#autoimmune disorders

[talkethtothehandeth]

If you have celiac and buy the brand Van’s for their waffles, please know that 9 days ago there was a recall because some of the packages of the gluten free waffles may contain “undeclared” wheat. And if you have celiac, you know “may” might as well mean “does”.

This recall only applies to boxes with the matching lot codes and numbers, and do not pertain to other products that Van’s has to offer. These boxes were distributed in AZ, CA, FL, GA, IL, NC, & WA. Please check your boxes immediately to ensure your own safety and save yourself the painful reactions to gluten. It’s advised the purchased packages be either thrown out (or given to someone who can eat wheat so as not to waste it) or return the product to where you’ve purchased it from.

“The U.S. Food & Drug Administration website published the recall July 3. It applies to certain packs of Van's Gluten Free Original Waffles with lot code UW40193L, expiration date Jan. 19, 2024, and UPC 0 89947 30206 4. According to the Van's recall, some of the packs of waffles may contain undeclared wheat.”

[disabled-models]

Bice, a model with alopecia universalis (AU), for Hearts Magazine

[chronicillnesshumor]

This meme was brought to you by connective tissue disorders

[she-is-ovarit]

"Approximately 80% of all patients diagnosed with autoimmune diseases are women."

For those of you who might wonder why this is the case, to shock nobody, we can add this to the list of mysterious medical conditions women experience that still remain elusive to the medical field.

However, there's some speculation:

Female sex hormones

The X chromosome

Microchimerism

Environmental factors

The microbiome

Antibodies

Interesting, considering female human beings actually have stronger immune systems than males.

To briefly talk about maybe the most overlooked and dismissed cause of high rates of autoimmune diseases in women, chronic stress (which presumably falls under "environmental factors") has been found to be strongly correlated with autoimmune diseases across multiple studies ("...up to 80% of patients reported uncommon emotional stress before disease onset), which can be triggered by even just one traumatic event, and anxiety disorders such as generalized anxiety disorder, panic disorder, PTSD, etc. are extremely high for women in comparison to men.

Women experience PTSD two to three times the rate as men do (source), panic disorder is 2.5 times more common in women and girls than in men and boys (source), and generalized anxiety disorder (which is often treated as trivial and grossly overlooked) is again 2-3 times higher for women and girls than it is for men and boys (source). Behaviorally chronic stress and trauma also often presents differently between the sexes - "fight or flight" for men and "tend and befriend" (fawn and freeze) for women.

Men are more likely to commit physical, psychological, and sexual violence and women are more likely to respond to this violence by continuously be on the receiving end of their behavior and never leaving, even when their children are caught in the middle.

Chronic stress means persistent high levels of cortisol in women's bodies. There is sexual dimorphism in our immune systems. High cortisol leads to Hypothalamic–Pituitary–Adrenal (HPA) axis dysregulation (please, learn more about this).

This leads to heart issues, susceptibility to infectious diseases and auto-immune disorders, an unexplainable debilitating chronic fatigue that can lead to a bedridden life, multiple sclerosis, the progression and reoccurance of cancers, earlier HIV disease progression, and dementia. There's also the bidirectional problem in which HPA axis dysregulation, created from high levels of cortisol from chronic stress in the first place, also in turn biologically causes increased anxiety.

So...

Approximately 80% of all patients diagnosed with auto-immune diseases are women.

And auto-immune diseases are found to be strongly, strongly linked with stress disorders.

And women are several more times likely to experience trauma and stress disorders than males across the board.

And when stress is triggered, men are more likely to throw punches or leave and women are more likely to freeze and people please.

And men are vastly less likely to seek out a therapist to fix their issues or even demonstrate empathy for other men, instead using women as emotional crutches and punching bags.

And freezing and fawning for women often means staying in those same conditions even when there's a risk of death.

And staying in those same conditions when a woman has children and the means those children learn those behaviors and likely develop chronic stress themselves, and the cycle of trauma continues.

And even when women leave those conditions, we're far more likely to end up in re-traumatizing situations as we seek out familiar dynamics.

