Week 189 of Changing to a healthy phenotype with sprouts

November 24, 2023November 28, 2023 gettingwell4 4-5 stars Advanced knowledge, Epigenetics, Immune system, Stress

1. I started eating 3-day-old microwaved Sango red radish sprouts ten weeks ago, but stopped two weeks ago due to stomach irritation. Earlier this year I tried them for a week using a different microwaving method, and found their glucoraphasatin pungency too much to stomach.

A technique of putting red radish sprouts in a bowl then into a Ziploc bag and using 40% power on my 1000W microwave for 10 seconds tamped their pungency down enough for a while. I use that technique every morning for a 3-day-old microwaved broccoli / red cabbage / mustard sprout mix.

I stopped eating Avena sativa oat sprouts in the evening because they don’t fit into a time-restricted eating regimen of ≤ 8 hours started last month. I still eat 3-day-old Avena sativa oat sprouts begun with 20 grams of hulled grains in the morning along with hulless Avena nuda oats.

I consider Avena nuda oats to be a sprouted grain food. After soaking 18-20 hours, about a quarter of the 82 g starting grains have visible sprouts when I eat them. 91% of Avena nuda oats visibly sprouted given a three-day germination period. So most of the Avena nuda oats that don’t show sprouts after soaking 18-20 hours have already started to germinate.

2. I’ve reduced food intake with TRE, and usually finish eating for the day before 4:00 p.m. This first item was reduced and the others deleted due to volume – too much food within 8 hours:

Advanced glycation end products-less chicken vegetable soup stretches for the prep day and three more days instead of two more days.
A daily avocado.
85 g hard tofu.
85 g precooked garbanzo / dark red kidney / pinto / black bean mix with untoasted sesame seeds. Will probably restart this the next time TPTB cause empty grocery store shelves.

I changed these two items after my sense of smell and taste improved:

I split 283 g of sliced white, crimini, portobello, and shitake mushrooms into the three leftover AGE-less chicken vegetable soup servings rather than into all four servings. Don’t need an umami bomb for prep day soup to taste good.
Stopped adding 3 g inulin daily to green tea. Don’t need a sweet taste.

Usually drink three cups of green tea and a cup of aluminum-free coffee before noon.

3. Supplements changed with TRE. Although the ProdromeNeuro loading dose and the 3-day-old broccoli / red cabbage / mustard sprout mix both have about 30-35 calories, I use the later mix as the start of TRE.

When I think an item’s desired results could be antagonized by having other items in the stomach, I’ll take it without eating anything else an hour before or an hour after. I’ll use meal numbers below rather than breakfast / lunch / dinner nomenclature as divisions among them are compressed.

Before Meal 1
– 3.2 g ProdromeNeuro, with nothing else an hour before or after
– 1.5 g yeast cell wall β-glucan (Glucan 300), with nothing else an hour before or after

Meal 1
– 3-day-old microwaved broccoli / red cabbage / mustard sprouts started from 10.7 g of seeds, with nothing else an hour before or after

Meals 2, 3, and 4
– 5 g total taurine
– 3.75 g total glucosamine hydroxychloride / 3 g total chondroitin sulfate, Kirkland Signature
– 3 g total acetyl-L-carnitine, Now
– 1.8 g total chondroitin sulfate, Now
– Hyaluronic acid, Nature’s Lab, 1 serving total
– 9 mg total boron, Swanson Triple Boron Complex

Meals 2 and 4
– Balance oil (total 1400 mg linoleic acid / 350 mg linolenic acid)
– 3 g total betaine anhydrous (TMG), Now
– 2 g total arginine alpha-ketoglutarate, Swanson

Meal 2 only
– Minerals and vitamins (RDA mainly), Kirkland Signature Daily Multi
– 25 mcg D₃

Meal 3 only
– 56.7 g desalted capers
– 28.35 g walnuts
– 5 g creatine
– 600 mcg Vitamin K₂ MK-7, Now

Meal 4 only
– 1.2 g lecithin, Now
– 30 mg zinc monomethionine / 0.3 mg copper, Now
– 25 mg lutein / 5 mg zeaxanthin
– 50 mcg D₃

After Meal 4
– 3.2 g ProdromeGlia, with nothing else an hour before or after

4. I’ll get blood tests next week without involving medical professionals other than Labcorp employees. I’ll compare results to a May 2023 annual physical done in the week I started retirement to see whether I’ve changed my phenotype to be more healthy during these less-stressful past six months.

An ulnar nerve anecdote

November 22, 2023 gettingwell4 2-3 stars Required further work, Beliefs, Cerebrum, Epigenetics

Two 2023 papers demonstrated the weak-sauce treatments currently offered to resolve elbow ulnar nerve pain:

“This case report investigated the use of ultrasound-guided nerve hydrodissection and platelet releasate injection for treating ulnar neuritis at the elbow.

The patient’s symptoms were first managed with home exercise and ulnar nerve hydrodissection at the elbow, which decreased but did not resolve her pain.

Platelet releasate injection of the ulnar nerve at the elbow was subsequently performed. Six weeks post-procedure, the patient reported additional pain improvement.

Despite these results, the patient was not completely symptom-free. Persistent symptoms were attributed to her concomitant neurogenic thoracic outlet syndrome.”

https://www.cureus.com/articles/133241-platelet-releasate-injection-as-a-novel-treatment-for-ulnar-neuritis-at-the-elbow-a-case-report/ “Platelet Releasate Injection as a Novel Treatment for Ulnar Neuritis at the Elbow: A Case Report”

When a diagnosis concludes with the word ‘syndrome’, we can be assured that medical professionals don’t know any specific cause. Expect physical therapy and/or drugs and/or surgery to be recommended, which will only address symptoms, not causes.

These practitioners proposed two experimental treatments, and somehow, the patient agreed to be a lab rat for both. If they were repeatedly questioned as to whether those two treatments would address causes, I’d expect responses similar to “That’s all we can do for you.”

In line with this decade’s revelations about the medical profession, the patient was also gaslighted. These practitioners asserted “changes to the patient’s lifestyle” as a reason neither treatment worked, although no such lifestyle changes were indicated.

Medical professionals are people whose early life experiences impel them to control other people with a license, among other driving factors. They won’t discuss items outside their ideas and beliefs, because these are defenses against their and their patients’ realities.

Next is a study of 111 elbow neuropathy patients (average age 55, median follow-up period of 880 days), one third of whom had various surgeries:

“There are three main potential mechanisms of recovery after nerve lesion: (1) resolution of conduction block, (2) collateral reinnervation, and (3) nerve regeneration.

Nerve function in chronic focal compression/entrapment neuropathies seems to improve mainly due to resolution of the conduction block and collateral reinnervation.

Contribution of nerve regeneration seems to be minor.

