Are sulforaphane supplements better than microwaved broccoli sprouts?

Armando asked a good question in Upgrade your brain’s switchboard with broccoli sprouts:

“Is there any way to consume sulphorafane in a supplement form? Rather than have to jump so many hops to consume it from broccoli.”

The relevant 2017 study’s sulforaphane amount was:

“100 µmol [17.3 mg] sulforaphane as standardized broccoli sprout extract in the form of 2 gel capsules.”

One answer in A pair of broccoli sprout studies was No:

  • “Plasma and urinary levels of total SFN [sulforaphane] metabolites were ~3–5 times higher in sprout consumers compared to BSE [broccoli sprout extract] consumers.
  • In sprout consumers, plasma concentrations were 2.4-fold higher after consuming the second dose than after the first dose.
  • Calculated SFN bioavailability from broccoli sprouts exceeded 100%.”

That study was from 2015, though. Are better products than broccoli sprout extracts available now?


Image from the US Library of Congress

During Week 5 of Changing an inflammatory phenotype with broccoli sprouts, back in May when I still believed impossible things like we would:

I contacted a distributor of a dried broccoli sprout powder for evidence of their claim:

“Independent assays confirm that EnduraCELL yields more Sulforaphane per gram and per dose than any other broccoli sprout ingredient available! These assays showed that EnduraCell yields around 3.5 times more SULFORAPHANE than the next highest broccoli sprout product.”

I’ve asked three times for the lab assays. They declined each time to provide the data.

The company founder has written several reviews, one of which is entitled Sulforaphane and Other Nutrigenomic Nrf2 Activators: Can the Clinician’s Expectation Be Matched by the Reality? In Section 6.5 Sulforaphane it stated:

“By calculation, MYR [myrosinase]-active whole broccoli sprout supplement yielding 1% SFN could deliver 10 mg SFN per gram of powder, corresponding to ~12 grams of fresh broccoli sprouts (dried powder retains ~8% moisture).

The 2017 study’s dosage of “100 µmol [17.3 mg] sulforaphane as standardized broccoli sprout extract” weighed a gram or less, for a 1.73% sulforaphane yield. A broccoli sprout powder that could deliver “3.5 times” may have a 3.5 x 1.73% = 6.1% sulforaphane yield.

Using worst-case calculations from Estimating daily consumption of broccoli sprout compounds and Our model clinical trial for Changing to a youthful phenotype with broccoli sprouts, I eat at least 76 grams of 3-day-old broccoli sprouts daily. That would be 76 g / 12 = 6.3 grams of a “whole broccoli sprout supplement yielding 1% SFN” or ≈ 1 gram of a powder yielding 6.1% sulforaphane.

I immerse 3-day-old broccoli sprouts in 100 ml distilled water, then microwave them on 1000W full power for 35 seconds to achieve up to but not exceeding 60°C (140°F) per Microwave broccoli to increase sulforaphane levels. Worst-case estimates are 21 mg sulforaphane without microwaving and 30 mg sulforaphane with microwaving. The equivalent weight of a broccoli sprout powder yielding 6.1% sulforaphane for the worst case of microwaved broccoli sprouts is (30 mg / 21 mg) x 1 g powder = 1.4 grams of powder.

This 30 mg / 21 mg worst-case ratio could also be used to calculate a best case. If it’s true that:

  1. “Whole broccoli sprout supplement yielding 1% SFN could deliver 10 mg SFN per gram of powder” and
  2. The equivalent weight of microwaved broccoli sprouts is at least (30 mg / 21 mg) x 1 g powder = 1.4 grams of a broccoli sprout powder yielding 6.1% sulforaphane,

then my daily sulforaphane dosage is at least 10 mg x 6.1 x 1.4 = 85 mg.


My answer to Armando’s question would be No for sulforaphane supplements. I’d consider a whole broccoli sprout powder after lab assays were personally verified.