And even when we're able to break free from this dynamic, because we're far more likely to seek out and stay in therapy, we're still left with trying to resolve chronic, disabling, sometimes life-threatening health issues caused by HPA-axis dysregulation from chronic stress.

While HPA-axis dysregulation in turn generates anxiety, which then creates high cortisol, which results in a feedback loop.

This was supposed to be a short post, but I want to leave off with solutions. Please don't give up on your mental health. Religiously go to therapy. Have extremely high standards for yourself in your relationships. Practice diaphragmatic breathing, meditation, exercise. It's been found that moving your body through exercise, Thai-chi, sports, short walks, dance, whatever (to the best of your ability, if you're able) can really help - just know your limits. If you're not there yet take liquid vitamins as needed (vitamin deficiencies such as low B-vitamins, low magnesium, low good fats, and D3 also cause chronic stress, immunity issues, and chronic fatigue). Make those medical appointments. Eat well, socialize, rest (especially during a PEM or immunity crash), aim for 64 ounces of water a day. Leave miserable situations when you find your chance to. Learn the language of your body and listen to it, and have patience. I've had periods of being bedridden and unable to work. I'm getting better, but it hasn't just been one thing that has been a "fix". If this list overwhelms you, just pick one thing that's most doable. We matter.

[gypsy-that-i-was]

I WILL have this….

[genzforbettergenerations]

Since I’ve never seen any kind of positivity post for this:

Shout out to people who get IV infusions weekly, biweekly, monthly, multiple times a year.

Shout out to people whose hands/arms/elbows/feet/legs are covered in scars and scar tissue. Shout out to people whose scar tissue hurts or locks up joints. Shout out to people who are covered in bruises after getting an IV.

Shout out to people whose veins roll or disappear, people who need multiple sticks or digging to get a vein. Shout out to people whose veins blow when getting IVs or during infusions. Shout out to people who feel like their veins have no more to give.

Shout out to people who cry or need someone to hold onto when getting an IV. Shout out to people who have anxiety or panic attacks when getting or thinking about IVs/infusions.

Shout out to people who will continue to need IV infusions into the foreseeable future. Shout out to people who will continue to need IV infusions for the rest of their lives. Shout out to the people who leave their IV in for several days, and thus need to cover it and continue with school, jobs, chores, etc, and sleep with it in.

Shout out to the kids and teens who need IV infusions.

Shout out to people who feel self-conscious about their IV scars. Shout out to people who worry about someone noticing them and treating them differently (though no one should be shamed for their scars, no matter how they got them).

Shout out to people who are traumatized from IVs/infusions. Shout out to people who have terrible memories associated with IVs/infusions.

Shout out to people who go to the hospital for infusions. Shout out to people who get infusions at home. Shout out to people who lose hours of their days while getting infusions.

You are no less worthy of love and positivity because you need IV infusions.

--

Anyone can reblog (and please do!), but only people who need (or have needed) regular/intermittent IV infusions should add on.

[titleknown]

Esoteric take, but I will say, the existence of autoimmune disorders pisses me off on an existential level.

Not just because of the people I've known who's lives they've fucked up but also because the idea of the bodily system meant to protect you randomly deciding "Now and forever, we have decided to cause problems on purpose" is just cosmically-enraging on a level that's hard to describe.

[justinnault]

Sodium Effects on Inflammation, Migraines & Acid Reflux AMA #104

Hey all! Buckle up because episode #104 of our AMA series is about to blow your mind. We're talking about something you might not expect: sodium! We all know salt adds flavor and keeps us hydrated, but there's a whole hidden world to this stuff.

This week, we're joined by Justin Nault, a super cool Certified Nutritional Therapist who specializes in keeping athletes and fitness enthusiasts fueled. He's here to spill the tea (or maybe the electrolytes?) on how sodium can actually help with some surprising things, like fighting inflammation, preventing those awful migraines, and even easing acid reflux.

Justin's gonna break down the science behind how sodium works its magic in our bodies and explain why getting the right amount is key to feeling fantastic. So whether you've been a Clovis Culture devotee for ages or are just joining the party, this episode is packed with info to help you level up your health game.