The majority of axons lost in chronic focal neuropathies probably never recover. Further studies using quantitative methods are needed to validate present findings.”

https://www.mdpi.com/2077-0383/12/12/3906 “No Major Nerve Regeneration Seems to Occur during Recovery of Ulnar Neuropathy at the Elbow”

Another interesting thing may have unexpectedly started with my 90-day trial of Prodrome Glia and Neuro products. Here’s an abbreviated look at what I’m tracking that omits intermittent fasting data:

Left ulnar nerve pain stayed the same or decreased two hours after a ProdromeGlia loading dose from Days 11-21. After adding a ProdromeNeuro loading dose at Day 22, my left ulnar nerve pain has unexpectedly stopped.

Any resistance exercise I’ve done during the past month would have aggravated my left ulnar nerve prior to the current regimen. Yesterday I clumped together reverse curls, regular bicep curls, bench presses, and triceps extensions, in that order, two sets each. I used lower weights than in the past, squeezed at the top of concentric motion, and returned slowly with eccentric motion for each rep.

Today on Day 25 the exercised muscles burn as expected, especially due to eccentric motion. But my left ulnar nerve is fine.

At the beginning, I thought that ProdromeGlia might eventually have an effect on left ulnar nerve pain, but not ProdromeNeuro. The first paper noted “The ulnar nerve begins in the axilla as a continuation of the medial cord of the brachial plexus, originally arising from the C8 and T1 nerve roots of the spinal cord.” I’ll guess that something upstream of my left ulnar nerve may also be involved in recent results.

Don’t agree with the second paper’s unevidenced assertion that “The majority of axons lost in chronic focal neuropathies probably never recover.” I’ve had intermittent left ulnar nerve numbness and pain for over five years, which is a lot longer than the 880-day median follow-up period of that paper.

Dr. Goodenowe presented his combined daily plasmalogen precursor dose as ~100 mg/kg. My analogous combined daily plasmalogen precursor loading doses are 7200 mg, appropriate for a person who weighs 72 kg. I weigh 155 lbs. / 70 kg.

More testing is warranted, of course. Maybe I’m just in-between an intermittent occurrence of left ulnar pain. So far, the way my current regimen is playing out, every day has something to make it Thanksgiving Day.

Brain restoration with plasmalogens

November 20, 2023October 7, 2024 gettingwell4 5+ stars Premium, Acetylcholine, Amygdala, Anterior cingulate cortex, Beliefs, Brain development, Brain hemispheres, Brainstem, Cerebellum, Cerebrum, Dopamine, Epigenetics, Glutamate, Hippocampus, Hypothalamus, Limbic system, Locus coeruleus, Lower brain, Memory, Neurochemicals, Primal Therapy, Serotonin, Stress, Thalamus Brain neurons, Control group, Corpus callosum, Dr. Arthur Janov, Genetic factors, Levels of consciousness, Neural plasticity, Neurodegenerative disease, Prefrontal cortex, Unconscious feelings, Unconscious memories

In this 2023 presentation for a professional audience, Dr. Dayan Goodenowe showed an example of what could be done (in the form of what he personally did at ages 53-54) to restore and augment brain structure and function over a 17-month period by taking plasmalogens and supporting supplements:

https://drgoodenowe.com/recording-of-dr-goodenowes-presentation-from-the-peptide-world-congress-2023-is-now-available/

Follow the video along with its interactive transcript. Restorative / augmentative supplements included:

Forms of MRI used to document brain structure and function changes were:

Brain volume decreases are the rule for humans beginning at age 40. Dr. Goodenowe documented brain volume increases, which aren’t supposed to happen, but did per the below slide of overall results:

“From a global cortical volume and thickness perspective, 17 months of high-dose plasmalogens reversed ~15 years of predicted brain deterioration.”

Specific increased adaptations in brain measurements over 17 months included:

Cortical thickness .07/2.51 = +3%.
White matter microstructure fractional anisotropy +8%.
Nucleus accumbens volume +30%.
Dopaminergic striatal terminal fields’ volume +18%.
Cholinergic cortical terminal fields’ volume +10%.
Occipital cortex volume +10%.
Optic chiasm volume +225%.
Nucleus basalis connectivity.
Neurovascular coupling signal controlled by noradrenaline integrity.
Amygdala volume +4% and its connectivity to the insula, indicating ongoing anxiety and emotional stress response.
Parahippocampus volume +7%.
Hippocampus fractional anisotropy +5%.

No changes:

Amygdala connectivity to the ventral lateral prefrontal cortex, the same part of the brain that relates to placebo effect.
Hippocampus connectivity.

Decreased adaptations in brain measurements included:

White matter microstructure radial diffusivity -10%.
Amygdala connectivity to the anterior cingulate cortex to suppress / ignore / deny anxiety response.
Amygdala connectivity to the dorsal lateral prefrontal cortex.
Entorhinal cortex volume -14%.
Hippocampus volume -6%.
Hippocampus mean diffusivity (white matter improved, with more and tighter myelin) -4%.

The other half of this video was a lively and wide-ranging Q&A session.

The referenced 2023 study of 653 adults followed over ten years showed what brain deterioration could be expected with no interventions. Consider these annual volume decrease rates to be a sample of a control group:

https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2806488 “Characterization of Brain Volume Changes in Aging Individuals With Normal Cognition Using Serial Magnetic Resonance Imaging”

Also see a different population’s brain shrinkage data in Prevent your brain from shrinking.

The daily plasmalogen precursor doses Dr. Goodenowe took were equivalent to 100 mg softgel/kg, double the maximum dose of 50 mg softgel/kg provided during the 2022 clinical trial of cognitively impaired old people referenced in Plasmalogens Parts 1, 2, and 3.

He mentions taking 5 ml in the morning and 5 ml at night because he used the Prodrome oil products. 1 ml of a Prodrome oil plasmalogen precursor product equals 900 mg of their softgel product.

“My brain is trying to minimize long-term effects of pain/stress by suppressing my memory of it. But this can only go on for so long before it becomes an entrenched state.

I have solved the sustenance side of the equation. I need to work harder to solve the environmental side.”

While I agree that we each have a responsibility to ourselves to create an environment that’s conducive to our health, the above phenomenon isn’t necessarily resolvable by changing an individual’s current environment. My understanding is that long-term effects of pain, stress, and related human experiences are usually symptoms of causes that started much earlier in our lives.

Adjusting one’s present environment may have immediate results, but probably won’t have much therapeutic impact on long-term issues. Early life memories and experiences are where we have to gradually go in order to stop being driven by what happened back then.

See Dr. Arthur Janov’s Primal Therapy for its principles and explanations. I started Primal Therapy at a similar age, 53, and continued for three years.

Continued with Part 2.

A smell and taste anecdote

November 13, 2023November 13, 2023 gettingwell4 2-3 stars Required further work, Amygdala, Brainstem, Cerebrum, Dopamine, Epigenetics, Hippocampus, Immune system, Limbic system, Lower brain, Memory, Neurochemicals, Stress Brain neurons, Control group, Genetic factors, Neural plasticity, Neurodegenerative disease

Two 2023 papers, starting with a study of smell and taste disorders:

“This study investigates the impact of etiology on the epidemiologic profile, disease severity, type of treatment, and therapy outcome in smell and taste disorders.

