Year: 2026

Eat broccoli sprouts to prevent or treat obesity

gettingwell4 4-5 stars Advanced knowledge, Stress

This 2026 rodent study made mice obese with a high-glycemic-index diet, and intervened with different doses of sulforaphane during and after inducing obesity:

“To our knowledge, this is the first study investigating therapeutic effects of sulforaphane (SFN) on obesity resulting from feeding with high-glycemic-index diet (HGID). To evaluate the potential role of SFN on energy metabolism, obesity development, and insulin resistance, effects were tested by administering SFN at different doses [oral 5 mg and 20 mg] in addition to HGID and after animals were made obese with HGID.

Energy, macronutrient, and fiber contents of the HGID used in the experiment and the isocaloric control group feed were kept equal. The only difference between HGID and the control group feed was composition of the starch. While starch in the HGID was a waxy corn starch consisting of 100% amylopectin, it was natural starch (75% amylopectin, 25% amylose) in the control group.

This study is strengthened by its:

  • Experimental design, in which SFN was administered at multiple doses both during exposure to HGID and after development of HGID-induced obesity, allowing for a comprehensive evaluation of its effects on energy metabolism, obesity progression, and insulin resistance.
  • Focus on specific components of HGID. To be able to separate effects of the HGI diet pattern, one of the long-standing criticisms regarding GI, from individual components it contains, especially dietary fiber, we were able to evaluate glycemic index interaction by keeping energy, macronutrient, and fiber contents of feeds equal and the starch composition different.

Several limitations should be acknowledged.

  • Potential adverse effects of the 5 mg/kg/day and 20 mg/kg/day doses of sulforaphane in this study were evaluated in terms of clinical signs. However, systemic adverse effects, particularly those affecting the brain, cardiovascular system, or other organs, were not assessed.
  • The relatively short duration of the SFN intervention (five weeks following development of obesity induced by a HGID) may have limited the ability to fully capture all potential changes in the measured variables. It may be beneficial to observe for a longer period in future studies to provide evidence that SFN reverses HGID-induced obesity.
  • The ideal dose of SFN has not yet been determined. Dose and bioavailability are considered important parameters that need to be clarified for SFN to be considered as an anti-obesity agent.

Results indicate that SFN may provide potential benefits both as a protective agent in the obesity development process and as a therapeutic approach after obesity has developed.

  • While SFN suppresses obesity development by combating increased energy consumption, body weight, deteriorated lipid profile, and decreased insulin sensitivity upon exposure to HGID, it supports obesity treatment with its aspects of reducing food consumption and body weight gain and improving glycemic control.
  • SFN may reverse adverse effects of HGID in a time- and dose-dependent manner by regulating postprandial insulin, restoring IRS1/IRS2 function, inhibiting gluconeogenesis through coordinated activation of signaling between sirtuins and PGC-1α, and shifting liver metabolism from lipid synthesis toward mitochondrial oxidation.”

https://www.mdpi.com/2072-6643/18/4/574 “Sulforaphane Against the Metabolic Consequences of a High-Glycemic-Index Diet: Protective and Therapeutic Mechanisms Associated with Obesity and Insulin Resistance”

A human equivalent to this study’s daily oral low sulforaphane dose is (5 mg x .081) x 70 kg = 28 mg, which is achievable by eating broccoli sprouts every day. People won’t tolerate quadrupling 28 mg to a human equivalent of the study’s 20 mg daily oral sulforaphane dose, so I didn’t curate this study’s high-sulforaphane-dose-specific findings.

Human age equivalents to this study’s 8-week-old, 23-week-old, and 28-week-old mice are respectively 18-25 years, 25-35 years, and 28-38 years.

A 42-month human study of broccoli sprouts’ effects on cognitive function

gettingwell4 4-5 stars Advanced knowledge, Epigenetics, Memory ,

A 2026 paper provided details of a 2020-2023 human trial of broccoli sprouts:

“In a 42-month randomized, double-blind, placebo-controlled trial, 26 participants aged 63–90  years with memory impairment were randomly assigned to receive either 30 mg/day of glucoraphanin (GLR) or placebo. The primary outcome was the change in Memory Performance Index (MPI) scores from the mild cognitive impairment (MCI) screen. This study evaluated the long-term efficacy of GLR supplementation on cognitive function in older adults at an elevated risk for Alzheimer’s disease (AD), including those with MCI.

Participants were instructed to take three capsules of either the GLR or placebo supplements daily for 42 months. The GLR supplement contained 30 mg of GLR purified from broccoli sprouts, along with 120 mg of mustard powder per three capsules. Mustard powder was included as a source of exogenous active myrosinase to enhance the enzymatic conversion of GLR to sulforaphane. The placebo supplement contained 0 mg of GLR.

No significant group difference was observed in the initial 6 months. A marginal difference in favor of GLR appeared in the later phase (30 and 42 months), including the 42-month endpoint.