Want to geek out further? Clovis.show has all the resources, detailed notes, and maybe even some secret bonus content (wink wink). Plus, if your brain is overflowing with questions about sodium or anything health-related, join our Clovis Academy Facebook group! It's a fantastic community where you can connect with like-minded folks and even submit questions for future AMAs.

So grab your favorite snack, salty or sweet, tune in, and let's unlock the hidden power of sodium together! This is gonna be epic!

[soontobecyborg]

me: has a small infection, nbd

my immune system:

[lordbeebrain]

Happiness is finally being able to wiggle your toes again, after not being able to do so for 4 months, due to your Multiple Sclerosis causing them to me stiff/numb 😮‍💨🥹😭❤️

I’m glad my recent Ocrevus infusion seems to be having positive effects ☺️

[disabled-models]

Mia Castro, a model with Hashimoto’s Disease, Hypermobile Ehlers-Danlos Syndrome (hEDS), and Tarsal Coalition.

[blueoaknx]

Mitochondrial Dysfunction in Autoimmune Disorders 

Mitochondria, the energy-producing organelles of eukaryotic cells, are involved in a myriad of cellular functions beyond ATP production, including calcium homeostasis, reactive oxygen species (ROS) generation, apoptosis regulation, and the modulation of immune responses. In autoimmune diseases, mitochondrial dysfunction is increasingly recognized as a key factor in disease pathogenesis. These disorders, characterized by the immune system's aberrant recognition and attack on self-antigens, often manifest in conditions such as systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), and multiple sclerosis (MS). This article delves into the mechanisms linking mitochondrial dysfunction to autoimmune disorders, highlighting cellular changes, signaling pathways, and potential therapeutic approaches.

Mitochondrial Function in Immune Cells

Mitochondria are critical for cellular energy metabolism, primarily through oxidative phosphorylation, which occurs in the inner mitochondrial membrane and generates ATP. However, their roles extend far beyond energy production. Mitochondria are involved in immune cell activation, differentiation, and the regulation of apoptosis. Immune cells, including T lymphocytes, B lymphocytes, dendritic cells, and macrophages, rely on mitochondrial function for their metabolic demands during immune responses. These cells undergo rapid changes in mitochondrial dynamics and energy production during immune activation.

Mitochondria also produce ROS as byproducts of oxidative phosphorylation, and these ROS, under normal conditions, function as signaling molecules that regulate immune responses. However, excessive ROS generation, stemming from mitochondrial dysfunction, can lead to oxidative stress, damage to cellular components, and dysregulated immune responses that are characteristic of autoimmune diseases.

Mitochondrial Dysfunction and Autoimmune Pathogenesis

In autoimmune diseases, mitochondrial dysfunction contributes to disease progression through multiple interconnected mechanisms, including dysregulated immune responses, enhanced oxidative stress, impaired mitochondrial dynamics, and defective apoptosis. The following section outlines key mechanisms linking mitochondrial dysfunction to autoimmune pathogenesis.

1. Oxidative Stress and Immune Dysregulation

Mitochondria are a major source of ROS, which are produced as intermediates during oxidative phosphorylation in the electron transport chain (ETC). Under normal conditions, ROS are tightly regulated by antioxidant systems, including superoxide dismutase (SOD), catalase, and glutathione peroxidase. However, in autoimmune diseases, mitochondrial dysfunction often results in increased ROS production, overwhelming the antioxidant capacity of the cell and resulting in oxidative stress.

Oxidative stress can damage cellular macromolecules such as lipids, proteins, and nucleic acids. In immune cells, excessive ROS lead to the activation of several signaling pathways, including the nuclear factor-kappa B (NF-κB) pathway, which promotes the expression of pro-inflammatory cytokines such as TNF-α, IL-6, and IL-1β. In systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), and multiple sclerosis (MS), ROS-induced activation of these inflammatory pathways amplifies the autoimmune response, driving tissue damage and inflammation.

Moreover, oxidative stress exacerbates the production of autoantibodies, particularly in diseases like SLE, where ROS contribute to the formation of immune complexes that target self-antigens, including nuclear components like double-stranded DNA (dsDNA) and mitochondrial antigens.

