Lupus

Posted on autoimmune conditions, Diet, Lupus, Sjögren’s Syndrome

Research case series presents food as medicine as a potential treatment for lupus and other autoimmune diseases

The research published in Frontiers in Nutrition describes the history of three women with lupus and Sjögren’s syndrome who achieved remission of symptoms following dietary changes alone.
The research published in Frontiers in Nutrition describes the history of three women with lupus and Sjögren’s syndrome who achieved remission of symptoms following dietary changes alone.


A new research case series published in Frontiers in Nutrition presents food as medicine as a potential treatment for autoimmune diseases, describing three patients with chronic autoimmune disease who showed remarkable improvement after following a predominantly raw dietary pattern high in cruciferous vegetables and omega 3 fatty acids. 
The research focused on three women with systemic lupus erythematosus and Sjögren’s syndrome who adopted a nutrition protocol that emphasized leafy greens, cruciferous vegetables, flax or chia seeds for omega-3 polyunsaturated fatty acids, and water, and included predominately raw foods. All three women reported that nearly all their symptoms of both diseases resolved after just four weeks of making the dietary changes.

Furthermore, all three patients have remained symptom-free, with two of them reporting no symptoms for more than six years without recent medication use. The research was published as part of an upcoming special issue of the journal focused on food as medicine and edited by the American College of Lifestyle Medicine (ACLM).
“Although the healing benefits of a predominantly plant-based eating pattern have been clearly demonstrated for cardiometabolic outcomes, clinical attention and research has been lacking on its effectiveness at treating and managing autoimmune diseases,” the study’s author, Brooke Goldner, MD, said. “The dramatic improvements in symptoms and quality of life reported by the three patients in this case series demonstrates what I see every day in my practice, that autoimmune diseases can quickly improve with optimal nutrition.
“My hope is that these cases generate greater recognition, making patients and clinicians aware of food as medicine as a treatment option for systemic lupus erythematosus and Sjögren’s syndrome. This case series also reflects the immediate need for more research into dietary changes as a potential treatment strategy for autoimmune disease.”  
Dr. Goldner herself has been free from debilitating lupus symptoms, including arthritis, photosensitivity, renal impairment, and antiphospholipid antibody clotting issues for over 18 years, which she attributes to the nutrition protocol.
Systemic lupus erythematosus is the most common type of lupus, an autoimmune disease in which the immune system attacks its own tissues, according to the U.S. Centers for Disease Control and Prevention. It has no cure and common symptoms include extreme fatigue, joint pain and swelling as well as hair loss. Sjögren’s syndrome is an immune system disorder that causes symptoms such as dry mouth and eyes and can accompany systemic lupus erythematosus.
The patients presented in the case series followed a strict customized, plant-based nutrition protocol called the Rapid Recovery Protocol (RRP), which was developed by Dr. Goldner and eliminates all processed food. The nutrition protocol shares similarities with a whole-food, plant-based diet but focuses “on predominately raw foods and high intakes of leafy greens and cruciferous vegetables, omega-3 polyunsaturated fatty acids (whole, ground flax or chia seeds; cold pressed flaxseed oil), and water.” Once remission was achieved, patients were allowed to begin a maintenance phase and incorporate cooked whole plant foods, and more fruits, nuts, seeds, and whole grains. 
The study publication includes a supplemental set of personal accounts from the three patients, who described in their own words their experience of achieving remission of symptoms within four weeks or less. One patient, a 40-year old who was diagnosed with lupus when she was nine months pregnant, reported experiencing symptoms since 2010 that included fatigue, extreme photosensitivity and leg pain that required her to spend much of the day lying down. After beginning the RRP protocol in 2017, she reported that her joint pain dissipated within weeks and that she could experience sunlight comfortably again.
“The most exciting thing for me was when I realized being in direct sunlight didn’t hurt my skin,” she said. “I’ll never forget the feeling of going to the beach two months after giving birth and enjoying the feeling of the warmth of the sun on my face and body.”
The second patient, a 54-year-old educator, experienced photosensitivity, butterfly rash, itchy scalp, and constant fatigue. Before starting the protocol, she was frequently hospitalized with pleurisy, an inflammation of the tissue separating the lungs and chest wall, and suffered from severe dry mouth that made it difficult to eat. She had brain fog and worried at one point she suffered from early-onset Alzheimer’s.
After completing the protocol, she said “I can walk everywhere. I can play with my kids, I can remember things, and I don’t have to write everything down. I can type, I can text, and I don’t take any painkillers anymore.”
The third patient, a 45-year-old teacher and mother of four, suffered from severe brain fog, debilitating fatigue, nerve pain, a grittiness in her eyes, and patches of skin that hurt as if they were sunburned, among other symptoms. She started the protocol in 2021 and said many of her symptoms went away within weeks.
“I was able to stay up late,” she said. “I wasn’t tired anymore. My skin and joint pain vanished. I didn’t feel nauseous anymore. My body felt amazing…It absolutely feels amazing to be well.”
Posted on Lupus