Week 10 of Changing to a youthful phenotype with broccoli sprouts

To follow up Week 9 of Changing to a youthful phenotype with broccoli sprouts:

1. I increased three of eight upper body exercises by 50% through adding another set. I did it because I didn’t feel muscle exhaustion after two sets like I’d previously felt. 🙂

Cognitively, see A claim of improved cognitive function and its follow on Upgrade your brain’s switchboard with broccoli sprouts.

2. It’s been inspirational at times, and at other times, dull, duller, dullest, to do what’s necessary and keep on track. But the efforts paid off when Week 9 was unlike any previous week!

I expressed appreciation in Our model clinical trial for Changing to a youthful phenotype with broccoli sprouts because scientific evidence provides great bases for intentional behavior. It’s still up to me to voluntarily carry out my part. And why wouldn’t I act when my healthspan and lifespan are the consequences? Except…

What if I’d been:

  • Tired of the hassle, or bored with self-imposed discipline, or lazy, and quit?
  • Projecting personal problems onto others, such that improving my present and future became less important than act-outs?
  • Distracted by, or believed propaganda, or participated in Madness of Crowds behavioral contagion, and missed day after day of required actions?

I may not have ever experienced Week 9’s intermediate-term benefits!

If I keep going past ten weeks, what long-term benefits could be expected?

Our model clinical trial didn’t say how researchers decided on a ten-week period for subjects to consume broccoli sprouts every day. I asked a study coauthor about trial duration, but no answer yet.

A few of the same coauthors answered generally in Reviewing clinical trials of broccoli sprouts and their compounds:

Biomarkers of effect are early stage end-points, for instance the modulation of phase 2 enzymes by glucosinolates. They need more time than biomarkers of exposure to be influenced by the dietary treatment.

Hence, length or duration of the study must be defined according to the biomarker measured to be modified, that is, to define perfectly the time of exposure to observe changes in relevant parameters. Gene expression is one important target for glucosinolates, and it requires a sufficient period of exposure to (de)activate signaling pathways involved.

It is crucial to find appropriate biomarkers of effect that are linked to later disease outcomes, and more investigation is needed in this sense. Post-study follow-up can be of great value in assessing the persistence of certain effects, or in discovering those that appear more long-term.

3. I’ll go into a clinic on Sunday for Day 70 truth tests. Here they are: Day 70 results from Changing to a youthful phenotype with broccoli sprouts!

Upgrade your brain’s switchboard with broccoli sprouts

Further investigating A claim of improved cognitive function, Part 3 of Rejuvenation therapy and sulforaphane offered:

“Improving brain function does not depend on neurogenesis as much as it does on synapse formation and factors such as NMDA receptors which decline in density with age.”

A PubMed “sulforaphane NMDA receptors” search turned up a 2019 cell study The glutathione cycle shapes synaptic glutamate activity:

Sulforaphane is a potent inducer of the Nrf2 transcription factor, has blood–brain barrier penetration, and might expand the size of the glutathione reservoir by our observation that it increases expression of GCL [glutamate cysteine ligase], the rate-limiting step in glutathione biogenesis. Our recent study in human subjects revealed that sulforaphane elevates peripheral glutathione levels and those of other brain metabolites.”

The referenced study was a 2017 Sulforaphane Augments Glutathione and Influences Brain Metabolites in Human Subjects: A Clinical Pilot Study:

“We found that the naturally occurring isothiocyanate sulforaphane increased blood GSH [reduced glutathione] levels in healthy human subjects following 7 days of daily oral administration. In parallel, we explored the potential influence of sulforaphane on brain GSH levels in the anterior cingulate cortex, hippocampus, and thalamus via 7-T magnetic resonance spectroscopy.

A significant positive correlation between blood and thalamic GSH post- and pre-sulforaphane treatment ratios was observed, in addition to a consistent increase in brain GSH levels in response to treatment. The sulforaphane response in brain GSH levels is not influenced by age, sex, or race.

The participants were given 100 µmol sulforaphane as standardized broccoli sprout extract in the form of 2 gel capsules, and instructed to ingest the extract each morning for 1 week.