Hyposmia has a prevalence of about 15%, while approximately 5% of the population suffers from anosmia. Multiple innervation of the taste mucosa with fibers from the seventh, ninth, and tenth cranial nerves assures robustness of the gustatory system compared to smell.

Conservative therapy employs corticosteroids, antibiotics, vitamins and and minerals as well as functional rehabilitation by olfactory training. Data regarding outcome of therapy were only available for 71 (26.3%) of patients. Only the sinunasal etiology was significantly more likely to show improvement after therapy (27.4% show improvement vs. 9.6% show no improvement).”

https://link.springer.com/article/10.1007/s00405-023-07967-1 “Characteristics of smell and taste disorders depending on etiology: a retrospective study”

This study was a little light on describing effective treatments for smell and taste problems. For example, olfactory training was said to have good therapeutic response. Looking it up, though, it seems to be whatever each practitioner feels like doing.

A review introduced the subject of olfactory ensheathing cells:

“Olfactory ensheathing cells (OECs) are glial cells of the primary olfactory nervous system, which are composed of the olfactory nerve and outer nerve fiber layer of the olfactory bulb. The primary olfactory nervous system is unique in that it can constantly regenerate.

It is now possible to remove olfactory bulb tissue and olfactory mucosa (outermost layer and lamina propria, which belong to the central nervous system and peripheral nervous system, respectively), which also suggests the potential value of OECs therapy in central nervous system and peripheral nervous system diseases. OECs can survive and renew in the central nervous system, and have been widely used in nerve regeneration and tissue repair.

Schwann cells (SCs) form the myelin sheath of the peripheral nerve, protect and nourish neurons, and play an irreplaceable role in the repair of peripheral nerve injury. There is no transcriptional difference between OECs and SCs. OECs are highly similar to SCs, and express the biomarkers of SCs.

Functional mechanisms of OECs in the treatment of neurological diseases include neuroprotection, immune regulation, axon regeneration, improvement of nerve injury microenvironment and myelin regeneration, which also includes secreted bioactive factors. Results obtained in clinical trials are not very satisfactory, and the effectiveness of these cell-based therapies remains to be proved.”

https://www.frontiersin.org/articles/10.3389/fimmu.2023.1280186/full “Potential therapeutic effect of olfactory ensheathing cells in neurological diseases: neurodegenerative diseases and peripheral nerve injuries”

Something interesting may have unexpectedly started with my 90-day trial of Prodrome Glia and Neuro products. Here’s an abbreviated look that omits my intermittent fasting and resistance exercise data:

Both product labels have a loading dose suggestion of 4-8 softgels (2 to 4 times the standard two-softgel dose) for 1-3 months. Two days after I started a Glia loading dose, my sense of smell, then sense of taste, were noticeably better.

I’ll guess that my primary olfactory nervous system glial cells are responding to these changes. At the beginning I thought that my peripheral nervous system Schwann cells might be affected regarding my left ulnar nerve. Since olfactory ensheathing cells are highly similar to Schwann cells, it doesn’t seem to be that much of a stretch to think that they could also be affected by my current regimen.

More testing is warranted, of course. I’ve had diminished smell and taste for decades, though. If the gardenias, roses, magnolias, honeysuckles, and other scents in past summers that had fainter scents than I remembered come across stronger, so much the better.

Vitamin K2 blood measurement

November 11, 2023November 12, 2023 gettingwell4 2-3 stars Required further work, Epigenetics

Two 2023 human studies used different measurement techniques to find similar results regarding Vitamin K₂ MK-7. The first compared 100 premenopausal women with 100 postmenopausal women with osteoporosis:

“Vitamin K (VK) as well as vitamin D (VD) plays an important role in osteoporosis. We developed a simple LC-MS/MS method for determination of VK1, MK-4, MK-7, 25(OH)D2, and 25(OH)D3 levels in human serum and validated the method in a study cohort of 200 patients.

MK-7 in plasma decreased earlier than VD in postmenopausal osteoporosis patients. MK-7 status is significantly associated with osteoporosis, and could be considered a predictable biomarker in diagnosis of osteoporosis in postmenopausal women.”

https://karger.com/anm/article-abstract/79/3/334/843963/Determination-of-Vitamin-K1-MK-4-MK-7-and-D-Levels?redirectedFrom=fulltext “Determination of Vitamin K1, MK-4, MK-7, and D Levels in Human Serum of Postmenopausal Osteoporosis Women Based on High Stability LC-MS/MS: MK-7 May Be a New Marker of Bone Metabolism” (not freely available)

Comparisons of postmenopausal women with and without osteoporosis are a necessary step before assigning MK-7 status as a diagnosis biomarker.

A second study sampled 518 people of various ages with unspecified health status:

“Biological properties of menaquinone-7, both those proven and those that remain to be investigated, arouse extensive interest. The most important of them is the prevention of age-related diseases.

A simple sample preparation method followed by liquid chromatography-tandem mass spectrometry-based method (LC-MS/MS) was used for selective and sensitive determination of K2MK-7 from 518 samples.

The highest degree of agreement of results with the lowest number of outliers and shortest whiskers is visible for the youngest age group. The lowest degree of agreement with the longest whiskers can be observed in males in the middle age group, i.e., 41–50 years old, with the highest values of outliers, not shown in Figure 4 for the sake of legibility, obtained in the oldest age group of females (11.7 ng/mL). The difference in the amount of vitamin K2MK-7 in females and males is noticeable in age group 41–50, which is when menopause often begins.

K2MK-7 values are significantly related to age of both females and males. Higher F-test values obtained for females not only confirmed the relationship between age and gender with content of vitamin K, but also indicated that in females, there is a greater distribution of K2MK-7 values depending on age.”

https://www.mdpi.com/1420-3049/28/18/6523 “Development, Validation, and Two-Year Application of Rapid and Simple LC-MS/MS-Based Method for the Determination of K2MK-7 in Blood Samples”

This study had more to do with establishing a simpler MK-7 measurement method than making other findings. Arbitrary age buckets weren’t informative without additional information regarding health status. Maybe these researchers’ workplace was similar to Labcorp or Quest where they didn’t interact with the blood donor?

Eat broccoli sprouts to inhibit brain cancer

November 7, 2023November 11, 2023 gettingwell4 4-5 stars Advanced knowledge, Epigenetics, Glutamate, Neurochemicals, Stress Brain neurons, Control group, Genetic factors

This 2023 rodent study by Our model clinical trial group investigated effects of broccoli seeds, 8-day-old sprouts, 95-day-old florets, and pure sulforaphane on glioma:

“This study employs a C6 rat glioma model to assess chemoprotective potential of aqueous extracts from broccoli seeds, sprouts, and inflorescences, all rich in sulforaphane (SFN), and pure SFN as positive control.

In plant material, seeds and sprouts exhibited a heightened concentration of aliphatic-type glucosinolates (GSLs), while broccoli heads showcased a more substantial amount of indole group GSLs. Similar to the GSL trend, the highest concentration of phenolic compounds was evident in sprouts, succeeded by seeds, with broccoli heads exhibiting a subsequent lower content.

