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Work your voluntary muscles today

gettingwell4 4-5 stars Advanced knowledge, Epigenetics, Immune system, Neurochemicals, Oxytocin, Stress, Telomeres ,

This 2020 review by the Aging as a disease research group highlighted their specialty:

“A theory that fits both the aging and the rejuvenation data suggests that aging is caused primarily by the functional (and notably, experimentally reversible) inactivation of resident stem cells, which precipitates deteriorated tissue maintenance and repair and leads to the loss of organ homeostasis.

The damaged and unrepaired tissues suffer changes in their biochemistry, including the molecular crosstalk with resident stem cells, which further inhibits productive, regenerative responses. The inflammatory and fibrotic secretome can then propagate systemically, affecting the entire organism.

Skeletal muscle accounts for almost 40% of the total adult human body mass. This tissue is indispensable for vital functions such as respiration, locomotion, and voluntary movements and is among the most age-sensitive in mammals.

Muscle is capable of active repair in response to daily wear and tear, intense exercises, or injuries. Muscle regeneration relies on the adult muscle stem cells, also called satellite cells.

Rather than a significant decline in the total number with age, most of the data support a dramatic lack of activation of muscle stem cells after injury and a concomitant lack in the formation of progenitors that are needed for repair.

Multiple experimental approaches have been used for tissue rejuvenation and/or systemic rejuvenation; these include ablation of senescent cells and re-calibration of key signaling pathways that are needed for productive stem cell responses. To test the success in experimental rejuvenation, 1-4 approaches are typically applied, and skeletal muscle is well-suited for assaying each one.”

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7007696/ “Skeletal muscle as an experimental model of choice to study tissue aging and rejuvenation”

The review had a short section on inflammation details. Not enough, and there’s no tissue repair. Continuing unchecked is a systemic issue that led the reviewers to their paradigm of aging as a disease.

The review concluded with a subject that’s taught in high school, and should be understood at least before college graduation. It’s curious that an item like sample size required emphasis. Maybe research that doesn’t adhere to basics is a current issue?

Week 3 of Changing an inflammatory phenotype with broccoli sprouts

gettingwell4 4-5 stars Advanced knowledge, Epigenetics, Immune system, Memory, Stress

To follow up Week 2 of Changing an inflammatory phenotype with broccoli sprouts:

1. I intend to follow the model clinical trial [1] and pause eating broccoli sprouts after ten weeks. The clinical trial subjects experienced benefits after stopping at Day 70, as measured at Day 90 and Day 160.

Sprouting broccoli seeds takes time and care every day. I may not have that time when everyone gets back to work.

Then again, I live in a state headed by Governor Klan Robes Blackface. Here’s his 1984 Eastern Virginia Medical School yearbook entry, 16 years after Martin Luther King Jr. was assassinated:


He has no empathy for people like the young black man – laid off for four weeks now – who was severely burned as a child, and who was enthusiastically working at Dunkin Donuts. Or the older lady who was trying to get her life back together at Hair Cuttery, still closed.

Who knows when or if people around here will get their jobs back? Politics are a magnet for the worst.

2. I’ve started to see encouraging signs. Over the last few years, I’ve tried to avoid walking long distances where the surface was tilted to my right in order to not overpronate my left foot and aggravate problems mentioned in Week 1.

That was neither an immediate concern during six-mile-long beach walks yesterday and today, nor have I felt any inflammation afterwards!

3. I have quart Mason jars for sprouting per many YouTube videos, but don’t use them. They’re unsuited for broccoli seeds, which don’t handle extra moisture well.

I’ve had good results with Russian-doll glass bowls. I use a strainer for Round 1, transfer them to a bowl, and wick out extra moisture with a paper towel during Round 2 before putting them back on a pantry shelf. It would be hard to maneuver a paper towel inside a Mason jar.


The bowl at the top left has been replaced by the next size larger than the bowl at the bottom left. Day 3 broccoli sprouts were too crowded to dry in the small bowl.

4. I had heartburn Friday and Saturday after eating 60 grams of 3-day-old broccoli sprouts in 100 ml of water processed with a 1000 W microwave on full power for 35 seconds. Today I removed a thousand spent broccoli seed coats before microwaving, and didn’t have heartburn afterwards. More experiments are required.

[1] 2018 Effects of long-term consumption of broccoli sprouts on inflammatory markers in overweight subjects curated in How much sulforaphane is suitable for healthy people?

Aging as an unintended consequence

gettingwell4 5+ stars Premium, Cerebellum, Epigenetics, Hippocampus, Hypothalamus, Immune system, Limbic system, Lower brain, Stress, Telomeres , , , , , ,

The coauthors of 2018’s The epigenetic clock theory of aging reviewed progress that’s been made todate in understanding epigenetic clock mechanisms.