Following sulforaphane administration, the increase in blood GSH was positively correlated with GABA, Gln [glutamine], Glu [glutamate], and GSH in the THAL [thalamus]. Although these correlations were not significant following multiple comparison, they remain suggestive. Power analysis calculations suggest that a sample size of n = 50 would yield a significant result, and this will be the focus of a future study.

As has been reported for cardiovascular and cerebrovascular diseases, longer treatment duration and/or higher dosages may be warranted. In a submitted study, we will report that peripheral GSH levels may be correlated with cognitive functions.”


One week of consuming sulforaphane wasn’t long enough to achieve much. Not enough subjects and “higher dosages may be warranted” were also thrown in to explain the lack of significant results.

Sulforaphane: Its “Coming of Age” as a Clinically Relevant Nutraceutical in the Prevention and Treatment of Chronic Disease estimated the “100 µmol sulforaphane” dosage to be 17.3 mg. Worst-case estimates made in Estimating daily consumption of broccoli sprout compounds are that since doubling the starting amount of broccoli seeds from one to two tablespoons in Week 6, I’ve consumed 30 mg sulforaphane with microwaving 3-day-old broccoli sprouts every day.

Something happened where the promised “In a submitted study, we will report that peripheral GSH levels may be correlated with cognitive functions” either wasn’t performed or wasn’t published. The follow-on 2019 study became a cell study instead of a 50+ person study.


The study’s thalamus findings provided plausible explanations for why eating a clinically relevant amount of broccoli sprouts every day since at least Week 6, Week 9 was so much different from the others. Sulforaphane changed a blood antioxidant which may have changed four thalamus metabolites.

The thalamus part of our brain is analogous to a switchboard. Signals pass through it to and from other brain areas.

Signals can be routed better when we clean up and upgrade wiring, and lower circuit resistance.

A claim of improved cognitive function

I’ll describe evidence for claiming improved cognitive function in Week 9 of Changing to a youthful phenotype with broccoli sprouts.

I read parts of over a hundred research papers last week. That required substantial concentration to understand them, and stay on topic while learning new items, which started new searches. This wasn’t a new development, it was just to a much greater extent. I also worked forty hours for my job.

The main chain of blog posts began when I relooked at the presentation in Reversal of aging and immunosenescent trends after remembering it included before and after photos per A hair color anecdote. The presentation prompted last week’s most frequent self-question, Why didn’t I see this before?

One possible explanation is that people don’t usually see things outside their conditioned perceptions. (1) Reevaluate findings in another paradigm illustrated this with an example of how different frameworks viewed the same hypothalamus study differently.

I was interested to see what sulforaphane research had in common with the presentation topics, which produced (2) Reversal of aging and immunosenescent trends with sulforaphane. That required gaining a better understanding of PubMed search techniques, which led to (3) A pair of broccoli sprout studies.

Numerous presentation topics resulted in (4) Part 2 of Reversal of aging and immunosenescent trends with sulforaphane. I investigated one of its cited papers in (5) A review of sulforaphane and aging, which required further searches, some of which are still on tabs of my browser.

I was happy to oblige special requests with (6) Tailoring measurements for broccoli sprouts and (7) Uses of the lymphocytes to monocytes ratio.

Could I have done all of what I did last week without changing my internal environment? What exactly are the effects of eating a clinically relevant amount of broccoli sprouts every day for nine weeks?

A plausible explanation is in Upgrade your brain’s switchboard with broccoli sprouts.

Week 9 of Changing to a youthful phenotype with broccoli sprouts

To follow up Week 8 of Changing to a youthful phenotype with broccoli sprouts:

1. This week has really been different.

A. Physically, on Friday Eve I worked out per my usual upper-body-workout-every four-days routine. I felt strong, and on one exercise I increased the weight by 33%. No problem doing the same number of reps and sets! Keeping good form was challenging.

Per Week 7, I eight-count each concentric rep slowly, then perform each eccentric rep to the same count, with a goal to reach muscle exhaustion during each set. Then pause and do another set.

What changed? Could I have done all this before?

No. I’d tried, making baby steps with increasing weight and keeping good form. But now I can, and I’ll do it again, along with other physical challenges.