Within freeze-dried aqueous extracts obtained from plant material samples, seeds exhibited the most substantial SFN content, trailed by sprouts and inflorescences. This hierarchy aligns with precursor GSL content, specifically glucoraphanin (GRA). These outcomes imply that approximately 5% of GRA content converted into SFN.

Sinapic acid derivatives emerged as the primary category of phenolic compounds. Higher concentrations of these phenolic compounds were observed in inflorescences, succeeded by seeds, and lastly, broccoli sprouts.

Aqueous extracts from seeds, sprouts, and inflorescences were administered to rats over 30 days before the introduction of C6-glioma cells. This specific time frame corresponds to a critical risk factor and initiation of the tumor niche in humans. The objective was to assess whether this consumption could protect against tumor development.

Tumor volume within the control SS group significantly increased compared to the sprout group. Volume fluctuations observed in the seed and inflorescence groups did not demonstrate any statistically significant differences when compared to the control group.

Subjects administered with 0.1 mg/kg of SFN displayed a notable decrease in tumor growth. A stark contrast is evident when compared to the corresponding control group (control OO) and the 0.7 mg/kg SFN-treated group.

These findings substantiate the notion that elevated doses of the pure compound might potentially assume a pro-oxidant role, while lower doses hold promise in fostering an environment rich in antioxidants and conducive to chemoprotection.

All experimental groups developed gliomas. However, the group administered with aqueous extract of broccoli sprouts and the group treated with pure SFN at 0.1 mg/kg exhibited formation of diffuse low-grade gliomas. Conversely, the remaining groups exhibited malignant characteristics, and manifested development of thrombosed vessels.

Incorporating broccoli sprouts into one’s regular diet emerges as a highly promising strategy for averting onset of specific types of cancer. It is the most cost-effective option for society when contrasted with consumption of nutraceuticals. While achieving a standardized effective dose of SFN via food consumption, such as sprouts, poses challenges, forthcoming clinical studies are poised to determine an appropriate dosage for shaping human intervention trials.”

https://www.sciencedirect.com/science/article/pii/S0753332223015184 “The preventive effects of broccoli bioactives against cancer: Evidence from a validated rat glioma model”

This study’s Discussion section had a lot of hand waving regarding broccoli seeds’ failure to outperform broccoli sprouts despite its 1.06 mg/kg to 0.63 mg/kg sulforaphane advantage. Although not specifically referenced, hormetic effects described in Sulforaphane in the Goldilocks zone and subsequent studies probably account for pure sulforaphane’s dose / response findings that 0.1 mg/kg better inhibited glioma than did 0.7 mg/kg.

For those who think this post’s title is over-the-top:

Although eating non-patentable broccoli sprouts is safe and cheap, how many people will wait for clinical trials to determine whether these rodent findings translate to humans?
If today there was already human clinical trial evidence confirming translatable findings, how many people would still wait for incorruptible, morally upright, honest, and trusted medical authorities’ approvals?

Plasmalogens, Part 3

November 5, 2023March 31, 2024 gettingwell4 4-5 stars Advanced knowledge, Acetylcholine, Brain development, Brain hemispheres, Brainstem, Cerebellum, Cerebrum, Dopamine, Epigenetics, Hippocampus, Hypothalamus, Immune system, Limbic system, Locus coeruleus, Lower brain, Memory, Neurochemicals, Stress, Thalamus Brain neurons, Control group, Genetic factors, Infants, Neural plasticity, Neurodegenerative disease, Prefrontal cortex

The 2022 plasmalogen clinical trial mentioned in Parts 1 and 2 bypassed peroxisome metabolism of cognitively impaired people per discussion of the below diagram:

Increasing the body’s fasting state with time-restricted eating, and preventing muscle atrophy with resistance exercise, were offered as the two most important ways to improve peroxisomal function.

I didn’t find any relevant 2023 human studies (where I could access the full study) on different non-drug treatments that I was willing to do. A 2023 review outlined aspects of peroxisomes, to include a few older human studies:

“Peroxisomes are small, single-membrane-bound organelles, which are dynamic and ubiquitous. Peroxisomes directly interact with other organelles, such as endoplasmic reticulum, mitochondria, or lysosomes. Peroxisomes exert different functions in various cells through both catabolic and anabolic pathways.

The main functions of peroxisomes can be categorized as reactive oxygen species (ROS) metabolism, lipid metabolism, and ether-phospholipid biosynthesis. Peroxisomes also play important roles in inflammatory signaling and the innate immune response.”

https://www.sciencedirect.com/science/article/pii/S2667325823001425 “Peroxisome and pexophagy in neurological diseases”

1. Since I haven’t recently tried the two main ways to improve peroxisomal function, I’ll give them a go over the next three months:

Expect to get my feeding timeframe to within eight hours. Don’t know about making it short like 6 hours, because my first meal of the day is 35 calories of microwaved cruciferous sprouts, then I wait an hour before eating anything else.
Resistance exercise progress should be measurable, as I recorded exercises during the first ten weeks of eating broccoli sprouts every day 3.5+ years ago.

2. Don’t know that I’ll recognize any cognitive improvements to the extent I did during Week 9.

I don’t have a young brain anymore, and I’m sure some decline could be measured in memory tests. But I’m not going to become a lab rat.
There’s an occasional annoyance that’s been going on for some time, especially when I’m distracted. It happens when I think of something to do, and it somehow becomes a short-term memory that I did it, instead of going into a Things To Do queue. It’s largely self-correcting. For example, regardless of what I paid, I’ll drive back to the grocery store self-checkout to retrieve a third bag that didn’t make it home. A pink-haired employee said young people leave their paid-for groceries behind all the time. It’s usually more of a reality disconnect for me than forgetfulness, because I have a memory that I performed the action. Definitely room for improvement.

3. Don’t know that I’d see biochemical changes such as some described in Part 1. Maybe I’ll move up an annual physical to compare it with the last one in May?

I already have very little oxidative stress, very little inflammation, low triglycerides, high HDL, and no major improvements are indicated on CBC / CMP / lipid panels.
Take supplements to ensure other things like acetylcholine neurotransmitter availability, one-carbon / methylation metabolism, vitamin / mineral adequacy.

4. I started the two Prodrome plasmalogen precursor supplements (ProdromeGlia and ProdromeNeuro) a week ago, and take their standard doses. My thought is that resultant plasmalogens won’t degrade very much if their primary use isn’t to immediately address oxidative stress and inflammation. That could give these extra plasmalogens a chance to make larger homeostatic contributions in myelin and membrane areas.

I don’t expect any particular effects to manifest. But I’m interested to see if these two areas would be affected:

My left ulnar nerve has been giving me problems for over five years, and several resistance exercises aggravate it. I’ve had two nerve continuity tests during that time to confirm. Numbness and pain are intermittent, though.
I still take acetaminophen several times a day for other pain.

None of the above treatments are specifically indicated. But if time-restricted feeding and/or extra plasmalogens have an effect on left ulnar or other pain, maybe I’ll be able to make better progress on resistance exercise.

