Defend yourself with taurine

This densely packed 2021 review subject was taurine:

“Taurine (Tau), a sulphur-containing non-proteinogenic β-amino acid, has a special place as an important natural modulator of antioxidant defence networks:

  • Direct antioxidant effect of Tau due to scavenging free radicals is limited, and could be expected only in a few tissues (heart and eye) with comparatively high concentrations.
  • Maintaining optimal Tau status of mitochondria controls free radical production.
  • Indirect antioxidant activities of Tau due to modulating transcription factors leading to upregulation of the antioxidant defence network are likely to be major molecular mechanisms of Tau’s antioxidant and anti-inflammatory activities.
  • A range of toxicological models clearly show protective antioxidant-related effects of Tau.”

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https://www.mdpi.com/2076-3921/10/12/1876/htm “Taurine as a Natural Antioxidant: From Direct Antioxidant Effects to Protective Action in Various Toxicological Models”


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Your lungs and Nrf2 activity

Two 2021 papers of Nrf2 activation effects on lung diseases, with the first a McGill University review:

“Oxidative stress and subsequent activation of Nrf2 have been demonstrated in many human respiratory diseases. The purpose of this review is to summarize involvement of Nrf2 and its inducers in acute respiratory distress syndrome, chronic obstructive pulmonary disease (COPD), asthma, and lung fibrosis in both human and experimental models.

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These inducers have proven particularly effective at reducing severity of oxidative stress-driven lung injury in various animal models. In humans, these compounds offer promise as potential therapeutic strategies for management of respiratory pathologies associated with oxidative stress, but there is thus far little evidence of efficacy through human trials.

Perhaps, by analogy with biologics, patients with demonstrated deficient antioxidant responses to their disease should be selected for study in future clinical trials.”

https://www.frontiersin.org/articles/10.3389/fphys.2021.727806/full “Role of Nrf2 in Disease: Novel Molecular Mechanisms and Therapeutic Approaches – Pulmonary Disease/Asthma”


A second paper was a human/rodent study of COPD:

“We investigated Nrf2 expression and epigenetic regulation, and mechanisms by which the Nrf2 signaling pathway in ferroptosis is related to COPD. These findings elucidated pathways of ferroptosis in bronchial epithelial cells in COPD, and revealed Nrf2 as a potential target for COPD treatment.

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DNA hypermethylation at specific CpG sites of the Nrf2 promoter in primary epithelial cells and in clinical lung tissues is correlated with decreased Nrf2 expression, which is related to COPD occurrence and development.”

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8684379/ “Hypermethylation of the Nrf2 Promoter Induces Ferroptosis by Inhibiting the Nrf2-GPX4 Axis in COPD”


Similar to this second paper’s CpG findings, Eat broccoli sprouts for your heart found:

“Sulforaphane (SFN) reduced Ang II‐induced CpG hypermethylation and promoted Ac‐H3 [histone H3 acetylation] accumulation in the Nrf2 promoter region, accompanied by inhibition of global DNMT [DNA methyltransferase] and HDAC [histone deacetylase] activity, and a decreased protein expression of key DNMT and HDAC enzymes. Overall, DNA methylation and histone deacetylation are considered to inhibit gene transcription with a synergistic effect.

Nrf2 can also be regulated independently of Keap1. Evidence indicates that SFN may indirectly activate Nrf2 by affecting activity of several upstream kinases.”

However, this second paper didn’t measure DNMT and HDAC inhibition, although their therapeutic effects in reducing oxidative injury and inflammation may have been present.

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Gut microbiota vs. disease risks

This 2021 review subject was risk relationships between diseases from the perspective of gut microbiota:

“There is a significant inverse relationship between the onset of Alzheimer’s disease/Parkinson’s disease (AD/PD) and cancer, but the mechanism is still unclear. Considering that intestinal flora can connect them, we briefly introduced the relationship among AD/PD, cancer, and intestinal flora, studied metabolites or components of the intestinal flora, and the role of intestinal barriers and intestinal hormones in AD/PD and cancer.