2. Mitochondrial Dynamics in Autoimmune Diseases

Mitochondrial dynamics, encompassing processes such as mitochondrial fission, fusion, and mitophagy, are critical for maintaining mitochondrial function and cellular homeostasis. Mitochondrial fission, mediated by proteins such as dynamin-related protein 1 (Drp1), leads to the division of mitochondria, while fusion, regulated by mitofusins (Mfn1/2) and optic atrophy 1 (OPA1), facilitates the merging of mitochondria to restore mitochondrial function and DNA integrity. Mitochondrial fusion is crucial for maintaining the respiratory capacity and metabolic flexibility of immune cells.

In autoimmune disorders, an imbalance in mitochondrial dynamics is often observed. For example, in rheumatoid arthritis (RA), T cells exhibit excessive mitochondrial fission and impaired fusion, leading to mitochondrial fragmentation, reduced mitochondrial membrane potential, and diminished oxidative phosphorylation capacity. This dysfunction contributes to the failure of immune cells to produce sufficient ATP during activation, resulting in altered cytokine production and a hyperactive immune response.

Similarly, in multiple sclerosis (MS), aberrant mitochondrial dynamics in oligodendrocytes and T cells contribute to neuroinflammation and demyelination. The dysregulated fission and fusion processes impair mitochondrial function, leading to increased oxidative stress, mitochondrial damage, and exacerbation of inflammatory cascades that damage myelin.

3. Mitochondrial-Derived Damage-Associated Molecular Patterns (DAMPs)

Mitochondria are also sources of damage-associated molecular patterns (DAMPs), which are intracellular molecules released upon cellular injury or stress. DAMPs, such as mitochondrial DNA (mtDNA), cardiolipin, and mitochondrial N-formyl peptides, serve as danger signals recognized by pattern recognition receptors (PRRs) on immune cells. These include toll-like receptors (TLRs), particularly TLR9, which recognizes mtDNA, and TLR2/4, which are involved in the recognition of mitochondrial lipids.

In autoimmune diseases, mitochondrial dysfunction leads to the release of mtDNA and other mitochondrial components into the extracellular space, where they act as endogenous ligands for PRRs. The activation of these receptors triggers inflammatory responses, including the activation of NF-κB, interferon pathways, and the inflammasome, all of which amplify immune responses and contribute to chronic inflammation and tissue damage.

In SLE, circulating mtDNA fragments have been detected in the serum, correlating with disease activity. The presence of mtDNA in the bloodstream is thought to exacerbate the activation of autoreactive immune cells and the production of autoantibodies, particularly those targeting nuclear antigens.

4. Impaired Apoptosis and Autoimmunity

Mitochondria are key regulators of apoptosis, particularly the intrinsic or mitochondrial pathway of cell death. The mitochondrial pathway is initiated by the release of pro-apoptotic factors such as cytochrome c and apoptosis-inducing factor (AIF) from the mitochondrial intermembrane space into the cytosol. This release activates caspases, leading to cell death. In autoimmune diseases, mitochondrial dysfunction often leads to defective apoptosis, which prevents the elimination of autoreactive immune cells.

In diseases like systemic lupus erythematosus (SLE), defective apoptosis of T cells and B cells contributes to the survival of autoreactive lymphocytes that would normally be eliminated through programmed cell death. The persistence of these cells results in the production of autoantibodies, including anti-dsDNA and anti-mitochondrial antibodies, which target self-tissues and exacerbate inflammation.

Moreover, impaired mitophagy, the process by which damaged mitochondria are selectively degraded by autophagy, further contributes to the accumulation of dysfunctional mitochondria, promoting sustained oxidative stress and inflammation.

Mitochondrial Dysfunction in Specific Autoimmune Disorders

1. Systemic Lupus Erythematosus (SLE)

In SLE, mitochondrial dysfunction plays a pivotal role in disease pathogenesis. Increased ROS production, defective mitophagy, and impaired apoptosis contribute to the activation of autoreactive T cells and B cells, leading to the production of autoantibodies. The release of mitochondrial DAMPs, such as mtDNA, amplifies the inflammatory response, and mitochondrial damage is directly linked to the severity of disease activity in SLE.

