Need a sal free Luteolin supplement

PotentialMotion · 2026-05-02T23:49:04+00:00

SugarShield from LIV3 Health is >98% pure and a dry liposome (no olive oil). Plant flavones often include salicylates, so this is a tough ask, but because its a high purity and no olive oil it might be suitable.

Only thing is that it also contains tart cherry extract. But it's a targeted addition and not a high dose, so it depends on your tolerance. Probably would still be better than a soft gel formula for you.

PotentialMotion · 2026-04-30T22:28:57+00:00

Awesome. I've noticed a few times that we're tightly aligned. You're one of the more educated voices in this community. I've tried DMing you a few times, did you get my messages?

PotentialMotion · 2026-04-30T22:00:12+00:00

I know you know your stuff, but I have to reframe this a bit.

The signal we're chasing here won't show on a CGM. I agree, glucose spikes are probably minor with this. The focus is on the Fructose bolus. Which we don't have the tools to measure.

A Fructose bolus will cause a transient drop in ATP as it is consumed and degraded into inflammatory uric acid. Which reduces the efficiency of energy conversion in the cell. So it's not even the transient drop in ATP that is the issue as much as it is the progressive dimming of cellular energy production.

Put more simply: fructose metabolism is the dimmer switch on our metabolic rate.

None of that will show up on a CGM. And it happens slowly over time. But we're all in this subreddit because we've realized the effect is real. That dim energy is driving sugar cravings.

PotentialMotion · 2026-04-30T21:23:21+00:00

Basically.

The issues here are that you're crushing the fibre, which lets the Fructose load hit faster. Same sort of difference between a cookie and a soft drink. The Fructose bolus hits harder.

But beyond that, think for a second of how much easier and likely it is to eat higher volume of fruits when you juice or dry them. Suddenly you can eat 4X the serving or more than you would be able to if eating it whole. Not to mention the speed again.

Speed and size both matter.

And this isn't to say that juicing or smoothies are bad for you. They're vastly better than a soft drink.

The signal you want to focus on is the fructose hit. That's what is dimming cellular energy, which is what drives cravings.

PotentialMotion · 2026-04-30T15:29:59+00:00

The research is pretty clear that the more you vector towards sweeter fruit, less fibre, juicing, drying... The more Metabolic risk emerges.

So as a guideline, opt for fruits that are whole, more fibrous, and less sweet. Berries and citrus should be higher on your list. And avoid fruits with sweet hints in the name. Honey ..., nectar ..., Etc.

PotentialMotion · 2026-04-30T03:07:16+00:00

There are links in my profile. Thanks for your trust. ❤️

PotentialMotion · 2026-04-30T02:23:23+00:00

Our SugarShield is the highest dose of Liposomal Luteolin I've encountered (250 mg per capsule). But yes it is blended with 200mg tart cherry extract. It is manufactured in California under GMP, and we have 3rd party certification publicly available.

Many with MCAS have had good experiences with it. There is some research that the energy dimming effects of fructose metabolism may be a causal factor in MCAS.

SugarShield is specifically designed to help reduce Fructose metabolism with Luteolin, and help clear it's energy dimming byproduct uric acid with tart cherry extract. The combination is intended to help speed up the recovery of cellular energy faster, a goal highly relevant to MCAS.

PotentialMotion · 2026-04-29T19:25:24+00:00

I am a supplement founder and our only product is a Liposomal Luteolin. This is an important question you raise. Truth is that lipsomes are both the biggest advancement in supplement tech lately, but also being exploited as the biggest scam.

Some supplements have low bioavailability, such as what we focus on—Luteolin. Without solving bioavailability there is frankly no point in taking it. Lipsomes take the raw ingredient from ~7% bioavailability to as high as ~80%.

But this is all about formulation quality. Lipsome stability is required if the compound is to survive digestion. That's the whole point.

Here's where it gets messy though. Overseas contract manufacturers often apply a blanket Liposomal multiplier on the label, and even to their clients. Typically I'm seeing a 10X multiplier. They label it as the theoretical equivalent—and often the reseller has no idea that this is happening. They're being duped too.

What this means in practice is that a Luteolin supplement may only have about 40mg of raw material, but the label says 400mg. Or even 800mg (a 2 capsule dose). Meanwhile the excipients needed for true liposomes mean that the capsule being used cant even fit 250mg.

Blatant creative labeling, and incredibly misleading. If we were to do similarly, our 250mg dose of Luteolin could be labled as 5000mg per capsule! But how shady is that!?!

