve been doing since the end of March. Maybe 28 weeks hasn’t been long enough to find out?

See the below discussion for a different point of view. I don’t think relative rates of metabolism between species would be more accurate than other measures because of individual differences among humans.

A chart from Microwave broccoli seeds to create sulforaphane of 10 people’s metabolisms after ingesting 200 μmol (35 mg) sulforaphane provides an example. Individual sulforaphane metabolites (DTC is dithiocarbamates) peak plasma measurements ranged from 0.359 μmol to 2.032 μmol, > 500%.

sulforaphane peak plasma

So we’re patient.


9 thoughts on “Week 28 of Changing to a youthful phenotype with broccoli sprouts

  1. I question the percent of lifespan method of determining equivalent therapy times. Drugs don’t care how long you are going to live. It would seem to me that relative rates of metabolism would be more accurate.

    I have been looking for studies which would measure relative therapy times for years and haven’t found a single one. Perhaps someone can direct me to some.

    • Hi Wayne! Thanks for commenting.
      Yes, you’re probably right. The study’s new human-rat relative biological age clock hasn’t been used elsewhere yet.
      In the Part 2 link is a IL-6 biomarker comparison of similarities between this study and our model clinical trial. What do you think?
      Unlike either of those studies’ subjects, I haven’t stopped treatments. I might if I get enough confirmation that a life stage reset has been produced.

      • I probably didn’t make myself very clear. It does make sense to me to use percent of lifespan to correlate the RESULT of a therapy. However, how long the therapy needs to be applied to get comparable results is completely unanswered as far as I have been able to determine. But I’m guessing it is closer to metabolic rate than lifespan.

        • Yes, I agree. The value of lifespan comparisons would be in using the new human-rat relative epigenetic clock.
          With IL-6 we got a rough idea of how our model clinical trial’s daily consumption of 117 μmol glucoraphanin by eating raw broccoli sprouts compares with the unknown Elixir treatment. Results between the studies were similar in that:
          1. IL-6 levels improved during early treatments through rat Day 8 and human Day 70, respectively.
          2. IL-6 levels continued decreasing shortly after treatments for 7 days (through rat Day 15) and 20 days (through human Day 90), respectively.
          3. IL-6 levels rose after rat Day 15 and human Day 90, respectively, but were still significantly below Day 0 values at rat Day 95 and human Day 160.
          Maybe if the trial’s coauthors reanalyzed samples with the human-rat relative epigenetic clock the picture of therapy times would become clearer. Since the trial subjects only had four samples, a future paired study that used this clock could provide better clarity.

          • We shall see. Methinks continuous oral consumption of broccoli sprouts vs. 4 intravenous hits every other day of Elixir is not the best comparison.

          • I should add that one of the targets of the Elixir Is the same as that of sulforaphane – nrf3. If the dosage were known to be optimal, then comparisons would perhaps be illuminating. In any event, your comparisons seem to hint that relative metabolic rates would be closer to required therapy times than relative lifespan. How fast epigenetic changes to the ARE promotor are accomplished would seem to be helpful but will be some time in coming.

            I should also add that I am an old man with an old brain (79) who has never taken a course in biology. My suppositions should be judged in that context!

          • And finally? it might be useful to consider the comments of Akshay in Josh’s earlier blog on the Elixir. He reported that they first used herbal supplements in rats and did not see noticeable results until two months of treatment. I am not certain that the administration was oral, but I think it was because he referenced the problem of low bioavailability.

            I have been taking a concoction of herbal nrf2 activators for about 4 months and will get some lab results in a couple of weeks. IL-6 is not available to me, but I will have hsCRP and some CBC ratios related to inflammation. I’ll get back to you. How about via email?

              • First, I note a typo in an earlier comment. It should of course be nrf2 not nrf3.

                I think I will have to pass on your kind offer of a guest blog. The number of data points I could muster and the extent of the controls are somewhat limited. I’d be happy to relate what I can to you, but it certainly wouldn’t warrant a blog. Thanks nonetheless.

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