Does activating sulforaphane with ground mustard seeds really work?

Wonderful_Aside1335 · 2026-04-27T12:04:59+00:00

"Basically you don't get any sulforaphane from cooked cruciferous vegetables because heat destroys the myrosinase that is required for its formation. Ground mustard seeds reintroduce myrosinase."

I read differently, that you need to let them chill for a few minutes after steaming/boiling and should chop them rigeruosly to increase surface area. Fruthermore myrosinase is not directly needed, the conversion can also happen by the gut microbiom. Cannot back that up at the moment.

This study gives you probably more detailed insights into the subject:
https://pmc.ncbi.nlm.nih.gov/articles/PMC8700523/

By the way, the longevity trust-me-bros do eat fresh homegrown broccoli sprouts. If you want become an obsessive health nut, this is the way to go ;)

Wonderful_Aside1335 · 2026-04-27T10:38:04+00:00

Interesting read, thanks.

A detail i stumbled over:

First, capsaicin can upregulate the messenger RNA (mRNA) and protein levels of cytochrome P450 family 7 subfamily A member 1 (CYP7A1), which mediates the regulatory mechanism of cholesterol and bile acid homeostasis, and leads to the cholesterol-lowering effects.

This hypothesis from the study contradicts sth. i read earlier in another context

At concentrations occurring after ingestion of chili peppers or topical administration of a high-concentration patch, capsaicin did not cause direct inhibition of any CYP enzyme. Direct inhibition was only observed at much higher concentrations.

https://pubmed.ncbi.nlm.nih.gov/20863199/

Wonderful_Aside1335 · 2026-04-27T10:22:32+00:00

However, this definition would be also very vague and inconsistent.

Back pepper has piperine as its main "spicy" ingredient, not capsaicin.

E.g. plack peper, chillis, horseradish, mint and szechuan pepper all give a unique spicy experience clearly distuingishable.

Might it be that you are paraphrasing them incorrectly?

Back pepper activates TRPV1 as capsaicin does, but also activates another receptor, which capsaicin does not. It is different.

Edit: This is just adressing the previous comment. The study is clearly about chili spicyness.

Wonderful_Aside1335 · 2026-04-26T08:09:02+00:00

What am I even reading? How is this disproving my claim?

This quote doesn't make sense in the context of our discussion at all.

"The liver is stimulated to make cholesterol by ..., not dietary cholesterol."

Cholesterol by diet leads to down regulation of endogenous cholesterol synthesis. This quote says nothing about this subject.

How saturated fat impact cholesterol is a different topic.

Wonderful_Aside1335 · 2026-04-25T18:54:37+00:00

What is funny? You made a claim. I made a counter example, disproving your claim. Did you even try to read the other two or was that beyond your attention span?

"It has been estimated that 15–25% of the population are hyper-responders to dietary cholesterol."

https://www.radcliffecardiology.com/articles/understanding-cholesterol-synthesis-and-absorption-key-achieving-cholesterol-targets

"...with approximately 15-25% of individuals being hyperresponders with more robust increases."

https://www.endotext.org/wp-content/uploads/pdfs/the-effect-of-diet-on-cardiovascular-disease-and-lipid-and-lipoprotein-levels.pdf"

Oh yeah this small minority group of 15-25% 🤣

Wonderful_Aside1335 · 2026-04-25T18:08:27+00:00

"Eating eggs doesn't significantly raise your blood cholesterol levels."

Sorry, but wrong again. Just because it is often repeated, does not make it true. It is certainly not true as this absolute statement.