The GLR group demonstrated superior performance on immediate recall and delayed free recall tests. MCI participants showed a greater MPI improvement with GLR.

Long-term GLR supplementation may help preserve cognitive function in individuals at elevated risk for AD, particularly those with MCI. Larger trials are warranted to confirm efficacy and clarify underlying mechanisms.”

https://www.frontiersin.org/journals/nutrition/articles/10.3389/fnut.2026.1740494/full “Efficacy of 42-month oral administration of glucoraphanin in preventing cognitive decline in individuals at elevated risk of dementia, including those with mild cognitive impairment: a randomized, double-blind, placebo-controlled pilot study”

Again, 42 is the answer! 🙂

This study was funded by the supplement manufacturer. There was no explanation of what the supplement’s “purified from broccoli sprouts” entails. Also, I didn’t mention results of voluntary group exercise because there was a long gap in the participants’ data due to government response to covid.

  • For comparison of this study’s 30 mg glucoraphanin dose, Our model clinical trial for Changing to a youthful phenotype with broccoli sprouts provided 30 grams of fresh broccoli sprouts that contained an estimated 51 mg of glucoraphanin for ten weeks. That study’s corresponding coauthor said of their 30 gram broccoli sprouts dose in Understanding a clinical trial’s broccoli sprout amount that “When we carried out tests with consumers, previous to the bioavailability studies, higher amounts per day were not easy to consume and to get eaten by participants.” There was no rationale provided for this study’s 30 mg dose other than citing two previous human studies that also used a 30 mg glucoraphanin dose.
  • For comparison of this study’s 120 mg mustard seed powder dose, my daily cruciferous food intake since five and a half years ago includes sprouted yellow mustard seeds started with 3.5 grams of seeds, along with sprouted broccoli and red cabbage started with 3.6 grams of each vegetable’s seeds, all sprouted for three days. I haven’t seen studies that show sprouting has effects on myrosinase enzyme activity.
  • This study cited Does sulforaphane reach the colon? which used 2% mustard seed powder to create sulforaphane from glucoraphanin. This study’s 120 mg mustard seed powder / 30 mg glucoraphanin is a lot more than 2%. My daily sprout intake started from 3.5 g mustard seeds / (3.6 g broccoli seeds +3.6 g red cabbage seeds) is also a lot more than 2%.

I’ve changed some items along the way, switching supplier from True Leaf to Johnny’s for organic broccoli seeds, and from non-organic Red Acre red cabbage seeds to True Leaf organic red cabbage seeds. I recently had to find another supplier of organic yellow mustard seeds when Naturevibe stopped carrying that product. I tried Food to Live, but their yellow mustard seeds when sprouted aren’t mild. I’ll next try Frontier Co-op to see if those are mild as advertised.

No hero will be rescuing your and your children’s neurodegeneration for you

gettingwell4 0-1 star Wasted resources, Dopamine, Epigenetics, Immune system, Memory, Neurochemicals, Stress , , ,

Starting this blog’s twelfth year by curating a poorly-done 2026 review of Nrf2 and its capability to change a person’s development of Parkinson’s disease. I’ll emphasize precedent conditions that if not effectively dealt with in youth, can’t prevent PD from occurring at some later life stage.

“This review explicitly examines how age-associated decline in NRF2 responsiveness intersects with redox imbalance, mitochondrial dysfunction, proteostatic failure, and neuroinflammation, core mechanisms shared between aging and PD. PD unfolds through a complex interplay of cellular stress and immune responses. Oxidative stress, mitochondrial dysfunction, and chronic neuroinflammation converge to damage dopaminergic neurons, with microglia playing a central role in amplifying this injury.

NRF2 emerges as a key regulator of antioxidant defenses, inflammatory balance, and mitochondrial protection, offering a promising target for clinical intervention. NRF2 activity favors the anti-inflammatory microglial over the pro-inflammatory phenotype. Decline in NRF2 inducibility with age impairs microglial clearance, promotes neuroinflammation, and reduces antioxidant defenses, while NRF2 activation restores protective functions and offers a promising therapeutic target.

Strategies aimed at restoring or enhancing NRF2 activity hold significant promise as disease-modifying interventions, not only to slow PD progression but also to promote resilience against the broader spectrum of age-associated neurodegenerative and inflammatory conditions.”

https://www.sciencedirect.com/science/article/pii/S0891584926000316 “NRF2 AT THE CROSSROADS OF PARKINSON’S DISEASE AND AGING: MECHANISTIC INSIGHTS AND TRANSLATIONAL PERSPECTIVES”

This review only gave lip service to PD progression outside of the brain, as if the importance of prodromal factors to a person’s neurodegeneration such as dysfunction in gut, eyes, skin, and olfactory systems can be minimized. But failure to recognize early what will doom a person to be unable to recover health in later decades is disingenuous. Since these reviewers omitted early interventions into PD prodromal factors, the best they came up with was interventions to “slow PD progression.”