B. Seven of this week’s blog posts may be evidence of improved cognitive function. Awakening was how it felt.

Is A claim of improved cognitive function sufficient evidence?

C. This 35th blog post for May comes after 30 posts in April. It wasn’t my goal to do one a day. It’s my goal to Surface Your Real Self. Did a few of them help?

I hope to do other things with my life in June. But the fact remains that humans are herd animals. We “think in herds, go mad in herds, while they [we] only recover their [our] senses slowly, one by one.” We’ll stay in the Madness of Crowds phase until enough people refuse to be propagandized.

2. As a result of reading A pair of broccoli sprout studies, I changed practices to start batches with one tablespoon of broccoli seeds twice a day so I could consume broccoli sprouts twice daily. Right now it’s a PITA task that requires optimization.

The two studies’ findings were:

  1. Broccoli sprouts are better than supplements.
  2. Eating sprouts twice a day is better than eating them once a day.
  3. When in doubt, refer back to Item 1.

3. I reordered broccoli seeds and will receive them next week. In the meantime, I introduced yet another unknown by consuming sprouts that came from a different vendor:

These seeds are smaller. Hundreds of seeds and seed coats annoyingly pass through my strainer, which didn’t happen with larger seeds. 3-day-old sprout sizes are smaller, and they smell and taste different.

Worst-case estimates made in Estimating daily consumption of broccoli sprout compounds would be higher with a smaller seed size. If I recalculated, though, they wouldn’t be worst cases anymore. So I’ll leave them at 21 mg sulforaphane without microwaving and 30 mg sulforaphane with microwaving from eating 3-day-old broccoli sprouts every day.

This vendor put “seed” four times on their label. The other vendor didn’t bother to put “seed” even once on their broccoli seed package label.

Like other vendors, they prefer buzzword marketing with “microgreen” and “sprouting” rather than provide useful consumer information such as number of seeds and broccoli variety characteristics. Will people buy “Broccoli Sprouting Seeds” but won’t buy Broccoli Seeds? Do people say “Cool beans!” anymore?

My reorder states there are ~720,000 broccoli seeds in that 5 lb. package. I’ll update with its volume after it arrives.

See Week 10 of Changing to a youthful phenotype with broccoli sprouts for follow ups.

We believe what we need to believe

While getting ready for bed tonight, I mused about how my younger brother had such an idealized postmortem view of our father. As he expressed six years ago in an obituary for our high school Literature teacher:

“I’ll remember my favorite teacher and how much he’s meant to my life. My father and Martin Obrentz were the two people who made me care about the things that make me the person I am today.”

Believe what you need to believe, David. But like I said five years ago in Reflections on my four-year anniversary of spine surgery:

“I don’t remember that my three siblings ever received a paddling or belting, although they were spanked. Even before he retired, 17 years before he died, the Miami-Dade County public school system stopped him and the rest of their employees from spanking, whipping, beating, and paddling children.”


It’s extremely important for a child to have a witness to their adverse childhood experiences. Otherwise, it’s crazy-making when these aren’t acknowledged as truths by anyone else. Especially by those who saw but disavow what they saw.

It didn’t really drum into my conscious awareness until tonight that I had such a witness. It wasn’t my mother, of course, since she directed most of my being whipped with a belt, and beaten with a paddle that had holes in it to produce welts. She has denied and deflected my experiences ever since then.

It wasn’t my siblings, regrettably for all of us. It wasn’t our Miami neighbors.

When I was twenty, I ran across a guy 300 miles north in Gainesville, Florida, named David Eisenberg, if I remember correctly. A couple of weeks after we met, he asked if my father was Fred Rice, Dean of Boys, West Miami Junior High School. He said he had been beaten by my father several times.

Those weren’t early childhood memories like mine. Those were experiences of a young man 12-15 years old during grades 7-9 that he remembered more than a decade later.

I was shocked. It came at a time when I wasn’t ready to face facts about my life, though. I needed fantasies, beliefs to smother what I felt.


