November 14, 2014 at 3:17 am #18341BenedictParticipant
Was reading (on this site) that new research shows that free fatty acids (FFA) are actually responsible for Gout flare ups, whilst the high purine foods (simply) fill your blood with uric acid and crystals etc.
What types of foods contain FFAs? Is it things that contain triglycerides? my we search didn’t really help me understand.
Am trying to make a list of foods to completely avoid at the moment (my last painful attack was a week ago so am trying to avoid any more attacks, if possible)/
Thanks!November 14, 2014 at 3:50 am #18346
Thanks for posting this, Benedict. It’s a new area of research, so facts are hard to come by.
Long ago, I learned that gout is not due to ‘sharp’ or ‘needle-like’ uric acid crystals digging into your joints. Rather, it is an immune reaction to the presence of foreign bodies. This works great for bacteria and other infections that can be killed when white blood cells engulf them. Not so good for uric acid crystals. They cannot be killed, so they just get engulfed and remain hidden.
That process explains many unusual aspects of gout. But the immune system, and related inflammatory and anti-inflammatory processes are very complex.
To make it simpler, scientists used mice, as things like injecting uric acid crystals and other torture seems more acceptable in mice than humans. This research revealed a specific Fatty Acid, C18:0 or stearic acid, that is clearly identifiable as a trigger for the inflammation process. I.e, uric acid crystals alone do not cause gout attacks, but they do in the presence of stearic acid.
For real life, things are not so easy. We eat a wide range of fatty acids. Some are anti-inflammatory, and some are pro-inflammatory. I’d love to be in a position where I could spend all day, every day, getting to the bottom of this. However, I think we have to wait for more gout research.
What I can do, is to produce a chart of stearic acid content. In real life, I think we need to consider other fatty acids, especially anti-inflammatory ones, so that we might switch certain foods to better choices for gout pain.
At the end of the day, of course, adopting anti-inflammatory diet practices is like preferring colchicine to allopurinol. We might get short term pain relief, but the constant presence of uric acid crystals is destroying joints. Going back to my opening paragraphs, I described how the immune system attacks uric acid crystals whenever it sees them. This happens every day, but we only notice it when the immune system gets swamped, and calls in reinforcements. That is the painful inflammatory process known medically as phagocytosis. Unfortunately, other white blood cells get caught up in the battle. These include the cells that were destined to repair bone, cartilage, and tendon. With that repair process compromised, you get slow joint destruction.
As I’m writing this, I’m thinking maybe I should restrict my forthcoming stearic acid food chart to people who promise to get their uric acid levels safe. Anyway, I have to produce the thing first, so let’s continue the discussion about free fatty acids and gout, whilst I try free up some time for a new food chart.November 15, 2014 at 5:12 am #18374BenedictParticipant
After reading various websites, I think you’re absolutely right that the priority has to be to reduce the uric acid levels long term. Am going to speak to my doctor to get me on allopurinol 100mg initially) as soon as possible.
In the short term, I bought some 1000 mg vitamin c tablets but noticed they have magnesium stearate – must be for the capsule shell. They’re vegetable capsules. I know magnesium stearate is created using stearic acid, which as you’ve said research shows could be a trigger for a flare up. So my question is whether these capsules are safe to take in the shortterm.
What do you think?
Many thanks for your advice.March 14, 2015 at 1:24 am #20287
Sorry for the delay in responding to this, @benedict – I missed your response.
I think magnesium stearate should be safe, though this is a knee-jerk reaction rather than properly researched knowledge. My thinking is that, since stearic acid has reacted with magnesium, it is no longer ‘Free’
I can’t find any obvious references to this, especially as the relationship between Free Fatty Acids and gout is so newly discovered. I will continue to look into this whenever I see some new research.
What do other gout sufferers think? If you keep this discussion alive, it will remind me to keep investigating FFAsMarch 14, 2015 at 6:56 pm #20292Ron AveryGuest
I found this article and it seems there is a definite co-relation between FFA’s and flareups if I am reading it correctly.March 16, 2015 at 8:21 am #20306
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Yes, you are reading that article correctly. This is the Joosten research that inspired my articles at https://gout-pal.com/gout-search/?q=joosten
Of most interest to me are some articles that have sprung from that research.