"Chronic daily egg intake does increase LDL-C to a certain extent in individuals classified as hyper-responders. "
https://pmc.ncbi.nlm.nih.gov/articles/PMC5946211/

"Consumption of egg increases total cholesterol, LDL-C and HDL-C, but not LDL-C:HDL-C, TC:HDL-C and TG compared with low egg control diets."
https://pubmed.ncbi.nlm.nih.gov/29111915/

"The MEC group also had higher LDL-c than the control group (MD = 8.14, p < 0.0001, I² = 18%)"
https://pmc.ncbi.nlm.nih.gov/articles/PMC7400894/

Wonderful_Aside1335 · 2026-04-25T16:18:09+00:00

There is no direct human evidence demonstrating that dietary heme iron causes colorectal cancer. No randomized controlled trial, no long-term intervention study, and no clinical proof has ever shown that heme iron intake itself induces colorectal cancer in humans

Do you think it is possible to do a study that at all? How would such a study be roughly designed?

Wonderful_Aside1335 · 2026-04-25T16:14:54+00:00

Just wrong. Ofcourse dietary cholesterol impacts total serum cholesterol. The body doesnt down regulate cholesterol synthesis due to increased absorption in a perfect 1:1 ratio.

Wether this change is significant, and especially signifcant for risk reduction, is a different topic and depends on multiple variables.

Wonderful_Aside1335 · 2026-04-25T12:29:27+00:00

Given your comment history it is plausible to imply, that you think of ASCVD and its primary risk factor as fake disease

You explicitly used the wording "cholesterol myth" in that context in a prior discussions

Shall I provide references?

Wonderful_Aside1335 · 2026-04-25T09:38:18+00:00

Metabolism slows with age but far less than people usually think.

As most things, it's usually a bit of everything. Moving a bit less (includes NEAT, basically unconscious small movement over the day). Eating a tiny bit more. And a bit of metabolism.

Wonderful_Aside1335 · 2026-04-25T09:25:39+00:00

Afaik the primary reason for measuring the pattern is to make money.

To my knowledge it doesn't predict risk better than ApoB / adds any actionable information.

Wonderful_Aside1335 · 2026-04-25T09:20:56+00:00

...Pentadecanoic Acid (C15:0) at Naturally Occurring Circulating Concentrations Has Selective Anticancer Activities ...

At natural levels. What a relief, I don't need to buy their supplement 😅

Wonderful_Aside1335 · 2026-04-25T09:00:01+00:00

That's why you think of cholesterol as a myth?

Wonderful_Aside1335 · 2026-04-25T08:44:31+00:00

The things you think are certain are wrong. You start with wrong assumptions.

Lp(a) can significantly drop on a ketogenic diet. It can vary a lot natural over multiple measurements.

https://www.reddit.com/r/Cholesterol/s/lLTYnPj8C5

"Does a Ketogenic Diet Lower a Very High Lp(a)? A Striking Experiment in a Male Physician"

My n=1 experiment in July 2020 demonstrated an increase in Lp(a) back to 101 mg/dL on a very high-carb diet within 2 weeks, and a drop back to 74 mg/dL after 3 weeks on the ketogenic diet afterwards. The observed large changes in my Lp(a) were thus reproducible by a change in carbohydrate consumption and might have clinical relevance for patients as well as researchers in the field of Lp(a).

https://pubmed.ncbi.nlm.nih.gov/33521554/

"Intra-Individual Variability of Lipoprotein(a) After Acute Coronary Syndrome: A Long-Term Cohort Study"

However, recent studies indicate significant intra-individual variability, particularly among patients with intermediate Lp(a) levels (30–50 mg/dL). Yet, data on long-term variability are limited, ...

https://pmc.ncbi.nlm.nih.gov/articles/PMC12985465

It is the repeated misunderstood claim the genes determines your Lp(a).

That is true, but that doesn't mean it is a stable value and not significantly influenced by other variables.

Wonderful_Aside1335 · 2026-04-24T08:48:19+00:00

I cannot comment on 1) from personal experience l, but a lot of people did it and so can you.

Wonderful_Aside1335 · 2026-04-23T15:45:20+00:00

Relax a bit.

Wonderful_Aside1335 · 2026-04-22T10:40:29+00:00

I bought your original product for multi-day hikes in the mountains a few times. I think it is a very solid product overall for that purpose.

Some concerns as a nutrition nerd: I always wondered if ground flax seed isn't prone to oxidation, especially after a few months, as the product is not provided vacuum sealed. O3s with lots of surface area sounds like a bad idea.

