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Research case series presents food as medicine as a potential treatment for lupus and other autoimmune diseases
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.”
How to deal with autoimmune disease flares- A Rheumatologist POV
Flares happen. We do everything we can to prevent them and understand why they occur, but sometimes, they just happen. This is true regardless of the inflammatory or autoimmune disease: lupus, arthritis, fibromyalgia, vasculitis, and all the others. As frustrating as they can be, there are things you can do to manage them with care and grace.
Possible trigger for autoimmune diseases discovered
One of the mysteries of immunology is that the function of B cells (green) in the thymus gland was previously unknown. Researchers have now been able to show that the immune cells help to prevent T cells from attacking the body. CREDIT Jan Böttcher, Thomas Korn / TUM
Immune cells must learn not to attack the body itself. A team of researchers from the Technical University of Munich (TUM) and the Ludwig Maximilian University of Munich (LMU) has discovered a previously unknown mechanism behind this: other immune cells, the B cells, contribute to the “training” of the T cells in the thymus gland. If this process fails, autoimmune diseases can develop. The study confirms this for Neuromyelitis optica, a disease similar to Multiple Sclerosis. Other autoimmune diseases may also be linked to the failure of this new mechanism.
The thymus gland functions as a “school for T cells” in children and adolescents. The organ in our chest is where the precursors of those T cells that would later attack the body’s own cells are discarded. Epithelial cells in the thymus present many molecules that occur in the body to the future T cells. A self-destruction program is triggered if any of them reacts to one of these molecules. T cells that attack the body’s own molecules remaining intact and multiplying, on the other hand, can cause autoimmune diseases.
New mechanism discovered
In Nature, the team led by Thomas Korn, Professor of Experimental Neuroimmunology at TUM and a Principal Investigator in the SyNergy Cluster of Excellence, and Ludger Klein, Professor of Immunology at LMU’s Biomedical Center (BMC), describe another previously unknown mechanism behind this.
In addition to the precursors of T cells, the thymus gland also contains other immune cells, the B cells. They develop in the bone marrow but migrate to the thymus in early childhood. “The function of B cells in the thymus gland has been a mystery that has puzzled immunologists for many years,” says Thomas Korn. The researchers have now been able to show for the first time that B cells play an active role in teaching T cells which targets not to attack.
MS-like disease due to malfunction in tolerance formation
Neuromyelitis optica is an autoimmune disease similar to multiple sclerosis (MS). While it is not yet known which molecules are attacked in MS, it is well-established that T cells respond to the protein AQP4 in neuromyelitis optica. AQP4 is most prominently expressed in cells of the nervous tissue, which then becomes the target of the autoimmune reaction. Frequently, the optic nerve is affected.
The researchers were able to show that in the thymus gland of humans and mice not only the epithelial cells but also B cells express and present AQP4 to the T cell precursors. If the B cells were prevented from doing so in animal experiments, AQP4-reactive T cell precursors were not eliminated and the autoimmune disease developed. This was also the case when the epithelial cells still presented the molecule. The team concludes from this that B cells in the thymus are a necessary condition for immune tolerance regarding AQP4.
Protection against subsequent interactions between T cells and B cells
“We suspect that this previously unknown process has evolved particularly to prevent dangerous interactions between autoreactive T and B cells in the lymph nodes and spleen, the so-called peripheral immune compartment,” says Ludger Klein. Once the immune system is developed, B and T cells can communicate and thus trigger highly effective immune reactions. This is useful when it comes to fighting pathogens quickly. On occasion, however, B cells may accidentally present the body’s own proteins, such as AQP4. If the T cells that react to AQP4 had not been sorted out in the thymus, this could lead to a sudden and violent large-scale attack on the body.
Possible cause of other immune disorders
“We assume that problems with the training of T cells by the B cells in the thymus can cause other autoimmune diseases as well,” says Thomas Korn. “After all, the B cells in the thymus present a whole range of the body’s own proteins. The corresponding interactions must be investigated in further studies.”
According to the researchers, likely suspects include antiphospholipid syndrome (APS) and certain forms of cerebral amyloid angiopathy. “Looking further into the future, this interaction in the thymus might be exploited to treat existing autoimmune diseases in a very targeted manner,” says Thomas Korn.
Study shows why women are at greater risk of autoimmune disease.
omewhere between 24 and 50 million Americans have an autoimmune disease, a condition in which the immune system attacks our own tissues. As many as 4 out of 5 of those people are women.
Rheumatoid arthritis, multiple sclerosis and scleroderma are examples of autoimmune disorders marked by lopsided female-to-male ratios. The ratio for lupus is 9 to 1; for Sjogren’s syndrome, it’s 19 to 1.
Stanford Medicine scientists and their colleagues have traced this disparity to the most fundamental feature differentiating biological female mammals from males, possibly paving the way for a better way to predict autoimmune disorders before they develop.
“As a practising physician, I see a lot of lupus and scleroderma patients because those autoimmune disorders manifest in the skin,” said Howard Chang, MD, PhD, dermatology professor and genetics professor and a Howard Hughes Medical Institute investigator. “The great majority of these patients are women.”
Chang, the Virginia and D.K. Ludwig Professor in Cancer Research and director of the RNA Medicine Program, is the senior author of the study, to be published Feb. 1 in Cell. Basic life research scientist Diana Dou, PhD, is its lead author.
The silence of the second X
Women have too much of a good thing: It’s called the X chromosome.
Throughout the mammalian kingdom, biological sex is determined by the presence of two X chromosomes in every female cell. Male cells pack just one X chromosome, paired with a much shorter one designated the Y chromosome.