World-first discovery may enable an effective long-term lupus treatment.

Summer Outdoor Safety for Elderly Nursing Home Residents

Australian researchers have discovered how to fix a defect that causes lupus. They hope their world-first discovery will offer effective long-term treatment.

Published in Nature Communications, the Monash University-led study found a way to reprogram the defective cells of lupus patients with protective molecules from healthy people.

Using human cells, the new treatment restores the protective side of the immune system that prevents autoimmunity, which occurs when the immune system attacks its own cells. The findings relate to the debilitating autoimmune disease lupus, which has no cure and limited treatments.

However, researchers hope this new method, developed in test tubes and proven in pre-clinical models, can also be developed for other autoimmune diseases such as diabetes, rheumatoid arthritis, and multiple sclerosis.

Humans all have proteins the immune system could attack, but this doesn’t happen in healthy people because of special cells called ‘regulatory T cells’ or ‘T-regs’ that protect from autoimmune disease. These are lacking in people who develop lupus and other autoimmune conditions.

Co-senior author Associate Professor Joshua Ooi, who heads Monash University’s Regulatory T Cell Therapies Group based at Monash Health, said the therapeutic effect was achieved by identifying specific protective molecules from healthy people and reprogramming ineffective lupus patient T-regs to restore their ability to switch off unwanted immune responses.

“We showed the effectiveness of this approach using human lupus patient cells, both in the test tube and in an experimental model of lupus kidney inflammation,” Associate Professor Ooi said.

“We were able to completely arrest the development of lupus kidney disease, without the use of the usual non-specific and harmful immunosuppressant drugs. It’s like a reset of the abnormal immune system back to a healthy state – kind of like a major software upgrade. That it uses the patient’s own cells is a very special part of this.”

About one in 1000 Australians has lupus, and rates are higher in First Nations communities. Nine in 10 people with lupus are female and most develop it aged 15-45. 

Co-senior author Professor Eric Morand, who is Dean of Monash University’s Sub Faculty of Clinical & Molecular Medicine and founded the Monash Lupus Clinic, described the treatment’s effectiveness as “profound” and a “game-changer”.

Study patients are managed at Monash Health, where Professor Morand is Director of Rheumatology. He said the research team was now designing clinical trials expected to start in 2026 to investigate whether this method was a long-term cure for people with lupus.

“The ability to target, specifically, the disease-causing immune defect, without the need to suppress the entire immune system, is a game-changer,” he said. “Even if the effects are only medium term, we are confident the treatment can be easily repeated as needed.”

Associate Professor Ooi previously discovered that a lack of specific T-regs to stop the immune system from targeting the body can lead to autoimmune disease. The new treatment would involve taking blood cells from the lupus patient, modifying them in the lab to restore this protective effect, then giving them back.

“This project relied on the generous involvement of patients, which enabled us to use human lupus cells every step of the way,” Associate Professor Ooi said. “This allows us to work as close to the human disease as possible in the lab.

“This is a unique characteristic of Monash University — state-of-the-art research labs side-by-side with clinicians and patients, in this case at Monash Health.”