1. Proven DNA methylation features of epigenetic clocks:

  1. “Methylation of cytosines is undoubtedly a binary event.
  2. The increase in epigenetic age is contributed by changes of methylation profiles in a very small percent of cells in a population.
  3. The clock ticks extremely fast in early post-natal years and much slower after puberty.
  4. Clock CpGs have specific locations in the genome.
  5. It applies to prenatal biological samples and embryonic stem cells.

While consistency with all the five attributes does not guarantee veracity of a model, inconsistency with any one will signal the unlikely validity of a hypothesis.”

2. Regarding what epigenetic clocks don’t measure:

“The effects of

  • Telomere maintenance,
  • Cellular senescence,
  • DNA damage signaling,
  • Terminal differentiation and
  • Cellular proliferation

have all been tested and found to be unrelated to epigenetic ageing.”

3. Regarding cyclical features:

“Both the epigenetic and circadian clocks are present in all cells of the body, but their ticking rates are regulated. Both these clocks lose synchronicity when cells are isolated from tissues and grown in vitro.

These similarities compel one to ponder potential links between them.”

This was among the points that Linear thinking about biological age clocks missed.

4. The reviewers discussed 3 of the 5 treatment elements in Reversal of aging and immunosenescent trends:

“It is not known at this stage whether the rejuvenating effect is mediated through the regeneration of the thymus or a direct effect of the treatment modality on the body. Also, it is not known if the effect is mediated by all three compounds or one or two of them.

What we know at this stage does not allow the formation of general principles regarding the impact of hormones on epigenetic age, but their involvement in development and maintenance of the body argue that they do indeed have a very significant impact on the epigenetic clock.”

Not sure why they omitted 3000 IU vitamin D and 50 mg zinc, especially since:

“It is not known if the effect is mediated by all three [five] compounds or one or two of them.”

5. They touched on the specialty of Aging as a disease researchers with:

“Muscle stem cells isolated from mice were epigenetically much younger independently of the ages of the tissue / animal from which they were derived.

The proliferation and differentiation of muscle stem cells cease upon physical maturation. These activities are initiated in adult muscles only in response to injury.“

6. The reviewers agreed with those researchers in the Conclusion:

“Epigenetic ageing begins from very early moments after the embryonic stem cell stage and continues uninterrupted through the entire lifespan. The significance of this is profound as the question of why we age has been attributed to many different things, most commonly to ‘wear-and-tear.’

The ticking of the epigenetic clock from the embryonic state challenges this perspective and supports the notion that ageing is an unintended consequence of processes that are necessary for

  • The development of the organism and
  • Tissue homeostasis thereafter.”


https://journals.sagepub.com/doi/10.1177/1535370220918329 “Current perspectives on the cellular and molecular features of epigenetic ageing” (not freely available)

Linear thinking about biological age clocks

gettingwell4 0-1 star Wasted resources, Epigenetics, Stress, Telomeres , , ,

This 2020 review by a Hong Kong company’s researchers compared and contrasted measures of biological age:

“More than a dozen aging clocks use molecular features to predict an organism’s age, each of them utilizing different data types and training procedures. We offer a detailed comparison of existing mouse and human aging clocks, discuss their technological limitations and the underlying machine learning algorithms. We also discuss promising future directions of research.

Biomarkers placed on an intuitive plane of Accuracy vs Utility. Bubble size depends on the number of clocks based on a corresponding aging biomarker.

Currently, DNAm [DNA methylation] is the most accurate and the most frequently used biomarker in biohorology. However, it is harder to apply a DNAm clock compared to clocks based on clinical blood tests. Moreover, DNAm marks often take a long time to emerge in response to aging interventions.

Chromatin structure and telomeres, while intriguing, are too labor intensive and error-prone to be practical.”

https://www.sciencedirect.com/science/article/pii/S1568163719302582 “Biohorology and biomarkers of aging: current state-of-the-art, challenges and opportunities”

We think about chronological age linearly. The reviewers hinted at but didn’t directly assess the extent to which techniques such as linear regression may also influence people to think linearly about biological age.

We experience cyclical changes every day (like sleep), month, season, and longer periods. The reviewers didn’t mention techniques that incorporate our cyclical experiences or assess cyclical biological age.

1. The reviewers pointed out some biological age clock linearity flaws:

“Most aging clocks base their BA [biological age] definitions either on CA [chronological age] or mortality risk. Mortality risk in its turn is derived from demographic tables and can be assumed to be a function of CA in most animals, including human.

Thus, aging clocks are ultimately treating CA as a substitute BA with the caveat that deviations from the actual CA signify better or worse physical fitness when compared to age matched controls. Such a design has several flaws.”