I don’t expect that the impacts of my childhood experiences will ever go away. After three years of Primal Therapy that ended a decade ago, at least mine don’t completely control my life anymore.

Dr. Arthur Janov put self-narratives of several patients’ experiences into his May 2016 book Beyond Belief which I partially curated in February 2017. It was partial because I couldn’t read much past Frank’s horrendous story in pages 89 – 105, “The Myth of a Happy Childhood.”

Do early experiences of hunger affect our behavior, thoughts, and feelings today?

Reposted from five years ago.


A 2015 worldwide human study Hunger promotes acquisition of nonfood objects found that people’s current degree of hungriness affected their propensity to acquire nonfood items.

The researchers admitted that they didn’t demonstrate cause and effect with the five experiments they performed, although the findings had merit. News articles poked good-natured fun at the findings with headlines such as “Why Hungry People Want More Binder Clips.”

The research caught my eye with these statements:

“Hunger’s influence extends beyond food consumption to the acquisition of nonfood items that cannot satisfy the underlying need.

We conclude that a basic biologically based motivation can affect substantively unrelated behaviors that cannot satisfy the motivation.


The concept of the quotes relates to a principle of Dr. Arthur Janov’s Primal Therapy – symbolic satisfaction of needs. Two fundamentals of Primal Therapy:

  1. The physiological impacts of our early unmet needs drive our behavior, thoughts, and feelings.
  2. The painful impacts of our unfulfilled needs impel us to be constantly vigilant for some way to fulfill them.

Corollary principles of Primal Therapy:

  • Our present efforts to fulfill our early unmet needs will seldom be satisfying. It’s too late.
  • We acquire substitutes now for what we really needed back then.
  • Acquiring these symbols of our early unmet needs may – at best – temporarily satisfy derivative needs.

But the symbolic satisfaction of derived needs – the symptoms – never resolves the impacts of early unfulfilled needs – the motivating causes:

  • We repeat the acquisition behavior, and get caught in a circle of acting out our feelings and impulses driven by these conditions.
  • The unconscious act-outs become sources of misery both to us and to the people around us.

As this study’s findings showed, there’s every reason for us to want researchers to provide a factual blueprint of causes for our hunger sensation effects, such as “unrelated behaviors that cannot satisfy the motivation.

Hunger research objectives could include answering:

  • What enduring physiological changes occurred as a result of past hunger?
  • How do these changes affect the subjects’ present behaviors, thoughts, and feelings?

Hunger research causal evidence for the effect of why people acquire items that cannot satisfy the underlying needmay include studying where to start the timelines for the impacts of hunger. The impacts potentially go back at least to infancy when we were completely dependent on our caregivers.

Infants can’t get up to go to the refrigerator to satisfy their hunger. All a hungry infant can do is call attention to their need, and feel pain from the deprivation of their need.

Is infancy far back enough, though, to understand the beginnings of potential impacts of hunger?

Do delusions have therapeutic value?

This 2019 UK review discussed delusions, aka false beliefs about reality:

“Delusions are characterized by their behavioral manifestations and defined as irrational beliefs that compromise good functioning. In this overview paper, we ask whether delusions can be adaptive notwithstanding their negative features.

We consider different types of delusions and different ways in which they can be considered as adaptive: psychologically (e.g., by increasing wellbeing, purpose in life, intrapsychic coherence, or good functioning) and biologically (e.g., by enhancing genetic fitness).”


A. Although the review section 4 heading was Biological Adaptiveness of Delusions, the reviewers never got around to discussing the evolved roles of brain areas. One mention of evolutionary biology was:

“Delusions are biologically adaptive if, as a response to a crisis of some sort (anomalous perception or overwhelming distress), they enhance a person’s chances of reproductive success and survival by conferring systematic biological benefits.”

B. Although section 5’s heading was Psychological Adaptiveness of Delusions, the reviewers didn’t connect feelings and survival sensations as origins of beliefs (delusions) and behaviors. They had a few examples of feelings:

“Delusions of reference and delusions of grandeur can make the person feel important and worthy of admiration.”

and occasionally sniffed a clue:

“Some delusions (especially so‐called motivated delusions) play a defensive function, representing the world as the person would like it to be.”

where “motivated delusions” were later deemed in the Conclusion section to be a:

“Response to negative emotions that could otherwise become overwhelming.”