According to existing evidence:

  • Bifidobacterium and Lactobacillus positively affect AD/PD and cancer;
  • Ruminococcaceae, Prevotellaceae, and Prevotella significantly improve on AD/PD but harm cancer; and
  • Blautia has universal anticancer ability, but it may aggravate AD pathology.

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This may partially explain the antagonistic relationship between neurodegenerative diseases and cancer. When some individuals suffer from one disease, their intestinal flora change to obtain a stronger resistance to the other disease than healthy individuals, which is consistent with statistical data.”

https://www.sciencedirect.com/science/article/pii/S0753332221011276 “Composition of intestinal flora affects the risk relationship between Alzheimer’s disease/Parkinson’s disease and cancer”


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Inevitable individual differences

This 2021 review subject was individual differences:

“We will focus on recent findings that try to shed light on the emergence of individuality, with a particular interest in Drosophila melanogaster.

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Another possible source of potential behavioral variability might come from the interaction of individuals with environmental microbes, from Wolbachia infections to changes in the gut microbiome. In this particular case, no genetic variation or neural circuit alteration would be responsible for the change in behavior.

Finally, from an evolutionary point of view, individuality might play an essential role in providing an adaptive advantage. For example, we have described that animals might use diversified bet-hedging as a mechanism to produce high levels of variation within a population to ensure that at least some individuals will be well-adapted when facing unpredictable environments.”

https://www.frontiersin.org/articles/10.3389/fphys.2021.719038/full “Behavior Individuality: A Focus on Drosophila melanogaster


Other papers on this subject include:

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Immune system aging

This 2021 review by three coauthors of Take responsibility for your one precious life – Trained innate immunity cast a wide net:

“Non-specific innate and antigen-specific adaptive immunological memories are vital evolutionary adaptations that confer long-lasting protection against a wide range of pathogens. However, these mechanisms of memory generation and maintenance are compromised as organisms age.

This review discusses how immune function regulates and is regulated by epigenetics, metabolic processes, gut microbiota, and the central nervous system throughout life. We aimed to present a comprehensive view of the aging immune system and its consequences, especially in terms of immunological memory.

aging immune system

A comprehensive strategy is essential for human beings striving to lead long lives with healthy guts, functional brains, and free of severe infections.”

https://link.springer.com/article/10.1007/s12016-021-08905-x “Immune Memory in Aging: a Wide Perspective Covering Microbiota, Brain, Metabolism, and Epigenetics”


Attempts to cover a wide range of topics well are usually uneven. For example, older information in the DNA Methylation In Adaptive Immunity section was followed by a more recent Histone Modifications in Adaptive Immunity section.

This group specializes in tuberculosis vaccine trained immunity studies, and much of what they presented also applied to β-glucan trained immunity. A dozen previously curated papers were cited.

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Glutathione primes β-glucan-trained immunity

Two 2021 papers on glutathione interactions with β-glucan, with the first studying human cells from healthy donors:

“(1→3)-β-D-Glucan stimulation induces epigenetic and transcriptomic changes in monocytes associated with increased glutathione (GSH) synthesis and metabolism. Intracellular glutathione levels were crucial in regulating several monocyte antifungal functions including resilience to oxidative stress, immunometabolism, nitric oxide production, phagocytosis, and cytokine production.

Our findings demonstrate an important role for GSH in immunity, and outline a better understanding of the acute response of monocytes to infections.”

https://www.frontiersin.org/articles/10.3389/fimmu.2021.694152/full “Glutathione Metabolism Is a Regulator of the Acute Inflammatory Response of Monocytes to (1→3)-β-D-Glucan”


A second study investigated the subject with a dozen rodent experiments:

“We demonstrated that antioxidation by GSH supported an environment essential for β-glucan-induced metabolic and epigenetic changes in monocytes. We found that GSH induced glycolysis and glutaminolysis in β-glucan-trained immunity in a mTOR-dependent manner.