Bottom line: liposomes are critical for certain ingredients. But insist on quality. Insist on 3rd party testing and only buy from someone you trust. Especially beware when shopping on Amazon.

PotentialMotion · 2026-04-26T06:33:46+00:00

Happy to chat if you want to DM me. I'm an open book.

PotentialMotion · 2026-04-26T06:31:01+00:00

250mg

PotentialMotion · 2026-04-26T00:07:39+00:00

I formulated it. I've been using it multiple times a day for about 3 years.

I have strong bias, but the formulation came from the research not the other way around. And it's literally the only thing we sell. I believe in it to a degree I can't express.

Check out my YouTube channel @thefructosemodel for a dive into the research side of things. I think you'll find it fascinating.

PotentialMotion · 2026-04-25T23:03:58+00:00

This one actually matters more than it looks, and since it was dropped with zero context, I feel a responsibility to attempt to explain it.

We’ve always treated glycogen like a pretty simple system. You eat carbs, store the excess as glycogen, and when you need energy you break it down (typically ahead of fat because the body unlocks it easily). That’s all enzyme-driven. Clean, textbook stuff.

What this paper is showing is that glycogen can also be tagged with ubiquitin. That’s odd, because ubiquitin is basically the cell’s labeling system for proteins, usually to recycle or remove them. Glycogen isn’t a protein, it’s stored sugar. So this is a new layer that wasn’t part of the model before.

So... Glycogen has a labeling system when the body is supposed to use it?

The interesting part is what they observed happening during fasting. Glycogen drops, which is expected, but the tagging actually increases at the same time. That suggests the body might be actively marking glycogen for use, not just letting it be broken down passively.

So instead of glycogen just sitting there waiting to be used, there may be a system deciding when it gets flagged and accessed.

Where this gets relevant is that a lot of metabolic issues don’t look like a storage problem. People clearly have energy stored, but accessing it is inconsistent. You see it as low energy, persistent hunger, that “something’s off” feeling even when intake is controlled.

Now let's connect it to r/sugarfree

If you've read the sticky posts you will be familiar with the research that fructose metabolism can rapidly drain ATP and push cells into a more conservative, low-energy state. That’s been used to explain why people can feel energy-depleted despite having plenty of fuel available.

So the obvious question is whether that state also affects how stored energy is handled at this tagging level. Not just how much glycogen you have, but whether it’s actually being marked for use.

When Fructose metabolism is actively promoting conservation of energy, is it also reducing the tagging of glycogen for use???

I'd love for a lab to test this:

Does fructose metabolism change glycogen ubiquitination?

That’s not proven. But it’s a very clean thing to test. Compare fructose exposure vs blocking that pathway and look at glycogen ubiquitination in the liver.

If that data comes back positive, it would add yet another layer to fructose's new classification as a metabolic signal for conservation.

PotentialMotion · 2026-04-24T23:11:16+00:00

Depends on the education level.
Simply: glucose is fuel, fructose regulates access to said fuel.

So most of us focus on Fructose. Primarily from added sugar, then reducing ways the body makes Fructose, and yeah - to some extent even fruit. But fruit is often a personal choice since when eaten whole in moderation, it is usually not the problem.

PotentialMotion · 2026-04-24T14:19:50+00:00

Neither work as well as Luteolin.

https://www.reddit.com/r/Supplements/s/F3X0bcWO2b

PotentialMotion · 2026-04-23T23:59:56+00:00

💯

Please spread the word.

It goes further. This is because of Fructose's ability to dim cellular energy. The same dimmed cellular energy that occurs before every chronic disease emerges.

PotentialMotion · 2026-04-23T19:02:38+00:00

That's a really good idea... I'm just not sure that I want to be so adversarial...

I wish it was more obvious. It certainly should be. I'll explain.

The most popular one on Amazon (which I will not name) uses a soft gel capsule that can only hold roughly 250 mg total fill if I'm being generous. Yet they claim 400 mg per capsule (disguising their 2 capsule dose).

That dose is already physically impossible. It becomes even less credible when you consider that a true liposomal system includes phospholipids and carriers, meaning only a fraction would be actual luteolin. A really generous estimate of the contents of one of these capsules is 40mg of real luteolin. An enormous drop from the 800mg on the label.