2. They pointed out non-linear characteristics of chromosomal telomere length:

“DNA lesions caused by oxidative stress are repaired less efficiently in telomeric regions, which causes frailty and subsequent telomere shortening. Oxidative stress levels may fluctuate due to habitat, life style, inflammatory diseases – factors that do not necessarily represent replicative clock ticking.

Telomere length typically fluctuates within ±2-4% per month. This led scientists to hypothesize that telomere attrition is an oscillatory process.”

Since cell components show cyclical phases, why wouldn’t cells and each higher living structural level likewise demonstrate cyclical phases? That avenue wasn’t explored.

3. They mentioned the non-linearity of epigenetic clocks:

“If an organism’s DNAm profile is not directly linked to the thermodynamic root of aging [entropy] but instead is a downstream product of competing processes, the applicability of DNAm aging clock methodology is at risk. In this case different aging clocks may not be equally good for different experiment settings.

While genetic, pharmacological and dietary interventions with proven effect on life expectancy change the methylation state of the age-associated CpG sites, they do so in different ways. Caloric restriction is more efficient in preventing methylation loss at hypomethylated sites and methylation gain at hypermethylated sites than rapamycin.

These findings imply that DNAm profiles do not simply gravitate towards the average with age and that there is no single pathway through which all aging processes are imbued into an organism’s epigenetic landscape.”

4. Genetic and epigenetic regulatory pathways were presented with linear thinking:

“Protein structures encapsulating DNA and regulating its accessibility (chromatin and histones) have also been shown to change with age. Moreover, DNAm machinery and histone modifications are interlinked and change throughout aging concordantly.

For example, DNA methyltransferases are attracted by the H3K36me mark. With aging it is less tightly regulated, and thus, more sporadic DNAm occurs, which ultimately translates to epigenetic clock ticking.”

An individual’s capability to regulate their own aging phenotype wasn’t addressed, only externally applied “aging interventions.” Diseases were considered chronological-“age-associated.”

Biological aging was neither viewed as a disease nor as an unintended consequence. If these researchers don’t grasp the foundations of their field of study, why do they work in the biological aging field? It isn’t just math.

  • Could this paper reflect one company’s desire to frame arguments in favor of the company’s offered solution?
  • Could this paper reflect a “chronological age is the cause” meme that satisfied organizational imperatives for sponsors like the Buck Institute for Research on Aging?
  • Or could it be that the reviewers had other paradigms?

What do you think?

Broccoli sprouts oppose effects of advanced glycation end products (AGEs)

gettingwell4 4-5 stars Advanced knowledge, Epigenetics, Hypothalamus, Immune system, Limbic system, Stress , , ,

This 2020 Australian/UK review subject was AGEs:

“AGEs are formed during cooking and food processing or produced endogenously as a consequence of metabolism. Deleterious effects of AGEs are underpinned by their ability to trigger mechanisms well known to elicit metabolic dysfunction, including activation of inflammatory pathways, oxidative stress and impaired mitochondrial oxidative metabolism. They have been widely implicated in complications of diabetes affecting cardiovascular health, the nervous system, eyes and kidneys.

Reactive carbonyl groups are constantly being produced via normal metabolism and when production overrides detoxification, AGEs accumulate. AGE formation may take several days or weeks to complete in the body.

Factors affecting AGE content of food depends on composition of protein, fat, and sugar and types of processing and cooking methods employed, predominantly on temperature and duration of preparation. Circulating free-AGEs concentrations are a good marker for dietary AGE intake while plasma protein-bound AGEs better represent endogenously produced AGEs.

Receptor for Advanced glycation end products (RAGE) signals via transcription factor NF-kB increasing gene expression of inflammatory mediators and production of ROS (reactive oxygen species).”

https://onlinelibrary.wiley.com/doi/abs/10.1002/mnfr.201900934 “The Role of Dietary Advanced Glycation End Products (AGEs) in Metabolic Dysfunction” (not freely available)

Let’s use the Australian 2019 Sulforaphane: Its “Coming of Age” as a Clinically Relevant Nutraceutical in the Prevention and Treatment of Chronic Disease as a reference for how sulforaphane may counter effects of AGEs:

1. “Activation of inflammatory pathways”

“Antioxidants in general and glutathione in particular can be depleted rapidly under conditions of oxidative stress, and this can signal inflammatory pathways associated with NF-κB. SFN [sulforaphane] has been shown to inhibit NF-κB in endothelial cells.