These results uncovered the GSH/mTOR/c-Myc signaling axis as the central effector of metabolic reprogramming in trained immunity. We revealed that the delicate GSH/ROS redox balance determines discrete, long lasting metabolic modifications that are causal to β-glucan-trained immunity.

Our results suggest that H3K27me3 demethylation is a necessary event. We identified H3K27me3 demethylation as a novel histone modification mark that was impaired by GSH deficiency in β-glucan-trained bone marrow derived macrophages.

We identified EZH2 as a potential tool to boost trained immunity under GSH deficiency conditions, or to enhance trained immunity in clinical settings where excessive inflammatory responses could be beneficial.

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Overall, these insights contribute to unraveling metabolic and epigenetic changes during trained immunity.”

https://www.sciencedirect.com/science/article/pii/S2213231721003669 “Glutathione synthesis primes monocytes metabolic and epigenetic pathway for β-glucan-trained immunity”


The second paper of Remembering encounters provides future benefits also explored this subject.

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Offspring brain effects from maternal adversity

This 2021 rodent study investigated conception through weaning effects on offspring from stressing their mothers:

“We investigated consequences of two prenatal insults, prenatal alcohol exposure (PAE) and food-related stress, on DNA methylation profiles of the rat brain during early development. We analyzed patterns in prefrontal cortex, a key brain region involved in cognition, executive function, and behavior, of both males and females, and found sex-dependent and sex-concordant influences of these insults.

The pair-fed (PF) group in the PAE model is a standard control for effects of alcohol in reducing food intake. However, compared to the PAE group that, albeit eating less, eats ad libitum, pair-feeding is a treatment in itself, with PF dams receiving a restricted ration, which results in both hunger and a disrupted feeding schedule. These stress-related effects could potentially parallel or model food scarcity or food insecurity in human populations.

We observed more DMRs (Differentially Methylated Regions) that showed decreased DNAm rather than increased DNAm in PF animals, suggesting that food-related stress may interfere with one-carbon metabolism and the pathways that deposit methylation on DNA. We also identified a sex-concordant DMR that showed decreased DNAm in PF animals in the glucocorticoid receptor Nr3c1, which plays a key role in stress responsivity and may reflect a reprogramming of the stress response.

This result is in line with previous studies that have shown that pair-feeding is a considerable stressor on dams, with lasting consequences on development, behavior, and physiology of their offspring. Altered DNAm of this key HPA axis gene may reflect broader alterations to stress response systems, which may in turn, influence programming of numerous physiological systems linked to the stress response, including immune function, metabolic processes, and circadian rhythms.

In PAE and PF animals compared to controls, we identified 26 biological pathways that were enriched in females, including those involved in cellular stress and metabolism, and 10 biological pathways enriched in males, which were mainly involved in metabolic processes. These findings suggest that PAE and restricted feeding, both of which act in many respects as prenatal stressors, may influence some common biological pathways, which may explain some of the occasional overlap between their resulting phenotypes.

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This study highlights the complex network of neurobiological pathways that respond to prenatal adversity/stressors and that modulate differential effects of early life insults on functional and health outcomes. Study of these exposures provides a unique opportunity to investigate sex-specific effects of prenatal adversity on epigenetic patterns, as possible biological mechanisms underlying sex-specific responses to prenatal insults are understudied and remain largely unknown.”

https://www.mdpi.com/2073-4425/12/11/1773/htm “Prenatal Adversity Alters the Epigenetic Profile of the Prefrontal Cortex: Sexually Dimorphic Effects of Prenatal Alcohol Exposure and Food-Related Stress”


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The impact of transgenerational epigenetic inheritance and early life experiences

A 2021 interview with McGill University’s Moshe Szyf:

There is a rejection of transgenerational inheritance as it goes against progressive thinking because it ties us to previous generations. The theory faces rejection because it sounds deterministic.