How interleukin-1? induces gouty arthritis is very technical, but notes that:
Overall, the study by Joosten and colleagues goes a long way to clarify the mechanisms by which IL-1? is produced in flares of gouty arthritis and the mechanisms that are thoroughly linked to endogenous signals that have considerable clinical validity. Thus, it is likely that gout could be classified as an autoinflammatory disease and, similar to other autoimmune diseases, is uniquely mediated by the production of IL-1?.
That ties in with lots of new research into new types of pain blockers that directly target these signals. That would seem to negate the effects of Free Fatty Acids.
My efforts, so far, have been heavily influenced by Purine-rich foods: an innocent bystander of gout attacks?, a fascinating editorial that combines Joosten’s research with additional research from Zhang.
Beyond that, prompted by your response, I’ve just searched for more current information about FFAs and gout. There is a remarkable amount of information – over 300 reports so far this year, of varying relevance. Perhaps one of the most interesting is a patent claim for treatment of gout pain and other inflammatory diseases using poly-unsaturated fats (PUFAs). The essence of the claim is that PUFAs only control inflammation with certain genetic types. That means I’ve got a task on my list now to understand more about “C allele at single nucleotide polymorphism (SNP) rs730012 (A-444C).”
I think the potential merits the investigation, as it looks like there is a strong possibility of treatment derived from various PUFAs including:
- Omega-3 and Omega-6 from borage, echium, flaxseed, canola, walnut (black, English, Persian), soybean, oat, hickory nut, butternut, beechnut, chia seed, marine algae.
- Omega-3 from fish, krill, crab, shrimp, lobster, mussel, octopus, oyster, clam
Practical treatments seem a long way off, but it looks like there might be help for gout sufferers in future, from both pharmaceutical gout pain blockers, and natural medicines.May 22, 2015 at 9:43 am #21391
I’ve just gained a fresh insight into the situation that gout flares only happen when uric acid crystals are present with something else. That “something else” is believed to be certain Free Fatty Acids (FFAs). Some new research explains some changes at cellular level that affect the way large white blood cells react to uric acid crystals.
I’m struggling to understand the science, so I’ll reproduce what I’ve read to see if anyone can add some clarity. My understanding of this so far is that there are two types of large white blood cells (macrophages). One (M2) fights inflammation, but the other (M1) promotes it. However, to produce inflammation, a signal or carrier (IL-1?) is needed. Uric acid crystals alone will not produce IL-1?, but a substance identified in the following reports as LPS, causes M2 white blood cells to produce IL-1? and thus inflammation occurs.
This is the full abstract of the report with my bold around the crucial conclusion:
Background/Purpose: Macrophages have been involved in both initiation and resolution of gout flares. Accordingly, these cells are characterized by their plasticity as the environment modulates their phenotype exerting inflammatory or anti-inflammatory functions depending on their activation or polarization state. Macrophages in the presence of interferon-? and lipopolysaccharide (LPS), what is known as classical activation, acquire an inflammatory phenotype and are also termed M1 macrophages. On the other hand, M2 or alternatively activated macrophages with IL-4 have anti-inflammatory and homeostatic functions. Equivalently, in the presence of granulocyte macrophage colony-stimulating factor (GM-CSF ) and macrophage colony-stimulating factor (M-CSF) macrophages become M1 or M2 respectively. As M-CSF is present in the blood stream at steady state some authors propose that M2 macrophages polarized with M-CSF could represent the population of resident macrophages. In this work we investigated M2 macrophages response to monosodium urate (MSU) crystals in vitro.
Methods: Macrophages were derived from peripheral blood monocytes of healthy donors after informed consent. Peripheral blood mononuclear cells were separated from whole blood by centrifugation with a density gradient. Monocytes were then isolated by negative selection with magnetic beads and cultured for 1 week with GM-CSF (1000 I.U./ml) or M-CSF (20 ng/ml) to obtain M1 or M2 macrophages respectively. Macrophages were then stimulated with MSU (200 ?g/ml), LPS (100 ng/ml) or both for 18 hours and quantification of IL-1? and IL-10 in supernatants was performed by ELISA. Activation of caspase-1 in M1 and M2 macrophages was analyzed by flow cytometry with the Caspase-1 FLICA? Detection Kit (Immunochemistry Technologies). Cytoplasmic pro-caspase-1 and pro-IL-1? were analyzed by western blot. Flow cytometry and statistics analysis were performed with the FACSDiva and GraphPad Prism 5 respectively.