C. Feelings weren’t extensively discussed until section 6 Delusions in OCD and MDD, which gave readers the impression that feelings were best associated with those diseases.

D. In the Introduction, sections 4, 5, and 7 How Do We Establish and Measure Adaptiveness, the reviewers discussed feeling meaning in life, but without understanding:

  1. Feelings = meaning in life, as I quoted Dr. Arthur Janov in The pain societies instill into children:

    “Without feeling, life becomes empty and sterile. It, above all, loses its meaning.

  2. Beliefs (delusions) defend against feelings.
  3. Consequentially, the stronger and more numerous beliefs (delusions) a person has, the less they feel meaning in life.

E. Where, when, why, and how do beliefs (delusions) arise? Where, when, why, and how does a person sense and feel, and what are the connections with beliefs (delusions)?

The word “sense” was used 29 times in contexts such as “make sense” and “sense of [anxiety, coherence, control, meaning, purpose, rational agency, reality, self, uncertainty]” but no framework connected biological sensing to delusions. Papers from other fields have detailed cause-and-effect explanations and precursor-successor diagrams for every step of a process.


Regarding the therapeutic value of someone else’s opinion of a patient’s delusions – I’ll reuse this quotation from the Scientific evidence page of Dr. Janov’s 2011 book “Life Before Birth: The Hidden Script that Rules Our Lives” p.166:

“Primal Therapy differs from other forms of treatment in that the patient is himself a therapist of sorts. Equipped with the insights of his history, he learns how to access himself and how to feel.

The therapist does not heal him; the therapist is only the catalyst allowing the healing forces to take place. The patient has the power to heal himself.

Another way Dr. Janov wrote this was on p.58 of his 2016 book Beyond Belief as quoted in Beyond Belief: The impact of merciless beatings on beliefs:

No one has the answer to life’s questions but you. How you should lead your life depends on you, not outside counsel.

We do not direct patients, nor dispense wisdom upon them. We have only to put them in touch with themselves; the rest is up to them.

Everything the patient has to learn already resides inside. The patient can make herself conscious. No one else can.”

https://onlinelibrary.wiley.com/doi/full/10.1002/wcs.1502 “Are clinical delusions adaptive?”

Reductionism vs. reductionism

This 2004 essay by an evolutionary biologist reviewed his field’s direction in the current century:

“Science is impelled by two main factors, technological advance and a guiding vision (overview). A properly balanced relationship between the two is key to the successful development of a science.

Without the proper technological advances the road ahead is blocked. Without a guiding vision there is no road ahead; the science becomes an engineering discipline, concerned with temporal practical problems.

Empirical reductionism is in essence methodological; it is simply a mode of analysis, the dissection of a biological entity or system into its constituent parts in order better to understand it. Empirical reductionism makes no assumptions about the fundamental nature, an ultimate understanding, of living things.

Fundamentalist reductionism (the reductionism of 19th century classical physics), on the other hand, is in essence metaphysical. It is ipso facto a statement about the nature of the world: living systems (like all else) can be completely understood in terms of the properties of their constituent parts.

This is a view that flies in the face of what classically trained biologists tended to take for granted, the notion of emergent properties. Whereas emergence seems to be required to explain numerous biological phenomena, fundamentalist reductionism flatly denies its existence: in all cases the whole is no more than the sum of its parts.”

Regarding cellular evolution:

“Modern concepts of cellular evolution are effectively petrified versions of 19th century speculations. Try to imagine a biology released from the intellectual shackles of mechanism, reductionism, and determinism.

Evolution, as a complex dynamic process, will encounter critical points in its course, junctures that result in phase transitions (drastic changes in the character of the system as a whole). Human language is a development that has set Homo sapiens worlds apart from its otherwise very close primate relatives, adding new dimensions to the phase space within which human evolution occurs. Another good critical-point candidate is the advent of (eucaryotic) multicellularity.