But if you understand what epigenetics is, it’s not deterministic. There is stability, and there’s also room for dynamic change.

The only way things change in the body for the long term is via epigenetics. We don’t know everything yet, new discoveries are yet to happen, and then we will just say, ‘Wow, it’s so obvious!’

The immune system is tightly connected to the brain and is directly affected by early adversity. Even though we will not be able to learn what’s going on in the brain, as far as epigenetics in living people, we will gain a lot of information from how the immune system responds to early adversity, and how this is correlated with behavioral phenotype and with mental health.

This brings into question the whole field of neuroimmunology, of which there is a lot of data. But it seems that a lot of psychiatrists are totally oblivious to these data, which is astounding, because the glucocorticoid hormone – the major player in this mechanism due to its involvement in early life stress as well as control of behavior – also controls immune function.

Nobody can live long enough to oversee a human transgenerational study. In humans, correlations are usually in peripheral tissue, where changes are small. The jury’s not out yet, but if evolution used it for so many different organisms, some of which are very close to us in the evolutionary ladder, it’s impossible that humans don’t use it.

How are current findings in animal models relevant to humans? How do we develop human paradigms that will allow us to achieve a higher level of evidence than what we have now?

  • One way is the immune-inflammatory connection to other diseases. I think this is where the secret of epigenetic aging lies, as well as epigenetics of other diseases.
  • Every disease is connected to the immune system. The brain translates the behavioral environment to the immune system, and then the immune system sends chemical signals across the body to respond to these challenges.

We need to understand that epigenetic programs are a network. Move beyond candidate genes, understand the concept of a network, and really understand the challenge: Reset the epigenetic network.

Epigenetics is going to be rapidly translated to better predictors, better therapeutics, and more interesting therapeutics. Not necessarily the traditional drug modeled against a crystal structure of an enzyme, but a more networked approach. Ideas about early life stress are critical and have impacted the field of childcare by highlighting the importance of early childhood relationships.”

https://www.futuremedicine.com/doi/10.2217/epi-2021-0483 “The epigenetics of early life adversity and trauma inheritance: an interview with Moshe Szyf”


Trained immunity genes

This 2021 human cell study investigated trained immunity responses:

“We integrated genetic, epigenetic, and functional validation data to shed light on regulation of trained immunity responses. This data integration revealed a novel role of SIGLECs and KDM4 genes on trained immunity responses.

  • Siglec-5 is an inhibitory receptor that dampens the immune response, and was found to display reduced levels of activation mark H3K4me3 upon β-glucan training.
  • Siglec-14 has a ligand-binding domain almost identical to Siglec-5 but in contrast to Siglec-5, leads to activation of the inflammatory response. Differential expression of Siglec-14 has been shown to play a role in incidence of premature delivery in Group B Streptococcus-positive mothers, COPD exacerbation, and susceptibility to tuberculosis.
  • Within the family of histone demethylases, members of the KDM4 family showed the strongest association with trained immunity responses via modulation of methylation at H3K9.

We observed a high degree of inter-individual variability in both β-glucan and BCG-induced trained immunity responses in both cohorts. Age showed no correlation with induction of trained immunity, whereas male individuals showed higher trained immunity responses as assessed by measuring TNF-α production and IL-6.

By studying processes underlying heterogeneity of trained immunity responses, we prioritized and identified important candidate genes and pathways implicated in trained immunity that could be novel targets for diagnostic and therapeutic purposes. KDM4 demethylases and Siglecs are also considered attractive therapeutic targets in oncology and other immune cell-mediated diseases.”

https://onlinelibrary.wiley.com/doi/full/10.1002/eji.202149577 “An integrative genomics approach identifies KDM4 as a modulator of trained immunity”


Most of what this study found can be extrapolated to yeast cell wall β-glucan’s effects.