Two key inflammatory cytokines were measured at four time points in forty healthy overweight people [our model clinical trial, Effects of long-term consumption of broccoli sprouts on inflammatory markers in overweight subjects]. Levels of both interleukin-6 (Il-6) and C-reactive protein (CRP) declined over the 70 days during which sprouts were ingested. These biomarkers were measured again at day 90, wherein it was found that Il-6 continued to decline, whereas CRP climbed again. When the final measurement was taken at day 160, CRP, although climbing, had not returned to its baseline value. Il-6 remained significantly below the baseline level at day 160.”

OMCL2019-2716870.010

2. “When production overrides detoxification”

“SFN significantly activates Nrf2 and as such has the potential to modulate the expression of genes associated with redox balance, inflammation, detoxification, and antimicrobial capacity, all key components of the upstream cellular defence processes.

Toxins presented to Phase 1 enzymes produce intermediate compounds which are sometimes more toxic to cells than the initial toxin. It is therefore important that Phase 2 is sufficiently active that intermediate products cannot accumulate in the cellular environment.

As a monofunctional inducer, SFN has been described as an ideal detoxifier, as its effect on Phase 1 is minimal compared with its significant activity on Phase 2.”

3. “Oxidative stress”

“As a mediator for amplification of the mammalian defence system against various stressors, Nrf2 sits at the interface between our prior understanding of oxidative stress and endogenous mechanisms cells use to deal with it. Diseases known to be underpinned by oxidative stress are proving to be more responsive to amplification of cellular defences via Nrf2 activation than by administration of direct-acting antioxidant supplements.

SFN, with absolute bioavailability of around 80%, is capable of increasing several endogenous antioxidant compounds via transcription factor Nrf2.”

4. “Complications of diabetes affecting cardiovascular health, the nervous system, eyes and kidneys”

“Nrf2 is ubiquitously expressed with highest concentrations (in descending order) in the kidney, muscle, lung, heart, liver, and brain. Nrf2 was shown to prevent endothelial cells from exhibiting a proinflammatory state. Nrf2 is required for protection against glucose-induced oxidative stress and cardiomyopathy in the heart.

Well in excess of 500 genes have been identified as being activated by SFN via the Nrf2/ARE [Antioxidant Response Element] pathway, and it is likely that this underestimates the number as others are being discovered. Of available SFN clinical trials associated with genes induced via Nrf2 activation, many demonstrate a linear dose-response. More recently, it has become apparent that SFN can behave hormetically with different effects responsive to different doses.

It [sulforaphane] is not only a potent Nrf2 inducer but also highly bioavailable so that modest practical doses can produce significant clinical responses. Other Nrf2 activators [shown in the above image] not only lack potency but also lack the bioavailability to be considered as significant intracellular Nrf2 activators.”

As mentioned in Changing an inflammatory phenotype with broccoli sprouts, per the above bolded part of section 3, I stopped taking N-acetyl-cysteine, the precursor to our endogenous antioxidant glutathione. I stopped taking curcumin last year due to no noticeable effects, probably because of its poor bioavailability. I may soon stop taking more vitamin E than the RDA, and β-carotene.

I changed my diet last summer to reduce AGEs, with mild effects. I expect stronger effects from also daily eating 60 grams of 3-day-old broccoli sprouts that yield 27 mg of sulforaphane after microwaving.

Reanalysis of findings from a senolytics clinical trial

gettingwell4 2-3 stars Required further work, Epigenetics, Stress

To follow up Preliminary findings from a senolytics clinical trial:

“The central hypothesis tested in our article is that a brief course of the senolytic drug combination, Dasatinib plus Quercetin (D+Q), can reduce senescent cell abundance in humans, specifically focusing on targeting adipose tissue in subjects with diabetes and kidney dysfunction, a condition in which adipose tissue senescent cell burden is known to be increased.

Although we reported a statistically significant decrease in skin senescent cells in the 9 subjects whose skin data were reported in the original article, that conclusion did not hold up upon reanalysis.

The overall conclusion of our article that D+Q can target senescent cells in humans holds upon reanalysis of the data, at least in adipose tissue and as reflected by a composite of blood SASP [senescence-associated secretory phenotype] factors, but we have not shown this in skin here.”

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6994619/ “Corrigendum to ‘Senolytics decrease senescent cells in humans: Preliminary report from a clinical trial of Dasatinib plus Quercetin in individuals with diabetic kidney disease’”

Reviewing clinical trials of broccoli sprouts and their compounds

gettingwell4 4-5 stars Advanced knowledge, Epigenetics , ,

This 2020 Spanish review analyzed recent clinical trials that used broccoli sprouts and their compounds. Stringent criteria for study selection resulted in few trials being considered:

  • “We reduced the timeframe to the last years, from 2012 to the present.
  • We focused our work on the data of studies carried out with human adults with different pathologies.
  • Articles [that] did not provide us with specific information about consumption of cruciferous foods or ingredients derived from Brassicaceae products, documents based on healthy volunteers, and patients with pathologies unrelated to our objective of study were also not included in the analysis.”