Co-first authors Peter Eggenhuizen, a PhD candidate and Research Fellow with the Centre for Inflammatory Disease Monash University, and Dr Rachel Cheong, former PhD candidate at the Centre for Inflammatory Disease Monash University, are confident the new method can be developed for up to 100 other autoimmune diseases such as diabetes, rheumatoid arthritis, multiple sclerosis, Sjögren’s syndrome, scleroderma, and myasthenia gravis.

“This breakthrough offers huge hope not only in lupus but across the spectrum of autoimmune diseases,” Mr Eggenhuizen said. “There is a huge range of autoimmune diseases that could be targeted with this approach.”

Added Dr Cheong: “The great thing is that because the treatment is very specific, it doesn’t harm the rest of the immune system. However, this means that the treatment needs to be carefully developed disease-by-disease, as each one is distinct.”

This research was supported by multiple national and international agencies, including the New-York headquartered Lupus Research Alliance, and was part of a body of work that won Professor Morand and Associate Professor Ooi the 2022 Victoria Prize for Science and Innovation in Life Sciences.

Case study – Vu Nguyen

Vu Nguyen, 39, was diagnosed with Lupus in 1995 aged nine after she developed swelling and pain in her joints. Almost 30 years later, Vu has experienced a range of symptoms, kidney biopsies and hospital stays. She had a stroke when she was 22 and now has epilepsy, which is secondary to lupus.

It took many years to stabilise Vu’s condition, which inspired her to establish Lupus Victoria. A Masters of Marketing graduate, Vu is completing psychological science post-graduate qualifications so she can counsel those who have the disease.

“My main symptoms are now bad functioning kidneys and my epilepsy,” Vu said. “With Lupus, it always changes. I’m currently in remission but I’ve had a lot of ups and downs with this disease. I think the lupus has made my body more prone to having the stroke and subsequent epilepsy. I am good at the moment. It’s just the epilepsy that’s currently attacking my body.

“This new treatment will really help people living with lupus; if the treatment was around 30 years ago it would have made a real difference for me. It could really cut down the many different types of medicines we take. With this procedure, we could possibly need just one treatment.”

Posted on Lupus, Multiple Sclerosis, Patient Talk, Rheumatoid arthritis

Multiple Sclerosis + Another Autoimmune Disease: Treatment Options

What if you have multiple sclerosis and an additional autoimmune disease such as rheumatoid arthritis or lupus? Can you take a single medication to treat both conditions. This video shows some data on treating multiple simultaneous autoimmune conditions and the importance of avoiding anti-TNF alpha blocking drugs if you have multiple sclerosis.

Posted on Lupus, Rheumatoid arthritis

RA and Lupus – Scientists reveal how our cells’ leaky batteries make us sick.

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Scientists reveal how our cells’ leaky batteries are making us sick

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“Now that we are beginning to understand how this inflammation starts, we might be able to prevent this process, with the ultimate goal of limiting inflammation and treating disease,” said researcher Laura E. Newman, PhD. CREDIT Courtesy Newman lab

Researchers have discovered how “leaky” mitochondria – the powerhouses of our cells – can drive harmful inflammation responsible for diseases such as lupus and rheumatoid arthritis. Scientists may be able to leverage the findings to develop better treatments for those diseases, improve our ability to fight off viruses and even slow ageing.

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The new discovery reveals how genetic material (mitochondria) can escape from our cellular batteries and prompt the body to launch a damaging immune response. By developing therapies to target this process, doctors may one day be able to stop the harmful inflammation and prevent its toll on our bodies.

“When mitochondria don’t correctly replicate their genetic material, they try to eliminate it. However, if this is happening too often and the cell can’t dispose of all of it, it can cause inflammation, and too much inflammation can lead to disease, including autoimmune and chronic diseases,” said researcher Laura E. Newman, PhD, of the University of Virginia School of Medicine. “Now that we are beginning to understand how this inflammation starts, we might be able to prevent this process, with the ultimate goal of limiting inflammation and treating disease.”