Update #1 11/13/2023

Update #2 11/22/2023

Update #3 12/13/2023 comments

Update #4 1/30/2024

Update #5 3/31/2024

Plasmalogens, Part 2

November 3, 2023November 9, 2023 gettingwell4 2-3 stars Required further work, Acetylcholine, Dopamine, Epigenetics, Hippocampus, Immune system, Limbic system, Memory, Neurochemicals, Stress Brain neurons, Control group, Genetic factors, Neurodegenerative disease

This post compares Dr. Goodenowe’s clinical trial mentioned in Part 1 with other researchers’ human plasmalogen studies this decade. One of its findings was:

“Figure 1A illustrates that plasmalogen precursor DHA-AAG dose-dependently elevated both direct and indirect target species [DHA-PL, DHA-PE, and (LA + AA)-PL] and had no effect on levels of biochemically unrelated PE species index (LA + AA)-PE.

DHA-AAG had a greater elevating effect on its direct target, DHA-PL than its indirect targets.

The 1-month washout period resulted in decreased levels of both direct and indirect target species and no effect on unrelated PE species.

Figures 1A,B illustrate that DHA-AAG is converted to its direct and indirect target species in humans as predicted from animal studies on similar AAG plasmalogen precursors (Wood et al., 2011d).”

Given this century’s background of numerous animal studies, there’s a need to know what translates to humans. Here are the three most recent human plasmalogen studies in descending order where I could access the full study:

2022

“Forty unmarried male students aged 18–22 years (20 in the plasmalogen group and 20 in the placebo group) were randomly allocated to either plasmalogen (2 mg per day) or placebo treatment of 4 weeks’ duration and ingested two capsules of 0.5 mg plasmalogen or placebo twice daily.

The primary efficacy outcome was the Total Mood Disturbance (TMD) T-score of POMS 2–Adult Short.

Secondary outcomes included the seven individual scales of POMS 2, other psychobehavioral measures (Athens Insomnia Scale and Uchida-Kraepelin test), physical performance test (shuttle run, grip muscle strength, and standing long jump), plasmalogen levels in plasma and erythrocytes, plasma levels of brain-derived neurotrophic factor (BDNF), urinary 8-hydroxy-2′-deoxyguanosine (8-OHdG), body mass index, and percent body fat.

Lipid composition of purified ether phospholipids from scallop is shown below. One capsule contained 0.48 mg of ethanolamine plasmalogen and 0.02 mg of choline plasmalogen. Plasmalogen and placebo capsules were prepared by a manufacturer (B&S Corporation, Tokyo).

There were no between-group differences in physical and laboratory measurements. It is suggested that orally administered plasmalogens alleviate negative mood states and sleep problems, and also enhance mental concentration.”

https://www.frontiersin.org/articles/10.3389/fcell.2022.894734/full “Orally Administered Plasmalogens Alleviate Negative Mood States and Enhance Mental Concentration: A Randomized, Double-Blind, Placebo-Controlled Trial”

There was no dose / response investigation, so there’s no data to corroborate that this 2 mg treatment produced these effects. It isn’t difficult to think of other factors that could influence the primary outcome of a 18-22 year-old unmarried male’s moods.

2020

“Effects of ascidian-derived plasmalogens on cognitive performance improvement were assessed in a randomized, double-blind, placebo-controlled study including Japanese adult volunteers age 45.6 ± 11.1 years with mild forgetfulness. An allocation controller who was not directly involved in the study equally, but randomly, assigned participants to either the intervention group (n＝33) or the placebo group (n＝33), based on normalized Cognitrax composite memory score (the primary outcome), sex, and age at time of screen. Participants were administered either one active capsule (200 mg medium-chain triglyceride (MCT) oil including ascidian plasmalogen oil) or placebo capsule (200 mg MCT oil) per day with water, any time during the day for 12 weeks.

Ascidian plasmalogen oil was extracted from ascidians (Halocynthia roretzi) and sold by NIHON PHARMACEUTICAL CO., LTD. Based on a previous study, 33％ of lipids contained in ascidians are phospholipids, 23％ of which are plasmalogens, and fatty acids of the sn-2 position of plasmalogens are mainly EPA, DHA, oleic acid, and arachidonic acid. The active capsule contains 1 mg plasmalogen.

Compared to the placebo group, the intervention group showed a significant increase score in composite memory (eight weeks: 3.0 ± 16.3 points, 12 weeks: 6.7 ± 17.5 points), which was defined as the sum of verbal and visual memory scores. These results indicate consumption of ascidian-derived plasmalogen maintains and enhances memory function.”

https://www.jstage.jst.go.jp/article/jos/69/12/69_ess20167/_article “The Impact of Ascidian (Halocynthia roretzi)-derived Plasmalogen on Cognitive Function in Healthy Humans: A Randomized, Double-blind, Placebo-controlled Trial”

Again no dose / response investigation, so no corroborating data. Standard deviations many times larger than a sample’s mean indicated wild variability (aka noise). Maybe intervention participants experienced memory loss (3.0 mean – 16.3 SD = -13.3; 6.7 mean – 17.5 SD = -10.8)? Yet statistics inferred a signal that allowed interpreting this treatment as producing meaningful positive changes in cognitive function.

“Ten Parkinson’s disease (PD) patients age 67.80 (7.41) years received oral administration of 1 mg/day of purified ether phospholipids derived from scallop for 24 weeks. Clinical symptoms and blood tests were checked at 0, 4, 12, 24, and 28 weeks. Blood levels of plasmalogens in patients with PD were compared with those of 39 age-matched normal controls.

B&S Corporation Co. Ltd. (Tokyo) was involved in provision of capsules containing ether phospholipids derived from scallop. Ethanolamine ether phospholipids (ePE) in plasma from PD and relative composition of ethanolamine plasmalogen (plsPE) of erythrocyte membrane in PD were significantly low as compared to those of age-matched normal controls.

Oral administration of purified ether phospholipids derived from scallop for 24 weeks increased plasma ePE and erythrocyte plsPE to almost normal levels, and concomitantly improved some clinical symptoms of patients with PD. Results indicate the efficacy of oral administration of purified ether phospholipids derived from scallop to some nonmotor symptoms of PD. Physiological mechanisms of the efficacy of purified ether phospholipid derived from scallop remained to be elucidated.”

https://www.hindawi.com/journals/pd/2020/2671070/ “Improvement of Blood Plasmalogens and Clinical Symptoms in Parkinson’s Disease by Oral Administration of Ether Phospholipids: A Preliminary Report

Again no dose / response investigation, so no corroborating data. These researchers asserted their 2017 study to be a plasmalogen gold standard, as did the other two above studies.

Here’s part of what Dr. Goodenowe said about that 2017 study in a 2019 review Plasmalogen deficiency and neuropathology in Alzheimer’s disease: Causation or coincidence?:

“They did not observe a significant elevation of plasma levels of plasmalogens in the treated group relative to the baseline. Lower dose of plasmalogens (1 mg twice daily) and the labile nature of the vinyl-ether bond might have limited absorption of the intact molecule and might have contributed to the lack of response in terms of plasmalogen levels in blood as well as the cognitive function. Reported instability of plasmalogens in acidic environments questions the stability of preformed plasmalogens in gastric juice during digestion which might reduce plasmalogen bioavailability.”