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Week 87 of Changing to a youthful phenotype with sprouts

This week I dialed back eating microwaved 3-day-old broccoli / red cabbage / mustard sprouts from twice a day to once a day. For my reasoning, here are two papers on broccoli sprouts and thyroid function, with the first a 2018 human study:

“We analyzed biochemical measures of thyroid function and thyroid autoimmunity in a subset of participants in a broccoli sprout clinical trial. The present work is a retrospective analysis of a subset of serum samples collected during a clinical trial conducted from mid-October 2011 to early January 2012.

130 individuals received placebo beverage, and 137 received broccoli sprout beverage for 84 consecutive days (12 weeks). Blood samples from day 0 and day 84 were analyzed in a subset of 45 female participants (19 placebo, 26 broccoli sprout beverage) for serum thyroid-stimulating hormone (TSH), free thyroxine (fT4), thyroglobulin (TG), anti-TG, and anti-thyroid peroxidase (anti-TPO) antibodies.

The percentage of patients with subclinical hypothyroidism (elevated TSH with normal fT4) was not significantly different between the two groups either before or after treatment.

subclinical hypothyroidism

Daily ingestion of a broccoli sprout extract beverage over 84 days had no deleterious effect on thyroid function tests or measures of thyroid autoimmunity. It may be prudent to evaluate thyroidal safety of plant-based food supplements on a case-by-case basis.”

https://www.sciencedirect.com/science/article/abs/pii/S0278691519300547 “Broccoli sprout beverage is safe for thyroid hormonal and autoimmune status: Results of a 12-week randomized trial” (not freely available)


A 2020 review by three of these coauthors summarized further details:

“One difference between the thyroid and other tissues is that ROS are not primarily a byproduct of its physiology, but an indispensable part of it. Thyroid follicular cells actively produce H2O2 to facilitate a cascade of redox reactions that sequentially oxidize iodide, iodinate tyrosine residues within Tg, and couple iodinated tyrosine residues of Tg to each other to form T4 and T3 (triiodothyronine).

There exists a fail-safe mechanism in which specific combinations of four Keap1 cysteines can form a disulfide bond to sense H2O2. This sensing mechanism appears to be distinct from that triggered by other Nrf2 inducers, such as electrophiles.

Findings from Keap1KD mice suggest that chronic genetic activation of Nrf2 signaling may have negative consequences for the thyroid gland. However, analysis of data from a clinical trial has shown that consumption of a broccoli sprout beverage (yielding pharmacologically active amounts of the Nrf2-activating compound sulforaphane) is safe for thyroid hormonal and autoimmune status during a 12-week administration period.

Nevertheless, it appears prudent to monitor thyroid function and thyroid volume (at least by palpation) in patients treated with Nrf2-modulating compounds in clinical trials or clinical practice.”

https://www.mdpi.com/2076-3921/9/11/1082/htm “The Keap1/Nrf2 Signaling Pathway in the Thyroid—2020 Update”


My Day 70 lab results for inflammation markers were great:

IL-6 2020

A year later, IL-6 was below the test’s detection limit, and high-sensitivity C-reactive protein could hardly have been better at 0.24 mg/L.

But TSH (reference interval 0.45 – 4.50 μIU/mL) increased from 3.01 to 7.50. Here’s what Labcorp Technical Review L8186 said:

“The panel concluded that despite the fact that serum TSH concentrations higher than 2.5 μIU/mL but less than 4.5 μIU/mL may identify some individuals with the earliest stage of hypothyroidism, there is no evidence for associated adverse consequences. Additionally, consequences of subclinical hypothyroidism with serum TSH levels between 4.5 μIU/mL and 10 μIU/mL are minimal, and the panel recommends against routine treatment of patients with TSH levels in these ranges.”

I went in last weekend to retest. Although the provider verbally agreed to test TSH, free T3, and free T4, a different test was ordered.