Nowhere in thinking about a symbiotic origin of the eucaryotic cell has consideration been given to the fact that the process as envisioned would involve radical change in the designs of the cells involved. You can’t just tear cell designs apart and willy-nilly construct a new type of design from the parts.

The organization of the mitochondrial endosymbiont is radically changed during its evolution, but that change is a degeneration to a far simpler “cell-like” design. The mitochondrial design could never evolve back to the level of complexity that its free-living [bacterial] ancestor had.

A common thread that links language and multicellularity is communication (interaction at a distance). In each case a complex, sophisticated network of interactions forms the medium within which the new level of organization (entities) comes into existence.

Our experience with variation and selection in the modern context does not begin to prepare us for understanding what happened when cellular evolution was in its very early, rough-and-tumble phase(s) of spewing forth novelty. Cellular evolution began in a highly multiplex fashion, from many initial independent ancestral starting points, not just a single one.”

https://mmbr.asm.org/content/68/2/173 “A New Biology for a New Century”


I came across this review by it being referenced in this researcher’s blog post:

Chinese Longevity Herb
I often don’t agree with him, but I subscribe to his blog because it’s interesting.

Organ epigenetic memory

This 2018 Japanese review subject was the relationships of organ memory and non-communicable diseases:

“Organ memory is the engraved phenotype of altered organ responsiveness acquired by a time-dependent accumulation of organ stress responses. This phenomenon is known as “metabolic memory” or “legacy effect,” which is similar to neuronal and immune memory.

Not only is the epigenetic change of key genes involved in the formation of organ memory but the alteration of multiple factors, including low molecular weight energy metabolites, immune mediators, and tissue structures, is involved as well. These factors intercommunicate during every stress response and carry out incessant remodeling in a certain direction in a spiral fashion through positive feedback mechanisms.

The systematic review revealed that each intervention type, that is:

  • Glucose lowering,
  • Blood pressure lowering, or
  • LDL-cholesterol lowering,

possessed unique characteristics of the memory phenomenon. Most of the observational periods of these studies lasted for > 10 years. Memory phenomenon was suggested to last for a long time and is thought to have a considerable effect on the clinical course of NCDs [non-communicable diseases].

Organs cannot possess consciousness, so it might not be appropriate to consider whether a recalling process exists in organs. However, the properties of organs are incessantly altered by external stimuli loaded on organs as if it is updating.

It is clinically important to investigate whether organ memory can be updated by our behaviors. Once organ memory is established in an organ, organ memory in each organ can influence one another and affect organ memory in a different organ.

Epigenome-modification enzymes, such as histone deacetylases and DNA methyltransferases, and transcription factors seem to be essential for the epigenetic regulation of gene expression, which is involved in the generation of organ memory. Cellular metabolism can epigenetically modulate the expression of genes that are related to the progression of diseases.”


1. The reviewers asserted:

“Organs cannot possess consciousness, so it might not be appropriate to consider whether a recalling process exists in organs.”

Memory studies don’t require this consciousness to investigate even the brain organ’s areas and functions. Researchers observe memory by measuring stimulus/response items like neuron activation and various levels of behavior. Consciousness is an emergent property.

2. Regarding recall: An organ’s “engraved phenotype of altered organ responsiveness” may not have recall itself, but it doesn’t have a separate existence apart from its body. An organ can’t be removed from its body for very long and still be part of its body.

When an organ is in its normal state as part of a body, it has access to recall-like functions via the “inter-organ communication of organ memory.” The review also mentioned:

“Organ memory in each organ can influence one another and affect organ memory in a different organ.

Evolution didn’t support unnecessary duplication for a kidney’s memory to include recall because it’s part of a body that includes a brain that has recall. Evolution didn’t duplicate functions of a kidney’s memory in a brain, either.

https://www.nature.com/articles/s41440-018-0081-x “Organ memory: a key principle for understanding the pathophysiology of hypertension and other non-communicable diseases” (not freely available)