Also see Part 1’s explanation of why using age-matched controls in plasmalogen studies is ridiculous.

Continued in Part 3.

Plasmalogens, Part 1

October 31, 2023November 3, 2023 gettingwell4 5+ stars Premium, Acetylcholine, Brain development, Brain hemispheres, Cerebellum, Cerebrum, Dopamine, Epigenetics, Hippocampus, Immune system, Limbic system, Lower brain, Memory, Neurochemicals, Stress Brain neurons, Control group, Corpus callosum, DNA methylation, Embryo development, Genetic factors, Infants, Neural plasticity, Neurodegenerative disease, Reciprocity

The person who knows the most about this subject is Dayan Goodenowe, PhD. Some recent publications include:

https://www.frontiersin.org/articles/10.3389/fcell.2022.864842/full “Targeted Plasmalogen Supplementation: Effects on Blood Plasmalogens, Oxidative Stress Biomarkers, Cognition, and Mobility in Cognitively Impaired Persons”

https://www.frontiersin.org/articles/10.3389/fcell.2022.866156/full “Brain ethanolamine phospholipids, neuropathology and cognition: A comparative post-mortem analysis of structurally specific plasmalogen and phosphatidyl species”

A sample of links freely available at https://drgoodenowe.com/.

1. Presentations to professional groups. Have your mouse ready to click the pause button.

https://drgoodenowe.com/dr-goodenowe-presents-at-the-iagg2023-in-yokohama-japan/ “A rare children’s disease that may be the key to reversing neurological decline in aging”

Includes videos of a treatment’s effects on a child.

https://neomarkgroup.wistia.com/medias/0qln0wy93t “The most influential biomarkers for aging and disease”

Despite the title, a considerable number of studies were presented on prenatal, infant, and early childhood development. He misspoke a few times, so read the slides.

“Phenotype is reality. Genotype is possibility. Communications links between different fields are very poorly connected in science.

Peroxisomes are islands. They don’t have DNA like your mitochondria do. Peroxisomal transport issues are important things to understand.

All aging-related cross-sectional analyses are on the rate of decline. You’re declining from a previous well state. Age-matched controls are the most ridiculous thing to do.”

2. I’ll highlight the longest of several interviews because there was plenty of room to expand on points. Maybe the best detailed explanations came as responses to that interviewer challenging with contrasting AD, traumatic brain injury, and cholesterol paradigms. Its transcript is more accurate than a usual YouTube interpretation, but there are still mistakes such as “fossil lipid” vs. phospholipid.

https://www.betterhealthguy.com/episode186 “Plasmalogens with Dr. Dayan Goodenowe, PhD”

“Science is how do you push things to its failure, until you can’t fail it again. We’ve lost that. It’s become more hypothesis proving.

Plasmalogens levels go up for a different reason than people think. The reason why it peaks in our 40s and 50s is because we’ve been myelinating. The white matter of our brain is still increasing. It’s not because we’re making more plasmalogens. It’s because the lake, the reservoir, gets full. What you’re measuring in blood is overflow from the lake. The lower plasmalogens start trickling down in your blood, the bigger drain that’s occurring on that system.

Low plasmalogens don’t just predict dementia in the elderly population. It predicts the rate of decline of that dementia. It predicts the rate of death.

The biggest drivers of plasmalogen manufacturing and the biggest reasons why they decrease with age, or in other circumstances is two things. One, the failure to maintain a fasting state of the human body. The second one is muscle atrophy.

Amyloid has absolutely nothing to do with Alzheimer’s, or dementia. It’s just a bystander on the road watching an accident happen.

Age-related cognitive decline is clearly where plasmalogens have the greatest impact. You’re always going to have mixed pathologies in the brain.

Nutritional availability of plasmalogens is virtually non-existent. As soon as they hit the hydrochloric acid of your stomach, they’re gone. They don’t make it past the stomach, or the upper intestine.”

I came across Dr. Goodenowe’s work last month from clicking a comment on this blog that linked back to her blog. Always be curious.

Continued in Part 2.

Dietary choline

October 29, 2023October 29, 2023 gettingwell4 4-5 stars Advanced knowledge, Acetylcholine, Epigenetics, Neurochemicals, Stress Control group, DNA methylation, Genetic factors

Two 2023 papers on choline intake, beginning with an analysis of 14323 people:

“Choline is an essential ingredient that is required for many biological processes in the human body, including formation of cell membranes, preservation of liver and kidney function, and production of neurotransmitters. For humans, only a small amount of choline can be endogenously generated through the liver. It is vital to supplement it in the diet to prevent deficiency.

Mean dietary choline intake was 316.5 ± 164.1 mg/d, and incidence of cardiovascular disease (CVD) was 8.8% in study participants.

New findings of our study are as follow:

In contrast to previous studies, higher dietary choline intake was associated with a lower incidence of CVD, especially incidence of stroke, in this large, nationally representative US population.

The protective role of higher dietary choline intake was accompanied by reduced inflammation and heart rate.

In the subgroup study, higher dietary choline intake – in participants aged ≥60 years, and in participants with BMIs < 30 kg/m2 – was found to be a protective factor for the presence of CVD.

Our results suggest that adequate choline intake acts against CVD, and choline deficiency should be avoided.”

https://www.mdpi.com/2072-6643/15/18/4036 “Association between Dietary Choline Intake and Cardiovascular Diseases: National Health and Nutrition Examination Survey 2011–2016”

A randomized control trial investigated choline intake effects on resistance exercise training:

“Choline plays crucial roles in several physiological processes, such as:

Neurotransmission, muscle contraction, and force generation via synthesis of chemical messenger acetylcholine;

Lipid transport via lipoprotein synthesis; and

Methyl-group metabolism as a precursor to betaine.

It supports cell membrane integrity/function as a precursor to phosphatidylcholine. Choline may also affect muscle responses to exercise via betaine, which is important for gene expression/protein synthesis.

The present study determined effects of different amounts of choline intakes (approximately 50%, 70%, and 120% of Adequate Intake (AI)) on muscle responses to resistance exercise training (RET). Three groups of 50-to-69-year-old healthy adults underwent a 12-week RET program, and submitted >48 diet logs (>4x/week for 12 weeks). Participants were randomly assigned to one of three choline groups in a double-blind manner: zero additional egg yolk (low), one additional egg yolk (medium = med), or three additional egg yolks (high) per day.

We found that low choline intake (~51% of AI) resulted in diminished strength gains compared to choline intakes of ~68% or ~118% of AI.

We observed that a high choline intake (greater than AI) did not provide additional positive effects on RET responses.

Together with choline, betaine was independently associated with change (%) in composite strength, suggesting that multiple mechanisms are at work.

There was no effect of choline consumption on any blood lipids and lipoproteins, indicating that a moderately low choline intake may not negatively affect blood lipid profiles.

Dietary cholesterol did not contribute much to variability of strength gains.