None of the 15 analyzed clinical trials were unqualified successes. Some of the problems noted were summarized in this critique of the largest study:

“The authors presented the results that there was a risk for T2DM [type 2 diabetes mellitus] with the intake of cruciferous foods and glucosinolates. However, this study presented big limitations because:

  • It did not review or consider the cooking procedures,
  • It did not quantify the amount of vegetables consumed on a daily or weekly basis, and
  • It did not quantify the glucosinolate contents in the different vegetables consumed. Besides,
  • The population sample was homogenous, because all of the participants were health-area workers, and the results are not extrapolatable to the general population. Finally, it should be highlighted that
  • Other nutrients and confounding factors were not considered in the study, and they could affect the development of these pathologies.”

“Figure 1 – General scheme of the glucosinolates (GSLs) and common hydrolysis products. ESP: Epithiospecifer proteins.”

https://www.mdpi.com/1420-3049/25/7/1591/htm “The Role of Brassica Bioactives on Human Health: Are We Studying It the Right Way?”

The reviewers’ answer to the title’s question “Are We Studying It the Right Way?” was NO. The 15 analyzed trials lacked one or more clearly defined measurements related to their target diseases:

“It is crucial that the outcome measure is of biological relevance; biomarkers or risk factors measured must be associated to the latter development of a disease. The degree of progression of the disease greatly influences the response observed.”

So: Why not consider Aging as a disease for clinical trials with broccoli sprouts and their compounds?

  1. “Lack of cure goes hand in hand with inability to accept that this [aging] is disease. It used to be that, please do not diagnose that there’s bacterial meningitis, because there is no cure. Whatever else you can come up with, do it first. Now, diagnose it as fast as possible, so we can put patients on antibiotics immediately. The same will happen to aging.”
  2. Several of the clinical trials’ methodological and statistical problems could be resolved with recognizing aging as a disease. “Healthy” old people who have no other diseases may be scarce, but there are large populations to sample control groups from among healthy and unhealthy young people, and unhealthy old people.
  3. The reviewers already have experience in using “healthy” 46 ± 6 year-old people in a clinical trial of broccoli sprouts and their compounds.
  4. A wide range of epigenetic clocks are available to test the efficacy of broccoli sprouts and their compounds with respect to human aging phenotypes.

As far as I can tell, epigenetic clocks haven’t been used in the subject area thus far! The review’s reference [7] from 2015 didn’t mention them.

Reference [55] was the October 2019 Sulforaphane: Its “Coming of Age” as a Clinically Relevant Nutraceutical in the Prevention and Treatment of Chronic Disease, which I’ve been using as the most current and comprehensive of the subject todate. Its references of broccoli sprouts and their compounds with respect to aging included:

“Nrf2 [nuclear factor erythroid 2-related factor 2] transcriptional activity declines with age, leading to age-related GSH [reduced glutathione] loss among other losses associated with Nrf2-activated genes. This effect has implications, too, for decline in vascular function with age. Some of the age-related decline in function can be restored with Nrf2 activation by SFN [sulforaphane].

A potent Nrf2 activator is capable of inducing hundreds of genes simultaneously. Of the phytochemicals with Nrf2 inducer capacity, Brassica-derived SFN is the most potent naturally occurring biomolecule known at this time.”

However, it had only one reference of DNA methylation, the 2015 The Role of Sulforaphane in Epigenetic Mechanisms, Including Interdependence between Histone Modification and DNA Methylation. Even that was a review rather than a study, and it had no mention of epigenetic clocks.

Maybe broccoli sprouts and their compounds’ effects on human aging is an area that just hasn’t drawn attention and funding?

Understanding a clinical trial’s broccoli sprout amount

gettingwell4 4-5 stars Advanced knowledge, Epigenetics, Immune system

To follow up Week 2 of Changing an inflammatory phenotype with broccoli sprouts, I contacted the model clinical trial’s corresponding coauthor to clarify a citation. Our correspondence was as follows:

Hello Dr.! Could you further describe Citation 11 of your 2018 clinical study Effects of long-term consumption of broccoli sprouts on inflammatory markers in overweight subjects or say where it may be found? “Services, F. a. D. A. F. U. D. o. H. a. H., 2001.” was cited for 30 grams of fresh broccoli sprouts being a half-serving.

Ref. 11. Sulforaphane: translational research from laboratory bench to clinic CA Houghton, RG Fassett, JS Coombes – Nutrition reviews, 2013.