Results: As expected, M1 macrophages produced inflammatory cytokines in response to LPS, whereas M2 macrophages were unable. Both M1 and M2 failed to produce IL-1? after MSU stimulation. However, when challenged with MSU and LPS, M2 macrophages produced IL-1? (mean+/-SEM, LPS 2.59+/-1.37 pg/ml, MSU+LPS 111.4+/-30.44 pg/ml, p= 0.0078) and reduced IL-10 production (mean+/-SEM, LPS 3738+/-230 pg/ml, MSU+LPS 1587+/-386.4 pg/ml, p= 0.0039). Resting M2 macrophages exhibited lower levels of active caspase-1 and pro-caspase-1. MSU stimulation increased active caspase-1 levels in both M1 and M2 macrophages and the presence of MSU and LPS had a synergic effect in pro-IL-1?.
Conclusion: M1 and M2 macrophages failed to produce inflammatory cytokines after MSU challenging, according with the fact that MSU crystals can be found in asymptomatic joints. However, after MSU phagocytosis, M2 macrophages were able to produce IL-1? after LPS stimulation, explaining the requirement of a trigger, such as a copious meal or alcohol intake, for the initiation of an acute flare in gout. M2 macrophages also had lower levels of caspase-1 and pro-caspase-1, than M1 macrophages.
Macrophages mediated response to uric acid crystals is modulated by their functional polarization. Available from: https://www.researchgate.net/publication/274699805_Macrophages_mediated_response_to_uric_acid_crystals_is_modulated_by_their_functional_polarization [accessed May 22, 2015].
I need to try and understand the LPS factor, and if, or how, it relates to Free Fatty Acids. I’m also trying to understand caspase-1 and pro-caspase-1.
If anyone can help with explanations, I’d be glad to receive your insight. If none of this makes sense, don’t worry too much. The main aim of proper gout control is to get rid of uric acid crystals. Once you do that, you can never get a gout attack. The science here might help us find better ways to manage gout pain prior to getting uric acid under control.May 22, 2015 at 10:43 pm #21395Ron AveryParticipant
I read and re-read this like 3 times and now I have a headache and still can’t wrap my head around it ! The patience and dedication you have is amazing and I applaud you.
I did however note one thing you said which for me and I believe all gout sufferers is critical – “The main aim of proper gout control is to get rid of uric acid crystals. Once you do that, you can never get a gout attack.”
What I read into this, and please correct me if I’m wrong, is that as long as I get my uric acid crystals under control I can eat all the FFA’s I want and drink all the alcohol I want and I won’t have a gout attack. Not that I would want to do this as It would most likely kill me in the long run with a heart attack or liver disease – but no gout !
Is this correct ?May 23, 2015 at 12:49 am #21396
Perfectly correct Ron.
I don’t think I’m alone in being more careful about my diet as I get older. I know many gout sufferers who use allopurinol as a prop for continuing unhealthy eating. For me, it worked the other way. Once I realized how easy it is to control gout, I wanted to enjoy my new-found freedom without the fear of heart disease (which is a paternal nightmare) or diabetes. I don’t want to turn into a foodie bore, but I think there are healthy ways to enjoy food. Less meat and interesting, spicy veg dishes is my way forward.
I’d love to find recipes that help avoid gout triggers for my GoutPal friends. As the scientists understand more about what causes gout attacks, I’m hopeful I can make progress on this. For years I’ve been intrigued by the fact that many people with high uric acid do not have gout attacks. That has the unappetizing name of asymptomatic hyperuricemia. It fascinates me.
If we can unlock the key of what combines with uric acid crystals to cause gout attacks, it makes the early months of allopurinol so much easier.
I find my head often in a whirl with some of the scientific journals. It’s very hard when every other word takes hours of research to understand the meanings. But I love these challenges! Of course, my real challenge is to understand it enough to explain it so it can be meaningful to everyone.
?If you can’t explain it to a six year old, you don’t understand it yourself.? – Albert Einstein
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