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Powering Inflammation

Mitochondria have their own set of genetic material, separate from the DNA that serves as the operating instructions for our cells. Scientists have known that this mitochondrial DNA, mtDNA, can escape into our cells and cause inflammation. But exactly what caused this has been a mystery until now.

“We knew that mtDNA was escaping mitochondria, but how was still unclear,” said Gerald Shadel, PhD, director of the San Diego-Nathan Shock Center of Excellence in the Basic Biology of Aging at the Salk Institute. “Using imaging and cell biology approaches, we’re able to trace the steps of the pathway for moving mtDNA out of the mitochondria, which we can now try to target with therapeutic interventions to prevent the resulting inflammation hopefully.”

Shadel and Newman, then a postdoctoral researcher in Shadel’s lab, and their collaborators used sophisticated imaging techniques to determine what was happening inside the leaky mitochondria. They found that a malfunction in mtDNA replication triggered the leak. This caused the accumulation of protein masses caused by nucleoids.

To try to fix this problem, the cell containing the faulty mitochondrion begins to export the excess nucleoids to its cellular trash bins. But the trash bins, called endosomes, can become overwhelmed by the volume of debris, the scientists found. These overburdened endosomes respond by releasing mtDNA into the cell – in short, the trash can overflows.

“We had a huge breakthrough when we saw that mtDNA was inside of a mysterious membrane structure once it left mitochondria. After assembling all of the puzzle pieces, we realized that structure was an endosome,” Newman said. “That discovery eventually led us to the realization that the mtDNA was being disposed of and, in the process, some of it was leaking out.”

The cell responds to this hazardous waste spill by flagging the nucleoids as foreign DNA, like a virus, and launches an immune response that results in harmful inflammation, the scientists determined.

“Using our cutting-edge imaging tools for probing mitochondria dynamics and mtDNA release, we have discovered an entirely novel release mechanism for mtDNA,” said researcher Uri Manor, PhD, former director of the Waitt Advanced Biophotonics Core at Salk and current assistant professor at UC San Diego. “There are so many follow-up questions we cannot wait to ask, like how other interactions between organelles control innate immune pathways, how different cell types release mtDNA, and how we can target this new pathway to reduce inflammation during disease and aging.”

Newman will continue to seek these answers in her new role at the UVA School of Medicine’s Department of Cell Biology. “We want to understand the physiological and disease contexts where this process can become activated,” she said. “For example, many viruses attack mitochondria during infection, so we will be testing whether mitochondria purposely use this pathway to sound the alarm against invading viruses, and whether over-reliance on this pathway to fight off infection can later trigger chronic diseases.”

Findings Published

Posted on Lupus

World-first discovery may enable an effective long-term lupus treatment

Australian researchers have worked out how to fix a defect that causes lupus, and hope their world-first discovery will offer effective long-term treatment.
Australian researchers have worked out how to fix a defect that causes lupus and hopes their world-first discovery will offer effective long-term treatment.

Australian researchers have worked out how to fix a defect that causes lupus, and hope their world-first discovery will offer effective long-term treatment.

Published in Nature Communications, the Monash University-led study found a way to reprogram the defective cells of lupus patients with protective molecules from healthy people.

Using human cells, the new treatment restores the protective side of the immune system that prevents autoimmunity, which is when the immune system attacks its own cells. The findings relate to the autoimmune disease lupus, a debilitating disease with no cure and limited treatments.

However, researchers hope this new method, developed in test tubes and proven in pre-clinical models, can also be developed for other autoimmune diseases such as diabetes, rheumatoid arthritis, and multiple sclerosis.

Humans all have proteins that the immune system could attack, but this doesn’t happen in healthy people because of special cells called ‘regulatory T cells’ or ‘T-regs’ that protect from autoimmune disease. These are lacking in people who develop lupus and other autoimmune conditions.

Co-senior author Associate Professor Joshua Ooi, who heads Monash University’s Regulatory T Cell Therapies Group based at Monash Health, said the therapeutic effect was achieved by identifying specific protective molecules from healthy people and reprogramming ineffective lupus patient T-regs to restore their ability to switch off unwanted immune responses.