Maybe these reviewers felt it would be outside the scope of this review to discuss early non-brain PD factors for more than one sentence? However, while PD is defined by striatal brain neurons, Nrf2 activity is much less in brain and central nervous system neurons than elsewhere in the body per Nrf2 Week #2: Neurons.

I disagree with these reviewers’ self-imposed emphasis on aging. Repeating ‘age-associated’ numerous times seemed as if they wanted to influence the reader into thinking age in and of itself was a cause for PD, rather than an imputed mathematical correlation. Their emphasis led to dumb mentions such as senolytics for no apparent reason than senescence is a ‘hallmark of aging’, and to meaningless ‘diseasome of aging’ characterizations, and to ignoring the existence of early non-age-associated PD diagnoses in 20- and 30-year-olds.

Whatever it takes to get published, I’d guess. Or maybe it’s that the number of omissions and useless points a review paper makes increases with the number of reviewers and their sponsors’ agendas.

For example, why was it permissible to dedicate lip service to ‘exposome’ factors like microplastics, environmental pollution, and viruses, but it’s still not permitted in 2026 to discuss research into the impacts on vascular disease and neurodegeneration of lipid nanoparticles and DNA contamination in what a large number of humans were exposed to by injected pharmaceuticals starting in late 2020? Not to mention two studies published in 2024 of over 2.5 million people whose incidences of neurologic issues, mild cognitive impairment, and Alzheimer’s disease rapidly increased after ‘vaccination’?

I’ve mentioned in this blog many times how it’s every human’s choice whether or not we take responsibility for our own one precious life. I suggest, if it’s not too late, do that for your children’s lives, too.

Celebrate Mozart’s 270th birthday

gettingwell4 Just me

“Mozart’s motet, Ave Verum Corpus, was composed in June of 1791, for his friend, Anton Stoll, a school teacher and choirmaster of the small parish church of St. Stephan in Baden, a spa-town located near Vienna which was famous for its hot thermal mineral springs. Mozart’s wife, Costanze, was pregnant with their sixth child and was ill, and so she was staying at the Baden spa for treatment (“taking the waters”).
The work was written almost as a payment to Stoll, who had often helped Mozart by making travel arrangements to and from Baden for Constanze. Writing very simply, Mozart was perhaps conscious of the limitations of a small-town choir, the manuscript for this work is dated June 17, 1791, and was presumably intended for the feast of Corpus Christi, which fell that year on June 23.”

Chronic inflammation is not a universal hallmark of human aging

gettingwell4 2-3 stars Required further work, Immune system, Stress

A 2025 human study of four geographically distinct populations investigated inflammation biomarkers:

“Inflammaging, an age-associated increase in chronic inflammation, is considered a hallmark of aging. However, there is no consensus approach to measuring inflammaging based on circulating cytokines.

We assessed whether an inflammaging axis detected in the Italian InCHIANTI dataset comprising 19 cytokines could be generalized to a different industrialized population (Singapore Longitudinal Aging Study) or to two indigenous, nonindustrialized populations: the Tsimane from the Bolivian Amazon and the Orang Asli from Peninsular Malaysia.

Much cytokine variation in these populations is probably due to the type and severity of current infections, not aging. Our results show that cytokines are not destiny with regard to inflammaging and chronic disease.

Even within industrialized populations, manifestation of inflammaging is highly heterogeneous. It may reflect immune dysregulation resulting from an evolutionary mismatch of physiology and environment, aligning with the notion that the hallmarks of aging are not universals, but rather common manifestations whose importance varies by context.

The Singapore Longitudinal Aging Study was similar to InCHIANTI except for IL-6 and IL-1RA. The Tsimane and Orang Asli showed markedly different axis structures with little to no association with age and no association with age-related diseases.

Inflammaging, as measured in this manner in these cohorts, appears to be largely a byproduct of industrialized lifestyles, with major variation across environments and populations.”

https://www.nature.com/articles/s43587-025-00888-0 “Nonuniversality of inflammaging across human populations” (not freely available) Thanks to Dr. Ian J. Wallace for providing a copy.

This study used the terms “industrialized” and “nonindustrialized” two dozen times without defining either, as if every reader knew what these researchers meant. Impreciseness wasn’t an accident, though. It invokes a meme rather than promote reader understanding. They did the same thing with not defining a significant biomarker, IL-IRA.

I’ll highlight one of the unmeasured and potentially important differences among these four populations, daily sunlight exposures. Although Singapore is one degree of latitude above the equator, sunlight availability doesn’t matter when the average 62-year-old retiree spends their days mostly indoors, and their nights viewing blue-light screens. What would be “industrialized” about this lifestyle?

Prevent your brain from shrinking studied brain volume effects of Tsimane diet and lifestyle.