Broccoli seeds and yeast?

This 2023 study created sulforaphane from broccoli seeds at room temperature using a yeast strain that expressed myrosinase enzyme:

“Myrosinase harboring high glucoraphanin-hydrolyzing activity is the key to prepare sulforaphane efficiently. Almost all the reported exogenous myrosinases are extracted obtained from plants by complex steps. In our previous study, it was proved that a Yarrowia lipolytica 20–8 carrying an Arabidopsis thaliana-derived myrosinase gene can be applied to hydrolyze glucoraphenin for efficient preparation of sulforaphene.

Before being evenly crushed, broccoli seeds were incubated at 100 ℃ for 1.5 h to eliminate endogenous myrosinases and epithiospecifier protein. One unit (U) of glucoraphanin-hydrolyzing activity was defined as the amount of enzyme that hydrolyzes glucoraphanin into 1 μmol glucose per minute.

Yeast whole-cell catalyst of Y. lipolytica 20–8 could yield 10.32 mg (58.22 μmol) sulforaphane from 1 g dried broccoli seeds within 15 min under mild reaction conditions with a conversion rate of 99.86%. This yeast whole-cell catalyst could be employed for efficient and reusable preparation of sulforaphane.”

https://www.sciencedirect.com/science/article/pii/S2590157523001104 “High-level and reusable preparation of sulforaphane by yeast cells expressing myrosinase”

These researchers referenced their 2021 study where they did the same thing with sulforaphene and radish seeds. That caused English-translation confusion in the Abstract and Conclusion sections.

This study’s yeast strain price and/or availability may preclude use for home sprouting. Arabidopsis thaliana is a road-side weed in Eurasia, though, so who knows what a functioning market could deliver?

3-day-old broccoli sprouts have the optimal yields heated broccoli seed powder at 55° C for only 5 minutes – which sufficiently inactivated epithiospecifier protein – vs. this study’s 1.5 hours at 100° C. Would you do that for five minutes, mix in yeast, then wait 15 minutes for a better sulforaphane yield?

Physical fitness and epigenetic clocks

April 23, 2023April 23, 2023 gettingwell4 5+ stars Premium, Epigenetics, Stress DNA methylation, Genetic factors

This 2023 human study of 144 men average age 68 investigated relationships among physical fitness measurements and three epigenetic clocks:

“We investigated relationships between physical fitness and age-adjusted values from residuals of the regression of DNAm aging clocks to chronological age (DNAmAgeAcceleration: DNAmAgeAccel) and attempted to determine the relative contribution of physical fitness variables to DNAmAgeAccel in the presence of other lifestyle factors.

Volume of oxygen (VO₂/kg) at ventilatory threshold and at Peak, fat free mass, calf circumference, serum HDL-C, daily intake of carbohydrates, iron, copper, vitamin C, and β-carotene were negatively related with DNAmAgeAccel.

Body fat, visceral fat area, and serum TG were positively related to DNAmAgeAccel.

Frequent alcohol consumption and past- and current-smoking status were associated with accelerated DNAmAgeAccel, while a morning lifestyle was associated with deceleration of it. Multiple regression analysis suggested that – rather than physical fitness – serum triglycerides, carbohydrate intake, and smoking status were significantly associated with DNAmAgeAccel.

In conclusion, the contribution of cardiorespiratory fitness to DNAmAgeAccel was relatively low compared to lifestyle factors such as smoking. However, this study reveals a negative relationship between cardiorespiratory fitness and DNAmAgeAccel in older men.”

https://www.medrxiv.org/content/10.1101/2023.04.12.23288187v1.full-text “Associations between cardiorespiratory fitness and lifestyle-related factors with DNA methylation-based aging clocks in older men: WASEDA’S Health Study”

Remembering life before birth

April 17, 2023April 17, 2023 gettingwell4 5+ stars Premium, Epigenetics, Immune system, Memory, Stress Control group, Embryo development, Genetic factors, Infants, Unconscious memories

This 2023 primate study investigated the body’s capability to remember prenatal experiences influencing later life:

“Maternal stressors and other environmental factors affect the developing embryo and fetus in ways that lead to increased susceptibility for chronic disease in later life. Developmental programming of chronic low-grade inflammation plays an important role in onset and progression of these diseases.

Establishing innate immune cell memory involves increased glycolysis, reduced oxidative phosphorylation, and expression of transcription factors which prime for pro-inflammatory activity. This memory relies on propagation of epigenetic modifications that develop in hematopoietic stem and progenitor cells (HSPCs), which can be passed on to progeny immune cells (i.e., macrophages).

These changes persist with altered epigenetic regulation for years after weaning – even when offspring are fed a conventional diet – predisposing offspring to inflammatory disease across their lifespans.

Several factors may initiate metabolomic reprogramming in fetal HSPCs:

We found increased chromatin accessibility of gene regulatory regions and RNA signatures supporting activation of factors with a major role in regulating macrophage inflammatory activation, including FOS/JUN, NF-κB, C/EBPβ, and STAT6.

Our prior work demonstrated a persistently altered histone code in liver tissue from juvenile animals.

Maternal diet-supplied lipids, including oleic acid, in hematopoietic tissues may play an important role in priming inflammation and metabolism in fetal HSPCs and bone marrow-derived macrophages with postnatal persistence.

Striking changes in fetal bone marrow and liver HSPCs observed here suggest that the primary driver for developmental programming of inflammation takes place in utero. However, we cannot rule out that exposure to maternal diet during lactation postnatally triggers shifts in microbiome composition or function contributing to inflammation.

Components of maternal diet, rather than maternal obesity per se, are a modifiable risk factor with potential to alter developmental programming of offspring immune systems.”

https://www.cell.com/cell-reports/fulltext/S2211-1247(23)00404-7 “Maternal diet alters long-term innate immune cell memory in fetal and juvenile hematopoietic stem and progenitor cells in nonhuman primate offspring”

And there are other ways we remember everything that happened then and along the way. Big clues are in our out-of-context responses to present day events.