The consistency of about 50% of AI is particularly significant, as much as 40% of the older population is consuming this low level of choline where there are no overt clinical signs of deficiency, and considering potential effects of choline on age-associated loss of muscle function. This research was supported by U.S. Poultry and Egg Association.”

https://www.mdpi.com/2072-6643/15/18/3874 “The Effect of Choline and Resistance Training on Strength and Lean Mass in Older Adults”

For over a decade, I supplemented phosphatidylcholine via a small amount of lecithin every day. I stopped that three years ago when I started supplementing betaine, thinking that I wouldn’t need as much choline oxidized to plentiful betaine.

Don’t have any choline blood tests to indicate whether or not that has been the right decision. It seems like there’s more risk than reward in continuing, though, so I’ll restart 1200 mg lecithin next week at $.07 a day. That provides about the same amount of choline as does one egg.

Rocket launch followed by telemetry plane

Activate Nrf2 to improve arthritis

October 27, 2023 gettingwell4 4-5 stars Advanced knowledge, Epigenetics, Immune system, Stress Control group, Genetic factors

This 2023 rodent study cited Eat broccoli sprouts for arthritis to test a Nrf2 activator’s effects on rheumatoid arthritis:

“We show that activation of Nrf2 efficiently improves arthritis of SKG mice, which develop T cell-mediated autoimmune arthritis by zymosan A injection. Oral administration of CDDO-Im, a representative chemical inducer of Nrf2, had effects of both prevention and treatment toward arthritis of SKG mice in an Nrf2-dependent manner.

We also found that Nrf2 activation through myeloid-cell lineage-specific Keap1 disruption did not achieve significant improvement in arthritis of SKG mice. Systemic Nrf2 activation or Nrf2 activation in other lineage cells including T cells, B cells and fibroblast-like synoviocytes linage cells is important for improvement of rheumatoid arthritis.

We propose that Nrf2 activation is an efficient therapeutic approach for rheumatoid arthritis.”

https://www.sciencedirect.com/science/article/pii/S0891584923005452 “Nrf2 activation improves experimental rheumatoid arthritis”

If professionals in medical-related fields cared about people, they would..

October 20, 2023October 20, 2023 gettingwell4 2-3 stars Required further work, Epigenetics, Immune system, Stress Control group, DNA methylation

Last month I came across an immune system inflammation biomarker I hadn’t known about, suPAR (soluble urokinase plasminogen activator receptor). This subject went into a queue of things I also didn’t know about, and I got around to looking at its 2023 research earlier this week.

It turns out suPAR was discovered in 1991. How some suPAR evidence fits into a segment of existing medicine and research will bore you to tears if you read https://www.mdpi.com/1422-0067/24/15/12376 “Plasminogen System in the Pathophysiology of Sepsis: Upcoming Biomarkers” up through Section 4.4. But it does thoroughly explain what suPAR is.

This paper managed to avoid addressing the point of 2018’s The arrogance of a paradigm exceeding its evidence as well as epigenetic findings of 2023’s Sex hormones and epigenetic clocks. I couldn’t find a better 2023 suPAR starting point, though.

Other 2023 suPAR papers bickered and equivocated using speech constrained by researchers wanting to keep their jobs and add to their CV. How about publishing papers telling the truth about whether or not quality medical care was provided using suPAR inflammation information? Since inflammation’s progression with disease or age isn’t exactly a mystery, what are suPAR’s prospects?

The most heartening 2023 paper I read provided good guidance for young adults:

“For verification of predicted correlations between plasma levels of suPAR and cardiovascular risk factors in younger populations, the current study analyzed data from young and healthy adults aged 25–41 years. A statistically significant inverse correlation between suPAR plasma levels and the HDL serum levels was found in male and female populations, as well as higher suPAR plasma levels in smokers compared to nonsmokers and past smokers.

A major strength of our study is the young and healthy study population lacked any relevant comorbidities, thus minimizing possible interference by unknown confounders. Investigating correlations of biomarker suPAR with cardiovascular risk factors and overall cardiovascular risk in a young and healthy population is important, since preventive measures to reduce the burden of cardiovascular risk factors and diseases should take place before irreversible damage is set.”

https://www.mdpi.com/2075-4418/13/18/2938 “The Association of suPAR with Cardiovascular Risk Factors in Young and Healthy Adults”

Higher suPAR in this study indicated preclinical symptoms with low-grade inflammation. If young adults ignore this signal, and don’t individually take responsibility for their own one precious life by investigating inflammation’s source, they may not be able to reverse later clinical conditions of many inflammation-related diseases.

The most disheartening paper provided details about how suPAR biomarkers continue to be ignored:

“We find that as a prognostic biomarker suPAR is challenged in it becoming as an object for clinical practice in the emergency department by the power of diagnostic practices and the desire for experience-based scripts that quickly enable the clinician to reach the right diagnosis. Although suPAR is enacted as a promising triage strategy suggesting a low or high risk of disease, the inability to rule out specific diagnoses and producing the notion of secure clinical actions make its non-specificity and prognostic character problematic in clinical practices.”

https://link.springer.com/article/10.1057/s41292-022-00296-2 “Challenges facing the clinical adoption of a new prognostic biomarker: a case study”

Didn’t agree with philosophical abstractions throughout this paper regarding a “new” biomarker from 1991.

Canadian Thanksgiving

October 10, 2023October 15, 2023 gettingwell4 Epigenetics, Immune system, Just me, Stress Control group, Embryo development, Genetic factors

Canadians were in dire straights yesterday, needing something to not be depressed about. It isn’t that US citizens are less depressed, but we have our Bill of Rights 1^st and 2^nd amendments that we adhere to.

Several of the people on this three and a half hour conversation were Canadians. Will you listen to them?

I learned a lot, such as possible transgenerational inheritance of effects from worldwide coerced actions. Bhakdi shortly after the 1 hour 6 min point was the easiest to understand, and also the scariest.

So what were you thankful for yesterday? Exposing facts?

But their taste

October 8, 2023October 8, 2023 gettingwell4 4-5 stars Advanced knowledge, Epigenetics Control group, Genetic factors

Two 2023 human studies of cruciferous vegetables’ consumer acceptance, starting with five species’ 7-day-old sprouts and 17-day-old microgreens:

“Sensory chemistry of Brassicaceae species is complex, reaching gustatory, olfactory, and pain nerves and receptors. Among organosulfur compounds, glucosinolates, their hydrolysis compounds, and sulfur-volatile compounds are responsible for their taste, aroma, and trigeminal characteristics (mainly, bitter taste, sulfurous aroma, and pungency/spicy sensations, respectively).

This work compared the sensory profiles and consumer acceptance between (S)prouts vs (M)icrogreens of the same species (kale, radish, rocket, broccoli, and mustard) under the same growing conditions, correlating them with phytochemical composition. On each sampling day (3, 5, 7, 12, 15, and 17 days), S&M were harvested, frozen, and freeze-dried for further analysis.