The stubby Y chromosome contains only a handful of active genes. It’s quite possible to live a full life without a Y chromosome. In fact, more than half of the people on Earth — women — lack Y chromosomes and do just fine. But no mammalian male or female cell can survive without at least one copy of the X chromosome, which holds many hundreds of active protein-specifying genes.
Still, having two X chromosomes risks the production, in every female cell, of twice the amount of the myriad proteins specified by the X but not the Y chromosome. Such massive overproduction of so many proteins would be lethal.
Nature has devised a clever, if complicated, workaround called X-chromosome inactivation. Early in embryogenesis, each cell in the nascent female mammal decides to shut down the activity of one or the other of its two X chromosomes. Once that decision is made, it’s handed down to these cells’ progeny in the developing fetus. That way, the same amount of each X-chromosome-specified protein is produced in a female cell as in a male cell.
As the researchers discovered, X-chromosome inactivation can lead to autoimmune disorders, but other factors can also cause these disorders — which is why men sometimes develop them.
The great equalizer
X-chromosome inactivation is achieved courtesy of a molecule called Xist. The gene for Xist is present on all X chromosomes, including the single one male cells have. But Xist itself is produced only when the X chromosome that its gene resides on is one of a matched XX pair — and is produced and deployed on only one pair member.
Xist consists of RNA, a substance best known for being a simple-minded messenger that shuttles genes’ instructions for making proteins to the intracellular machines that make them. Yet RNA can do a whole lot more than schlep genetic information. There are as many different kinds of so-called long noncoding RNA (lncRNA) molecules — lengthy RNA stretches that don’t carry instructions for making proteins — as there are of the protein-encoding RNA variety. These lncRNA molecules can park themselves on stretches of chromosomes and change the likelihood that the cellular machinery charged with reading the genes in those locations will do so.
Xist, a type of lncRNA, is much longer than most. Xist coats long sections of one of a female mammalian cell’s two X chromosomes — but always just one — cutting that chromosome’s output to zero or close to it. The other X chromosome, left undisturbed, pumps out just enough RNA-encoded instructions to keep the cell humming.
But Xist’s nestling into the extra X chromosome generates odd combinations of lncRNA, proteins that bind to it, other proteins that bind to those proteins, and DNA some of those proteins cling to. These complexes can trigger a strong immune response, Chang and his colleagues have learned.
In 2015, Chang’s group identified close to 100 proteins that either bound to Xist or that bound to those proteins, collectively enabling this molecule to lay anchor along gene-specifying regions of the X chromosome.
Inspecting this Xist “parts list,” Chang realized that many of Xist’s collaborator proteins were known to be associated with autoimmune disorders. Might the RNA-protein-DNA complexes generated in the course of X-chromosome inactivation be triggering the notoriously high rate of autoimmunity in women compared with men? That question was the impetus for the new study.
What if males made Xist?
To eliminate possible competing causes such as female hormonal action or aberrant protein production by the supposedly silenced second X chromosome, the researchers tossed the Xist ball into the male court. They sewed the gene for Xist into the genomes of two different strains of male lab mice. One strain is quite susceptible to autoimmune symptoms mimicking lupus, with females more susceptible than males. The other is resistant to it.
The inserted Xist gene had been modified in two ways. It could be turned on or off by chemical means, pumping out Xist only when the scientists wanted it to. The Xist gene was also tweaked slightly so that its RNA product would no longer silence the genes of the male mouse’s chromosome into which it was stitched.
Merely inserting that modified Xist gene had no noticeable effect on the mice. But the Xist produced from the inserted gene, once that gene was activated, still formed characteristic complexes with almost all the proteins found earlier to be collaborating closely with Xist.
Now, the scientists could ask: Is a bioengineered male mouse that’s been coaxed to produce Xist more prone to autoimmunity than a normal male mouse, which never produces it, or than a male in whom the gene for Xist has been inserted but not activated?
By injecting an irritant known to induce a lupus-like autoimmune condition in the susceptible mouse strain, the investigators could compare its effect on males who made Xist with its effect on normal males, who made none.
In these susceptible mice, males in which the Xist gene was activated developed lupus-like autoimmunity at a rate approaching that of females — and considerably more so than non-bioengineered males.
The absence of autoimmunity in some female or Xist-activated male mice in the susceptible strain showed that not just activation of Xist but also some kind of tissue-damaging stress (caused, in this case, by injection of the irritant) is required to get the autoimmunity ball rolling.
In the autoimmune-resistant strain, activating Xist in bioengineered male mice wasn’t enough to induce autoimmunity — as might be predicted by the fact that in this strain even females seldom develop autoimmunity. That suggests that not only Xist activation but also an appropriate genetic background is necessary for autoimmunity to develop.
These constraints on autoimmunity are fortunate, because if there were none all women might be more susceptible to develop immunity, Chang noted.
Toward a better autoimmunity-screening panel
An early step in the development of autoimmunity is the appearance of autoantibodies: antibodies targeting one’s own tissues or cell products. Autoantibodies to the contents of cell nuclei are called anti-nuclear antibodies. Close examination of blood samples from about 100 patients with autoimmunity showed the presence of autoantibodies to many of the complexes associated with Xist. Some of these autoantibodies were specific to one or another autoimmune disorder, indicating their potential utility in identifying particular emergent autoimmune disorders before symptoms develop. Autoantibodies to still other Xist-associated proteins spanned several disorders, designating them as possible common markers of autoimmunity.
“Every cell in a woman’s body produces Xist,” Chang said. “But for several decades, we’ve used a male cell line as the standard of reference. That male cell line produced no Xist and no Xist/protein/DNA complexes, nor have other cells used since for the test. So, all of a female patient’s anti-Xist-complex antibodies — a huge source of women’s autoimmune susceptibility — go unseen.”