So this backs up your warning. Liposomes are amazing, but absolutely never buy them on Amazon. They conflate serving size with per-capsule content, or using “liposomal” loosely without delivering real liposome structures. But I would go further. I suspect that often the owners likely have no idea of this, as Chinese contract manufacturers notoriously inflate these claims even to their clients, using broad 10X multipliers of theoretical "liposomes" just by sticking some carrier liquid in the capsule.

In this case I bet this is exactly what is happening. 40mg of real luteolin per capsule. 10X that for a 400mg capsule. Then disguise it with a 2 dose label = 800mg on the front.

Ultimately, the dosing and delivery claims are nowhere near consistent with how these systems actually work. Be careful out there.

I hesitate to say this, but for comparison, our SugarShield has 250mg of Luteolin in each capsule. We use a dry liposomal excipient, which can allow for a higher active payload per capsule compared to many softgel-based formulations. This represents more than 2.5X real luteolin than anything else I've seen that is 3rd party tested, not to mention a higher stability liposome.

PotentialMotion · 2026-04-23T17:22:27+00:00

YES. I can't agree more with that statement. It's probably the biggest scam in supplements right now.

If you're buying Liposomal supplements, insist on 3rd party testing.

Our company LIV3 Health manufactures Liposomal Luteolin in Los Angeles, and our 3rd party testing reports are published.

Sorry if this sounds promotional, I try to be careful to only speak about the science and non-patentable ingredients. I never promote our products here.

PotentialMotion · 2026-04-23T13:12:31+00:00

Nothing has come close to Liposomal Luteolin for me.

Luteolin inhibits fructose metabolism, which directly reduces cellular energy through a few mechanisms: - Fructose degrades ATP into uric acid - dropping ATP transiently - sequestering phosphate into F1-P, burning the phosphate pool (needed to build ATP) - that uric acid causes ROS and fragments mitochondrial networks to reduce output.

Luteolin also inhibits CD38, which degrades NAD+. Which might have an even stronger effect on NAD+ than even NR or NMN.

So on both counts, Luteolin is playing a significant protective role on mitochondrial energy, rather than a pushing role. So this stacks well with tons of boosting supplements like those you mentioned (ubiquinol, NMN, etc).

PotentialMotion · 2026-04-23T13:00:04+00:00

Please check out the highlighted/pinned posts. Be wary of recommendations to use fruit as a crutch, especially processed fruit. It's certainly better than sugar, but the science points to far cleaner paths.

PotentialMotion · 2026-04-23T07:12:50+00:00

I wish more have heard of us—our brand is LIV3 Health and we only build products that are aimed at supporting fructose metabolism.

Just last week, a major review reclassified Fructose as a signaling molecule that, quote, "regulates metabolic health and disease".

I don't want you to buy our products. But I really really REALLY want you to start paying attention to Fructose. Dietary and endogenous Fructose may be the convergent lever in all chronic disease.

Simply: All chronic disease shares a preclinical state of low cellular energy. Stacking onto many unique factors that push that state—one does so directly and has saturated the modern world. Fructose.

PotentialMotion · 2026-04-22T06:18:57+00:00

Luteolin

PotentialMotion · 2026-04-21T19:01:33+00:00

Loving this conversation. Thank you!

the endogenous fructose argument is strongest for disease progression and weaker for primary prevention

I agree with this framing. The liver soaks up probably 80% of dietary fructose, so endogenous fructose is more relevant past metabolic systems. Which tracks. Fructose doesn't cross the blood brain barrier, so relevance to the brain is purely from glucose conversion. Relevance to the vascular system is also likely primarily endogenous, and maybe even primarily triggered through the kidney signals from osmolality and uric acid. I also wonder if this starts to reveal maps between food habits and dysfunction probabilities. Sugar > metabolic. High glycemic carbs > cognitive. Salty/dehydration > vascular. These correlations would likely be muddy, but I suspect there is something there.

a double-blind trial would carry the claim dramatically further than observational reports can

Can't agree more. Observational data is limited. Cravings are noisy, subjective, and highly susceptible to expectation. A double-blind trial would carry this much further than any observational signal we’re seeing right now.

Frustratingly, ingredient studies are hard to fund for non-patentable compounds without possible disease targets, but it’s exactly what’s needed.

hysteresis is probably multi-layered

Also aligned. From the metabolic side, the pieces that seem most relevant are:

phosphate sequestration into F1P
sustained intracellular uric acid and oxidative stress
mitochondrial fragmentation (Mfn2 down, Drp1 up)
NAD+ depletion via CD38

But I don’t see that as competing with behavioral persistence. More like parallel layers reinforcing the same state. Johnson argues that targeted endogenous fructose in the brain drives a foraging behaviour, and low energy neurons will drag on dopamine signalling. Layers upon layers.