TSH was still high at 5.85 μIU/mL. Other measurements (Total T4, T3 Uptake, and Free Thyroxine Index) aren’t suitable substitutes for free T3 and free T4. I’ll specify Labcorp test numbers next time.


My hypothesis is that preconditioning my endogenous ARE system twice daily worked alright elsewhere, but not for my thyroid. We’ll find out in 2022 whether halving the electrophilic activations of my Nrf2 signaling pathway has any effect on thyroid measurements.

I don’t take anything with, or an hour before or after these very reactive isothiocyanates. I continue to eat 3-day-old oat sprouts twice a day with other foods.

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Uses of the neutrophils-to-lymphocytes ratio

This 2021 review subject was recent history and uses of the neutrophils-to-lymphocytes ratio parameter to indicate systemic inflammation and stress:

“NLR is widely used across almost all medical disciplines as a reliable and easily available marker of immune response to various infectious and non-infectious stimuli. NLR reflects dynamic relationships between innate (neutrophils) and adaptive (lymphocytes) cellular immune response during illness and various pathological states.

A normal range of NLR is between 1–2, and values higher than 3.0 and below 0.7 in adults are pathological. NLR between 2.3–3.0 may serve as an early warning of cancer, atherosclerosis, infection, inflammation, psychiatric disorders, and stress.

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Neutrophils play a pivotal role in innate immune response including phagocytosis, and release of a variety of cytokines and molecule mediators. Lymphocytopenia is a hallmark of stress while inflammation is due to demargination, redistribution, and accelerated apoptosis.

Opposite changes in neutrophil and lymphocyte counts are a multifactorial dynamic process depending on regulation of various immunologic, neuroendocrine, humoral, and biologic processes such as margination / demargination, mobilization / redistribution, accelerated / delayed apoptosis, influence of stress hormones, and sympathetic / parasympathetic nervous system imbalance. NLR is the best expression of a tight functional relation between two fundamental immunocompetent leukocyte populations.”

https://doi.org/10.4149/bll_2021_078 “Neutrophil-to-lymphocyte ratio, past, present and future perspectives”


The fourth study of Uses of the lymphocytes-to-monocytes ratio also commented on NLR.

Sunday morning stroll

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Eat broccoli sprouts to prevent radiation damage

This 2021 rodent study investigated effects of sulforaphane on skin damage from irradiation:

“Radiotherapy is currently the main treatment for various cancers. We observed the protective effect of sulforaphane (SFN) on radiation-induced skin injury (RISI), including oxidative stress and inflammatory response indexes, and Nrf2 expression with its downstream antioxidant genes:

  • SFN prevented DNA damage caused by radiation.
  • SFN prevented and treated radiation-induced skin inflammation.
  • SFN prevented radiation-induced oxidative stress in skin.
  • Activation of Nrf2 and expressions of its downstream genes in skin induced by SFN.

Nrf2 downstream antioxidant genes induced by SFN

Mice were randomly assigned to one of four groups (n = 8), including control group (CON), SFN group, irradiation (IR) group, and IR plus SFN (IR/SFN) group (* p < 0.05 vs. CON; & p < 0.05 vs. IR).

Our most innovative discovery was that SFN provided skin protection from IR. At present, there are a few drugs to treat RISI in clinical patients, but the effect is not very ideal, or some may cause certain side effects.

SFN extracted from natural broccoli has no toxicity and is easily accepted for usage in clinic. According to our findings, SFN will provide a new strategy for clinical treatment and prevention of RISI in the future.”

https://www.mdpi.com/2076-3921/10/11/1850/htm “Sulforaphane-Mediated Nrf2 Activation Prevents Radiation-Induced Skin Injury through Inhibiting the Oxidative-Stress-Activated DNA Damage and NLRP3 Inflammasome”


This study’s findings probably also apply to less-severe skin damage caused by sun exposure.

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Is liver damage reversible?