If you check in the table 2, about clinical trials, different studies using broccoli sprouts were establishing daily dosage around 60 g/day (e.g. 56 – 68, etc.). In a similar way, in our previous studies for bioavailability with broccoli sprouts (Domínguez-Perles et al.) we also considered 30 g and 60 g was 1/2 and 1 portion per day, respectively, of broccoli sprouts.

When we carried out tests with consumers, previous to the bioavailability studies (Domínguez-Perles et al., Baenas et al.), higher amounts per day, were not easy to consume and to get eaten by participants. The people or general public in Spain is not very familiar (yet) with these fresh sprouts as may be in USA, or UK, for example. That why we took a “realistic” amount of broccoli sprouts per day, to be incorporated in daily diet.

Of course, with higher amounts we could even probably see better results, but that would not be realistic for a food to be incorporated in daily diet – the purpose of the “prevention” perspective of this work.

I hope that I help you to understand why we selected that amount or the doubts about it. Thank you very much for your interest in the work.

Thank you very much Dr.! It’s encouraging that healthy people were the subjects of your 2018 clinical trial.

May I obtain your permission to use your excellent explanation as a follow up to my blog post?

I and several other people are using your study as the model to improve our health during this lockdown. There have been a lot of errors on my part, but our methods are improving.

Yes, you can use the information, of course. The participants were “healthy” overweight subjects (without medication or treatments of any disease, just adults with overweight). Please, keep safe and have a nice week.

Attached to the last email was his latest coauthored review The Role of Brassica Bioactives on Human Health: Are We Studying It the Right Way? published March 30, 2020, curated in Reviewing clinical trials of broccoli sprouts and their compounds.

“Figure 1 – General scheme of the glucosinolates (GSLs) and common hydrolysis products. ESP: Epithiospecifer proteins.”

Forcing people to learn helplessness

gettingwell4 4-5 stars Advanced knowledge, Beliefs, Brainstem, Cerebrum, Cortisol, Epigenetics, Hippocampus, Hypothalamus, Limbic system, Locus coeruleus, Lower brain, Memory, Neurochemicals, Stress , , , ,

Learned helplessness is a proven animal model. Its reliably-created phenotype is often the result of applying chronic unpredictable stress.

As we’re finding out worldwide, forcing humans to learn helplessness works in much the same way, with governments imposing what amounts to martial law. Never mind that related phenotypes and symptoms include:

  • “Social defeat
  • Social avoidance behavior
  • Irritable bowel syndrome
  • Depression
  • Anxiety
  • Anhedonia
  • Increased hypothalamic-pituitary-adrenal (HPA)-axis sensitivity
  • Visceral hypersensitivity” [1]

Helplessness is both a learned behavior and a cumulative set of experiences. Animal models demonstrate that these phenotypes usually continue on throughout the subjects’ entire lifespans.

Will the problems caused in humans by humans be treated by removing the causes? Or will the responses be approaches such as drugs to treat the symptoms?

A major difference between our current situation and the situation depicted below is that during communism, most people didn’t really trust or believe what the authorities, newspapers, television, and radio said:

Image from Prague’s Memorial to the Victims of Communism

[1] 2014 GABAB(1) receptor subunit isoforms differentially regulate stress resilience curated in If research provides evidence for the causes of stress-related disorders, why only focus on treating the symptoms?

Week 2 of Changing an inflammatory phenotype with broccoli sprouts

gettingwell4 4-5 stars Advanced knowledge, Epigenetics, Immune system, Memory, Stress

To follow up Changing an inflammatory phenotype with broccoli sprouts:

1. My traveling companion used a kitchen scale to measure the weight of broccoli sprouts at Day 3. She started them from one tablespoon of broccoli seeds, and they weighed 60 grams!

The model clinical trial [1] used 30 grams to produce great results:

“The intervention consisted of a 10-week period which included daily consumption of a portion (30 g) of raw, fresh broccoli sprouts. This amount is consistent with a half-serving.”

I asked the study’s corresponding coauthor for clarification of “a half-serving.” Our conversation is at Understanding a clinical trial’s broccoli sprout amount.

Eating a 60 gram “full serving” of 3-day-old broccoli sprouts yielding 27 mg of sulforaphane after microwaving [2] fits [3]‘s guidelines:

“The daily SFN [sulforaphane] dose found to achieve beneficial outcomes in most of the available clinical trials is around 20-40 mg.”

2. My current microwaving time for 60 grams of 3-day-old broccoli sprouts in 100 ml of water with a 1000 W microwave on full power is 35 seconds. Their temperature gets up to 57°C. YMMV.