Previous studies reported the decrease of glucosinolates and sulforaphane from day 4 of germination. Previous studies also indicated that designing crop improvement strategies for sensory traits based on ∑GLS content would be flawed, as it does not consider relative differences in sensory characteristics of different GLSs and isothiocyanates, nor contributions from other GLS hydrolysis products.

Consumers tested 5 brassica species’ 7-day-old sprouts and 17-day-old microgreens. Each consumer was served ∼ 10 g of each sample coded with 3-digit numbers and the questionnaire. Water and unsalted crackers were provided between samples for palate cleaning.

Consumers were asked to taste each sample, express their overall liking and ‘attribute’ liking using a 9-point hedonic scale (1 = dislike extremely, 5 = neither like nor dislike, and 9 = like extremely). The question ‘How much do you like the ‘attribute’ of this sample?’ was used for global satisfaction/overall, and different attributes (appearance, leaves color, hypocotyl color, size, bitterness, spicy, astringency, herbal-vegetal and ID flavor).

Differences among samples depended more on brassica species than growing stage (S&M).

In rocket S&M, no attributes were found in the critical corner. Rocket^S and Rocket^M were also characterized by the lowest values of ∑GLS. Rocket^S presented the highest GLS₅ glucoerucin content, which does not have bitter taste.

Although no differences were found in global, bitterness, and spicy consumer satisfaction degree between S&M of radish and mustard species, penalty analysis indicated a need to improve excess intensity of bitterness and spicy in Radish^S and Mustard^S.

4 out of 5 sprout samples needed improvements, while only 2 out of 5 microgreens samples needed improvements. Sprouts are richer in organosulfur compounds than microgreens, although it depends on the species.

An interesting research line would be to study odor-active compounds of these products and link them with consumer preferences. Other vegetable crops could be included, such as cereals and legumes.”

https://www.sciencedirect.com/science/article/pii/S0925521423001722 “How does the phytochemical composition of sprouts and microgreens from Brassica vegetables affect the sensory profile and consumer acceptability?”

This study treated all conditions to 16 hours light/8 hours darkness throughout. If I wanted naturally developed sprouts at Day 7, I’d follow other studies’ methods and keep germinating seeds in darkness through Day 3 to simulate their natural below-ground conditions, then provide white or blue light after Day 3. So I consider this study’s 7-day-old and 17-day-old sprouts to be both microgreens because they got their leaves at Day 3.

Hadn’t thought of a pain aspect to eating sprouts before reading this study. I’d guess a consumer’s hedonic rating of “dislike extremely” would correspond.

I switched to equal starting weights of broccoli, red cabbage, and mustard seeds 2+ years ago during Week 56 to produce 3-day-old sprouts. That combination takes the edge off individually unpleasant attributes while preserving their beneficial effects.

Couldn’t do that with radish sprouts earlier this year. I might try again if my right thumb doesn’t stop hurting, after I find a tactic that tones down their intensity.

An association analysis of 2129 adults aged 40–80 years found:

“The proportion of participants who ate cruciferous vegetables over two days was 29.5% among bitter tasters, significantly lower than that (35.7%) among non-tasters (P = 0.04) after adjustment of age, gender, race/ethnicity, dietary energy intake, physical activity, education, smoking, and income levels.

Bitter taste sensitivity was associated with less consumption of cruciferous vegetables and a high likelihood of obesity, which may mediate its association with diabetes.”

https://pubs.rsc.org/en/content/articlelanding/2023/FO/D3FO02175K “Bitter taste sensitivity, cruciferous vegetable intake, obesity, and diabetes in American adults: a cross-sectional study of NHANES 2013–2014” (not freely available)

Bridging Nrf2 and autophagy

October 4, 2023January 19, 2025 gettingwell4 4-5 stars Advanced knowledge, Acetylcholine, Dopamine, Epigenetics, Glutamate, Memory, Neurochemicals, Stress Brain neurons, Genetic factors, Neurodegenerative disease

Three more 2023 papers that cited Precondition your defenses with broccoli sprouts, starting with a review:

“Examining crosstalk between Nrf2 antioxidant signaling and autophagy provides insights into how they are interconnected and proteins that mediate their communication. These factors are potential therapeutic targets for diseases with both autophagy dysfunction and oxidative stress.

A working model illustrates mechanisms of bridging factors (SQSTM1, TFEB, Sestrin2, TRIM16, Ca²⁺, and miRNAs) connecting autophagy (left) and the main antioxidant Nrf2-Keap1-ARE pathway (right) and feedback loops between these factors.

A network forms that connects Nrf2, SQSTM1, TFEB, and mTOR.

Other non-canonical autophagy regulatory proteins like Sestrin2 and tripartite motif-containing protein 16 (TRIM16) also participate in regulation of Nrf2 and mTOR via direct or indirect interactions.

Ca²⁺ is the most widespread intracellular messenger whose role in autophagy has been studied extensively.

At post-transcriptional level, microRNAs have been reported to impact both the regulation of autophagy and Nrf2 antioxidant signaling.

Since these regulatory proteins seem intricately entangled, potential side effects in practical scenarios should also be taken into consideration. Further studies on understanding the complex crosstalk between autophagy and antioxidant pathways are yet to be conducted.”

https://www.frontiersin.org/articles/10.3389/fcell.2023.1232241/full “An update on the bridging factors connecting autophagy and Nrf2 antioxidant pathway”

A second review subject was improving autophagy:

“Lysosomes are crucial degradative organelles that maintain cellular homeostasis. During the pathogenesis of neurodegenerative diseases and aging, functions of lysosomes are impaired, and lysosomal degradative capacity is consequently reduced.

Transcription factor EB-mediated lysosome biogenesis enhances autolysosome-dependent degradation, which subsequently alleviates neurodegenerative diseases. Small-molecule compounds that enhance TFEB activity and lysosome biogenesis are potential therapeutic agents.”

https://journals.lww.com/nrronline/fulltext/2023/11000/enhancement_of_lysosome_biogenesis_as_a_potential.7.aspx “Enhancement of lysosome biogenesis as a potential therapeutic approach for neurodegenerative diseases”

A third review tied mitochondrial participation into these processes:

“Mitochondria play an essential role in neural function, such as supporting normal energy metabolism, regulating reactive oxygen species, buffering physiological calcium loads, and maintaining the balance of morphology, subcellular distribution, and overall health through mitochondrial dynamics. Given recent technological advances in the assessment of mitochondrial structure and functions, mitochondrial dysfunction has been regarded as the early and key pathophysiological mechanism of cognitive disorders.

Mitochondrial dysfunction caused by acute and chronic brain injury is difficult to be distinguished because they may exhibit similar structural and functional impairments. Mitochondrial physiological function and morphology are integral, so when one is damaged, the other is also involved.

We recommend that all of the above methods can be used to explore mitochondrial dysfunction in different pathological pathways of cognitive disorders. Results may be related to special pathological pathways, sensitivity of the method, experiment cost, and degree of proficiency.”

https://journals.lww.com/nrronline/fulltext/2024/04000/latest_assessment_methods_for_mitochondrial.18.aspx “Latest assessment methods for mitochondrial homeostasis in cognitive diseases”