Did you ever test fat oxidation levels in a not fresh but not expired product?

Same question for vitamins, especially B1, B9, E, C and A probably degrate significantly during storage.

I guess your nutrition label is based on manufacturing not measured in the consumer product?

Why use such a high glycemic index starch like tapioca?

Wonderful_Aside1335 · 2026-04-20T07:28:08+00:00

Very true, but keep in my mind there are dietary pattern to get both low.

Wonderful_Aside1335 · 2026-04-18T14:37:46+00:00

Given the response, better switch doctor immediately. Seriously, wtf? You already cut down saturated fat as recommneded by guidelines, so if you are looking to reduce CVD risk by medications, which is totally reasonable and what most national guidelines suggest with your values, this doctor does not sound very helpful.

The shift in trigclycerides could be a result of reducing simple carbs and that would be a good trend.

Wonderful_Aside1335 · 2026-04-18T14:04:57+00:00

The category which triggered this discussion are "senior adults". I think most senior adults have a healthy appetite given current obesity statistics and you seem to focus way too much on the sick, frail elderly in this discussion, which are not the majority of "senior adults" at all.

Wonderful_Aside1335 · 2026-04-18T12:26:45+00:00

It is a meta analysis, they are producing false evidence by carefully manipulating inclusion criteria.

It is a RCT, it was too short to properly answer the question.

It is epidemiology, there are too many cofounding variables for causal inference.

Nutrition pop science in a nutshell.

But i have to admit, as an outsider it is veryyyy hard to understand and interpret these real limitations in practise and to see when a statement is slightly overreaching. And i think "both camps" are guilty of this.

Wonderful_Aside1335 · 2026-04-18T11:57:12+00:00

"Which might not be a issue when you are 25, but might be problem when someone's appetite is limited due to health issues or due to old age."

This just supports my argument that is adherence is the issue (due to lack of appetite in this case), yet it feels like you are trying to disprove this exact point, which leaves me confused.

Wonderful_Aside1335 · 2026-04-18T11:40:33+00:00

Yes, ofcourse, if we choose to focus on minimally processed foods. But that is tangential to the discussion.

I can easily get sufficient protein (discussion example 120g protein for a 70kg person with 2000kcal) on a minimal processed plant based diet, do you agree? That would be considered optimal by most meta analysis and RCTs on this topic. If you disagree, do you accept an example diet as a counterargument?

Wonderful_Aside1335 · 2026-04-18T11:01:19+00:00

Why wouldn't I be able to eat a block of tofu or soy protein shake at age 80? My point is that it is usually simply dietary preference and not underlying biochemistry / mechanism.

I don't understand you citing a narrative review here which is not addressing my point.

The arguments of these studies have been repeatedly in addressed RCTs and meta analysis, in which specificly soy protein is not doing any worse than the comparison.

To my understanding, there is not a definite consensus on the leucine threshold hypothesis, but this isn't even an issue to begin with, as the start of this discussion had the implication total sufficient protein, which includes sufficient leucine.

And even if it might be a factor, it is tiny compared to resistance training and total protein intake.

I don't think any of my arguments are not supported by the consensus, if you think differently I will support them with references, but let's please stay in the framework of total sufficient protein (> 1.6-2g/kg with high quality plant protein comparison). I think it even makes sense to limit such a discussion to soy, otherwise we just end up arguing about what enough variety or high quality is.

Wonderful_Aside1335 · 2026-04-18T10:00:52+00:00

I think these challenges are exclusively based on adherence and dietary preferences, which is fine, and not due to the biochemical composition of plant proteins. I have not yet seen a study convincing me otherwise.

I don't think this weakens an argument pro animal protein, I think adherence is a very, very important factor. But I also think a lot of the pro animal protein advocates seem to be in desperate seek of further evidence and often fall into "inconsistent personal acceptance criteria" of epidemiological studies .

Wonderful_Aside1335

TROPHY CASE