I immediately cool down the microwaved broccoli sprouts in a colander. See Enhancing sulforaphane content for changes. Go up to the 60°C cliff but don’t fall into the 70°C 65°C canyon:

cliff

The desired range [2]:

“In the temperature range of 50–60°C, a positive correlation was observed between GLR [glucoraphanin] or SFR [sulforaphane] contents and temperature. However, these two physiochemical contents were negatively correlated with temperature when it increased to 70°C.”

3. I had several days of failed crops during Week 2. I switched over to Russian-doll glass bowls with success:

I’d guess that failures were related to excess moisture, which broccoli sprouts hate, hate, hate! Look closely at the top left Day 0 tray below:

Notice concentric raised ribs that are about 1/16″ high. Their effects may have either kept broccoli seeds too wet over a 3-day period, or promoted bacterial growth (although I ran them through a dishwasher after Day 3).

4. I started to put items on the edge of my microwave’s carousel because they don’t heat evenly when placed in the center. I thought uneven heating was a problem that was solved a long time ago, but not for the microwave I bought (Sharp model SMC1131C, which was the least expensive at Best Buy on the day I needed a carousel microwave oven.)

[1] 2018 Effects of long-term consumption of broccoli sprouts on inflammatory markers in overweight subjects curated in How much sulforaphane is suitable for healthy people?

[2] 2020 Microwave cooking increases sulforaphane level in broccoli curated in Microwave broccoli to increase sulforaphane levels and Growing a broccoli sprouts Victory Garden

[3] 2019 Sulforaphane: Its “Coming of Age” as a Clinically Relevant Nutraceutical in the Prevention and Treatment of Chronic Disease curated in How much sulforaphane is suitable for healthy people?

Flatten the Panic Curve April 13-17, 2020

gettingwell4 4-5 stars Advanced knowledge, Amygdala, Beliefs, Brainstem, Immune system, Limbic system, Lower brain, Memory, Primal Therapy, Stress , , ,

To better understand our internal origins of panic, here’s Dr. Arthur Janov’s interpretation of a 2013 Iowa study Fear and panic in humans with bilateral amygdala damage (not freely available):

“Justin Feinstein did a study with those who had a damaged amygdala, the hub of the emotional system. They did not have normal fear responses. But if oxygen supplies were lowered and carbon dioxide supplies were increased, mimicking suffocation (increasing acidity of the blood) there were panic attacks.

Where in the world did those attacks come from? Certainly not from the usual emotional structures.

They believe it includes the brainstem! Because the lowering of oxygen supplies and adding carbon dioxide provoked the lower structures to sense the danger and reacted appropriately.

Very much like what happens to a fetus when the mother smokes during pregnancy and produces those same effects.”

Since those of us who chronically experience panic aren’t going into therapy over this weekend, what else can we do?

1. Stop looking at the John Hopkins Panic map.

2. Search out realistic news such as: “Change in [New York state] ICU admissions is actually a negative number for the first time since we started this intense journey.”

3. Stop clicking sensational headline links.

4. Question your information, and investigate multiple views. Trust has been lost:

  • Dr. Scott Jensen, a Minnesota physician for 35 years and state senator, on the inappropriate CDC / WHO guidelines for reporting COVID-19 deaths:

    “It’s ridiculous. The determination of cause of death is a big deal. The idea that we’re going to allow people to massage and game the numbers is a real issue because we’re going to undermine trust.

    I would never put down influenza as the cause of death. Yet that’s what we’re being asked to do here.”

  • The same day, Dr. Fauci arrogantly grouped physicians in with conspiracy theorists if they didn’t conform to these bordering-on-fraudulent CDC / WHO guidelines:

    “Every time we have a crisis of any sort, there’s always this popping-up of conspiracy theories. I think the deaths that we’re seeing are coronavirus deaths, and the other deaths are not being counted as coronavirus deaths.”

    Telling people to trust him – a bureaucrat who hasn’t been in active practice for over three decades – because he had far superior medical judgment than did practicing doctors who for years continuously see patients?

  • Consider the evidence.
  • Don’t accept lies you feel uneasy about. Trust your internal BS detector.

Which herd will you choose to belong to?

https://nypost.com/video/bison-stampede-terrorizes-family-trapped-in-car/

or

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

gettingwell4 5+ stars Premium, Epigenetics, Primal Therapy , , , , , , ,

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 need” may 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?

Lowering US pneumonia death counts to increase COVID-19 death counts

gettingwell4 4-5 stars Advanced knowledge, Immune system

To follow up CDC directs the US to attribute deaths from other causes to COVID-19, my sending its information to Tucker Carlson yesterday morning may have contributed to the information being broadcast nationally yesterday evening. The transcript at Tucker Carlson: Possible That Doctors Are Classifying Conventional Pneumonia Deaths As COVID Deaths, Increasing The Count included:

“For many years, the CDC has tracked the total number of Americans who die each week from pneumonia. For the last few weeks, that number has come in far lower than at the same moment in previous years.