2. Rheumatoid Arthritis (RA)

In RA, mitochondrial dysfunction in immune cells, particularly in synovial T cells and macrophages, is associated with increased mitochondrial fragmentation, oxidative stress, and dysregulated immune activation. ROS and mitochondrial-derived DAMPs contribute to the chronic inflammatory environment in the synovium, driving the production of pro-inflammatory cytokines and promoting joint destruction.

3. Multiple Sclerosis (MS)

Mitochondrial dysfunction in MS primarily affects oligodendrocytes, the myelinating cells in the central nervous system. Impaired mitochondrial function in these cells contributes to neuroinflammation and demyelination. Additionally, T cells with dysfunctional mitochondria play a role in the perpetuation of inflammation, leading to the destruction of myelin and axonal injury in the CNS.

Therapeutic Implications

Targeting mitochondrial dysfunction presents a promising therapeutic strategy for autoimmune diseases. Potential approaches include:

Mitochondrial Antioxidants: Compounds like MitoQ, MitoTEMPO, and other mitochondrial-targeted antioxidants can help reduce oxidative stress, protect mitochondrial function, and alleviate inflammation.

Modulating Mitochondrial Dynamics: Agents that promote mitochondrial fusion or inhibit excessive fission, such as Mfn2 activators, could restore mitochondrial integrity in immune cells, reducing inflammation and improving immune regulation.

Enhancing Mitophagy: Stimulating mitophagy through compounds such as spermidine or activation of the PINK1/PARK2 pathway may help remove damaged mitochondria and reduce the accumulation of mitochondrial DAMPs.

Targeting Mitochondrial DAMPs: Inhibiting the release of mtDNA and other mitochondrial DAMPs using TLR inhibitors or blocking downstream signaling pathways may reduce the inflammatory response in autoimmune diseases.

Conclusion

Mitochondrial dysfunction is a key factor in the pathogenesis of autoimmune diseases. Through mechanisms such as increased oxidative stress, impaired mitochondrial dynamics, and dysregulated apoptosis, mitochondrial dysfunction exacerbates immune activation and inflammation. The accumulation of mitochondrial-derived DAMPs further amplifies the autoimmune response. Targeting mitochondrial health offers a promising therapeutic strategy to mitigate the effects of mitochondrial dysfunction and improve disease outcomes in autoimmune disorders.

[eregyrn-falls]

Image description for the original post:

A tweet from David Wallce (but his name and his Twitter handle are cut off), quoting an article from pme.uchicago.edu titled "Inverse vaccine' shows potential to treat multiple sclerosis...". The quote in the tweet is:

"A new type of vaccine developed by researchers at the University of Chicago has shown in a lab setting that it can completely reverse autoimmune diseases like multiple sclerosis and type 1 diabetes -- all without shutting down the rest of the immune system."

Below this is a link to the article quoted

Upon clicking, the article is subtitled, "In a new study, Prof. Jeffrey Hubbell and fellow researchers describe a new “inverse vaccine” that in a lab setting can stop autoimmune reactions which attack a person’s healthy tissues, as seen in diseases multiple sclerosis, type I diabetes, or rheumatoid arthritis." It was written by Sarah C. P. Williams.

The article is dated September 11, 2023.

End description.

(The subsequent reblogs in this thread give a lot of very welcome context! But it's useful to have the original post in plain text for accessibility too.)

[supernovaodessa]

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[shamistate]

Shamis Tate Explains The Connection Between Neuropathy and Autoimmune Disorders

Neuropathy, a condition marked by nerve damage, often intersects with autoimmune disorders, leading to a complex interplay of symptoms and challenges. In this video, Shamis Tate delves into the relationship between neuropathy and autoimmune disorders. With five key subheadings, we will explore the mechanisms linking these conditions, common autoimmune diseases associated with neuropathy, diagnostic approaches, treatment options, and lifestyle adjustments for managing symptoms.