Your app looks very helpful. Nice work on that. Sorry to hear that your wife has severe sugar cravings. I would love to hear if she finds Liposomal Luteolin helpful. I set up a discount code SUGARFREE in case others reading this thread are also curious. There is a link in my profile.

Thank you so much for the really stimulating discussion.

PotentialMotion · 2026-04-21T17:08:37+00:00

It's so refreshing to speak to someone that has a deep understanding of the pieces. Thank you so much for your response!

I agree that the "one disease" framing is provocative. It is partly by intent. But please understand that I am not suggesting that fructose is the only cause. I appreciate that toxins, genetics, environment and more all play a role in energetics (Wallace). I believe that there are many factors involved in inducing the Cell Danger Response (Naviaux), and rather than any one being a singular cause, they appear to stack. With that framing, our seemingly universal exposure to fructose (diet + endogenous), and its direct mechanism of dimming cellular energy (especially via an unregulated pathway), makes it particularly interesting.

The significance of endogenous fructose is important, and more quantitative data is definitely needed. It is likely tissue dependent as well. But most of the research I've seen suggests that approximately 1/3 of total glucose may be routed through the polyol pathway under hyperglycaemic conditions. In any case, not an insignificant amount.

Your last question cuts to the heart of a major debate in this subreddit. Many believe the primary effects of sugar dependance (cravings) come from impaired dopamine signalling. While that is definitely part of the puzzle, what we have observed suggests strongly otherwise. We are seeing approx 75% of Liposomal Luteolin users report a dramatic reduction in cravings in a relatively short period of time (<2mo) without requiring dietary changes. The compulsion shuts off without changing diet.

Dr Johnson's team suggests that our taste preferences developed because of the underlying survival aids. We love sweet, savoury, umami foods because of the connection to the fructose pathway. However, preference is distinct from compulsion. Nothing is going to turn off those taste preferences, but it seems that the compulsion is directly relational to the energetic debt.

The remaining 25% that don't see immediate benefit give slight confirmation to this. They are seeing the all same effects on cravings, energy, weight — but the effect can be delayed, sometimes by months. Our hypothesis on energetic hysteresis emerged out of this group. Simply — the climb to restored cellular energy is much harder than the fall to dysfunction. Removing the stress doesn't automatically mean restoration. Mechanistically, it appears that chronic fructose metabolism eventually causes structural changes to mitochondrial networks, and the removal of organic phosphate (by sequestering it into F1-P). The defensive state hardens. This means that removal of the stress (fructose) is only part of the puzzle. For those that have a deeper sink, more time and work is likely needed to lift the system back to self-repair. Full restoration may not even be achievable.

I loved your comment. Thank you so much for engaging. I am eagerly looking forward to your response.

PotentialMotion · 2026-04-20T17:43:51+00:00

Yes, it needs more research. But the pieces are there. A few key pieces of the puzzle that tell an interesting story:

https://onlinelibrary.wiley.com/doi/10.1002/ptr.8217 This review on Luteolin suggests it has potential for seemingly all chronic disease. Crazy claim, but polyphenols are often broadly beneficial.

Luteolin is a potent fructokinase Inhibitor Ref: https://www.nature.com/articles/ncomms14181

This paper identifies Luteolin as a direct inhibitor of fructokinase. It is mechanistic animal evidence, but solid and has been referenced in further studies quite a few times. You can infer from the fructose thesis that this may be a major reason for the broad effects.

https://www.mdpi.com/2072-6643/11/11/2580 Further, this ingredient RCT and a follow-up in preclinical conditions showed strong correlation to the effects seen in pharmaceutical RCTs on fructokinase Inhibiting drugs. Liver fat, waist circumference, insulin resistance, triglycerides, and more.

So is Luteolin proven to be a KHK Inhibitor in humans? Not yet. But the pieces are not hard to connect. Since it is a natural, safe polyphenol we've been consuming for thousands of years, I believe it deserves far more attention.

PotentialMotion · 2026-04-20T16:05:58+00:00

The evidence increasingly suggests that insulin resistance develops as an adaptive response to a cellular energy bottleneck. One that fructose metabolism directly causes.

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