How could that be? It seems entirely possible that doctors are classifying conventional pneumonia deaths as COVID-19 deaths. This would mean the epidemic is being credited for thousands of deaths that would have occurred if the virus never arrived here.”

Not sure where to find the information supporting “For the last few weeks, that number has come in far lower than at the same moment in previous years.”

Cui bono questions midway through John Hopkins will be herding the US public toward the cliff April 6-10, 2020:

  1. This change in medical reporting has had / will have what effects on the headlines we’ve seen and will see?
  2. Who has benefited / will benefit from (medical, economic, social, and political) reports on and actions taken with the change in medical reporting to: “COVID-19 being the underlying cause more often than not.”
  3. Who has suffered and will suffer from these reports and actions?

CDC directs the US to attribute deaths from other causes to COVID-19

gettingwell4 4-5 stars Advanced knowledge, Immune system

To follow up the If people don’t stand up for their rights, their rights will be forgotten point, which YouTube has taken down:

“We don’t die of the virus. We die of pneumonia.”

The CDC at https://www.cdc.gov/nchs/nvss/covid-19.htm has been issuing guidance to merge deaths from other causes into a WHO code U07.1 that assigns COVID-19 as the primary cause of death. For example, click the March 24, 2020 “Notification of new ICD code introduced for COVID-19” guidance to see:

“The underlying cause depends upon what and where conditions are reported on the death certificate. However, the rules for coding and selection of the underlying cause of death are expected to result in COVID-19 being the underlying cause more often than not.“

Click the April 2, 2020 “New Releases: Final Guidance and Provisional Death Counts” guidance to see:

“Provisional counts for COVID-19 deaths are based on a current flow of mortality data in the National Vital Statistics System (NVSS), and will include:

  • A weekly provisional count of deaths in the United States due to COVID-19
  • A provisional count of deaths from all causes
  • Percent of previous year’s deaths (the number of deaths received compared to the number of deaths expected based on data from previous years)
  • Pneumonia deaths (excluding pneumonia deaths involving influenza)

Pneumonia deaths are included in the provisional counts because deaths due to COVID-19 may be misclassified as pneumonia deaths in the absence of positive test results, and pneumonia may appear on death certificates as a comorbid condition. Thus, increases in pneumonia deaths may be an indicator of excess COVID-19-related mortality.”

  1. How probable is it now that US deaths from pneumonia will NOT be attributed to COVID-19?
  2. This change in medical reporting has had / will have what effects on the headlines we’ve seen and will see?
  3. Who has benefited / will benefit from (medical, economic, social, and political) reports on and actions taken with the change in medical reporting to: “COVID-19 being the underlying cause more often than not.”
  4. Who has suffered and will suffer from these reports and actions?

If people don’t stand up for their rights, their rights will be forgotten

gettingwell4 4-5 stars Advanced knowledge, Beliefs, Epigenetics, Immune system, Memory, Stress

YouTube took down this interview and a follow-on interview It was known to everybody that the lockdown would cause a catastrophe.

Here’s an interview last week with a German epidemiologist, Professor Wittkowski, who isn’t on a government payroll:

“First of all the elderly and fragile should be separated from the population where the virus is circulating. Everyone else, especially the children, should keep going to school, because they will be the primary impetus for herd immunity.

Flattening the curve prolongs the time a virus stays in the population. People staying indoors keeps the virus healthy.

Like every other respiratory disease, without government intervention, the pandemic would already be over like it’s over in China and South Korea. Except, both in China and South Korea, social distancing started very close to the peak. By keeping the virus from running its course, they are now having a second wave of cases. It will keep on if we don’t let it complete.

There’s nothing to be scared about. This is a flu epidemic like others, maybe more severe. What’s changed is the internet. People get their information in a few seconds, rather than a week.

Tracking a respiratory disease is impossible. Even in times of social distancing. Nature has ways to make sure we survive.

The standard for AIDS reporting, i.e., the date of infection separated from the date of reporting, is not being followed.

If we had herd immunity now, we wouldn’t have a second wave in the fall. Herd immunity typically lasts for a couple of years. If we prevent herd immunity, it is certain that a second wave will occur.

Testing doesn’t stop anything. Antibody testing will give us estimates of herd immunity, which would be useful.

We don’t die of the virus. We die of pneumonia.

The downside of starting containment is that we should not believe that we are more intelligent than mother nature when we were evolving. Mother nature was pretty good at making sure we were a good match for the diseases that we happened to see virtually every year.

I think people, especially in the United States, are more docile than they should be. People should talk with their politicians, question them, ask them to explain. Because if people don’t stand up to their rights, their rights will be forgotten.”