“We showed the effectiveness of this approach using human lupus patient cells, both in the test tube and in an experimental model of lupus kidney inflammation,” Associate Professor Ooi said.

“We were able to completely arrest the development of lupus kidney disease, without the use of the usual non-specific and harmful immunosuppressant drugs. It’s like a reset of the abnormal immune system back to a healthy state – kind of like a major software upgrade. That it uses the patient’s own cells is a very special part of this.”

About one in 1000 Australians has lupus, and rates are higher in First Nations communities. Nine in 10 people with lupus are female and most develop it aged 15-45. 

Co-senior author Professor Eric Morand, who is Dean of Monash University’s Sub Faculty of Clinical & Molecular Medicine and founded the Monash Lupus Clinic, described the treatment’s effectiveness as “profound” and a “game-changer”.

Study patients are managed at Monash Health, where Professor Morand is Director of Rheumatology. He said the research team was now designing clinical trials expected to start in 2026 to investigate whether this method was a long-term cure for people with lupus.

“The ability to target, specifically, the disease-causing immune defect, without the need to suppress the entire immune system, is a game-changer,” he said. “Even if the effects are only medium term, we are confident the treatment can be easily repeated as needed.”

Associate Professor Ooi previously discovered that a lack of specific T-regs to stop the immune system from targeting the body can lead to autoimmune disease. The new treatment would involve taking blood cells from the lupus patient, modifying them in the lab to restore this protective effect, then giving them back.

“This project relied on the generous involvement of patients, which enabled us to use human lupus cells every step of the way,” Associate Professor Ooi said. “This allows us to work as close to the human disease as possible in the lab.

“This is a unique characteristic of Monash University — state-of-the-art research labs side-by-side with clinicians and patients, in this case at Monash Health.”

Co-first authors Peter Eggenhuizen, a PhD candidate and Research Fellow with the Centre for Inflammatory Disease Monash University, and Dr Rachel Cheong, former PhD candidate at the Centre for Inflammatory Disease Monash University, are confident the new method can be developed for up to 100 other autoimmune diseases such as diabetes, rheumatoid arthritis, multiple sclerosis, Sjögren’s syndrome, scleroderma, and myasthenia gravis.

“This breakthrough offers huge hope not only in lupus but across the spectrum of autoimmune diseases,” Mr Eggenhuizen said. “There is a huge range of autoimmune diseases that could be targeted with this approach.”

Added Dr Cheong: “The great thing is that because the treatment is very specific, it doesn’t harm the rest of the immune system. However, this means that the treatment needs to be carefully developed disease-by-disease, as each one is distinct.”

This research was supported by multiple national and international agencies, including the New-York headquartered Lupus Research Alliance, and was part of a body of work that won Professor Morand and Associate Professor Ooi the 2022 Victoria Prize for Science and Innovation in Life Sciences.

Case study – Vu Nguyen

Vu Nguyen, 39, was diagnosed with Lupus in 1995 aged nine after she developed swelling and pain in her joints. Almost 30 years later, Vu has experienced a range of symptoms, kidney biopsies and hospital stays. She had a stroke when she was 22 and now has epilepsy, which is secondary to lupus.

It took many years to stabilise Vu’s condition, which inspired her to establish Lupus Victoria. A Masters of Marketing graduate, Vu is completing psychological science post-graduate qualifications so she can counsel those who have the disease.

“My main symptoms are now bad functioning kidneys and my epilepsy,” Vu said. “With Lupus, it always changes. I’m currently in remission but I’ve had a lot of ups and downs with this disease. I think the lupus has made my body more prone to having the stroke and subsequent epilepsy. I am good at the moment. It’s just the epilepsy that’s currently attacking my body.

“This new treatment will really help people living with lupus; if the treatment was around 30 years ago it would have made a real difference for me. It could really cut down the many different types of medicines we take. With this procedure, we could possibly need just one treatment.”