This 2021 rodent study measured sequential liver changes caused by a high-fat diet:

“Using a longitudinal mouse study of diet-induced obesity in male mice, we investigated kinetics of hepatic DNA methylation and gene expression compared to those of obesity-induction to assess if they could be causal for development of insulin resistance. We aimed to find out if these changes were reversed by massive weight loss induced by vertical sleeve gastrectomy or metformin treatment.

We identified two CpG sites within exon 1 of Fgf21 that became gradually hypomethylated upon HFD feeding. DNA demethylation started between week two and four, to become significant at week five, and significantly correlated with hepatic Fgf21 gene expression.

These DNA methylation changes preceded development of insulin resistance, and were potentially causally involved in increased Fgf21 expression and plasma levels associated with insulin resistance. This points to a key regulatory function of gene body DNA methylation, which was eventually a compensatory response to counteract the developing insulin resistance.

HFD-induced decrease in Fgf21 DNA methylation could not be reversed by vertical sleeve gastrectomy or metformin treatment. As soon as weight loss slowed down or mice started to re-gain weight, differences in DNA methylation were no longer detected compared to sham-operated mice.

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As the altered DNA methylation pattern was acquired during adulthood in differentiated cells, our data emphasize that metabolic programming via DNA methylation is dynamic and not restricted to fetal development. This supports the concept that individuals can actively influence their DNA methylation patterns by lifestyle choices.

Our data indicate that DNA methylation alterations in key metabolic tissues can be acquired by an obesogenic diet, and not easily be reversed by interventions common in obese and diabetic subjects.”

https://www.sciencedirect.com/science/article/pii/S0955286321003272 “Dietary induction and reversal of obesity and insulin resistance is associated with changes in Fgf21 DNA methylation in liver of mice”


This study attempted two interventions that didn’t have desired effects. All about the betaine mentioned others that may reverse liver epigenetic changes.

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Eat broccoli sprouts for your liver

This 2021 rodent study investigated sulforaphane pretreatment’s role in reducing liver injuries:

“As a double blood supply organ of the portal vein and artery, the liver is highly sensitive to ischemia, and is one of the common organs to suffer from hepatic ischemia-reperfusion injury (HI/RI). HI/RI leads to overproduction of reactive oxygen species (ROS).

  • Overdoses of ROS promote reaction of lipid peroxidation and generation of the extremely aggressive oxidants nitric oxide (NO) and malondialdehyde (MDA).
  • HI/RI decreased antioxidant enzyme activity of glutathione (GSH), catalase (CAT), and superoxide dismutase (SOD).
  • Sulforaphane (SFN) intervention significantly decreased levels of MDA and NO by increasing activity of GSH, CAT, and SOD.

Inflammation is the most serious secondary injury experienced in HI/RI.

  • Monocyte chemotactic protein 1 (MCP-1) is involved in an inflammatory reaction with regulation of monocytes, T lymphocytes, and NK cells. MCP-1 can also increase infiltration of inflammatory cells by activating NF-κB.
  • Tumor necrosis factor-α (TNF-α) is a promoter of the inflammatory response. Interleukin-6 (IL-6) is an inflammatory mediator in the acute reaction period.
  • SFN treatment significantly decreased HI/RI-induced expression of TNF-a, IL-6, and MCP-1.

sulforaphane and liver inflammation

In conclusion, SFN has a protective effect on HI/RI. The mechanism is associated with activating Nrf2/HO-1 signaling to suppress oxidative stress and inflammation.”

https://www.sciencedirect.com/science/article/abs/pii/S0966327421000794 “Sulforaphane alleviates hepatic ischemia–reperfusion injury through promoting the activation of Nrf-2/HO-1 signaling” (not freely available)


A human equivalent of this study’s 5 mg / kg sulforaphane dose was (.161 x 5 mg) x 70 kg ≈ 56 mg. For comparison, my estimated daily sulforaphane intake from microwaved sprouts is 52 mg.

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