AIP Diet – What is the Autoimmune Protocol?

AIP Diet Day 1 - Autoimmune Protocol Meals & Snacks - YouTube


AIP Diet is starting for me! I’m doing the AIP diet to quell a Hashimoto’s Flare and I’m taking you along for the journey. I explain what the Autoimmune Paleo Protocol (AIP diet or also known just as the Autoimmune Protocol) is and also what I ate for AIP for Day 1 breakfast and lunch.. Note: I follow the Autoimmune Paleo Protocol developed by Dr. Sarah Ballantyne, which is called the AIP Diet. The Autoimmune Protocol by Dr. Amy Myers is very similar but slightly different in what has to be eliminated (like in the Paleo version, black pepper is eliminated)

Health disparities and inequities impact Black and Latino Americans with multiple sclerosis, says new study

Lilyana Amezcua

Lilyana Amezcua CREDIT Ricardo Carrasco III

Minority populations in the US with multiple sclerosis and other autoimmune diseases experience poorer outcomes due to modifiable social conditions, according to a new USC study. Social determinants of health (SDOH) – things like where people are born, grow up, live, work and age – are unevenly distributed, leaving many people of color with fewer resources to ensure their own well-being.

“For Blacks and Latinos with MS or other autoimmune diseases, access to neurological specialists is rare and diagnostic tools are limited,” said lead researcher Lilyana Amezcua, MD, an associate professor of clinical neurology at the Keck School of Medicine of USC, program director of the Multiple Sclerosis Fellowship and director of the Keck Huntington Beach Multiple Sclerosis Infusion Program. “Our study shows that, before we look at biological factors as the cause of the disparities we see in health outcomes, we should first assess the role of SDOH and how we might modify them to make a difference.”

The study was just published in JAMA Neurology.

Surveying the field

To investigate the role of SDOH, researchers performed a narrative review of medical literature from three major bibliographic databases of life sciences and biomedical information, focusing on studies published between January 2014 and March 2021. They searched thousands of journals for terms related to race, ethnicity, disparity and inequity in connection with certain autoimmune diseases, including multiple sclerosis (MS) and neuromyelitis optica spectrum disorder (NMOSD). What they discovered was revealing – and what they did not find was equally telling.

“Normally, one would expect there to have been much more data available for a survey like this, but racial and ethnic populations, particularly with regard to MS, are quite underrepresented. In prior studies, only about one percent of literature reflects these minority populations. In clinical trials, less than 10 percent include African Americans or Latinos,” Amezcua said. “This is a disservice to these communities because there are more than 20 disease-modifying treatments for MS.”

Health disparities and inequities in autoimmune diseases

Despite the paucity of studies including people of color, the data indicate that when it comes to MS and NMOSD, Black and Latino Americans – who traditionally have lower income, education and health literacy – are more likely to experience health disparities such as greater disease severity and faster disease progression than white Americans. Black people also have a higher risk of developing MS and NMOSD and are more likely to die from the disease. The review did not include Asian Americans because data for this group was even scarcer.

The review also revealed significant inequities in accessing health care, leading to diagnostic delays, and underuse of services such as outpatient neurological care, case management, technology, equipment, nursing and modification services.  

The role of SDOH

For MS in particular, the review showed SDOH such as low income and low education were associated with lower utilization of health services by people of color. Unemployment was associate with poorer outcomes for Black patients. The study also found that negative illness perception is another SDOH associated with racial and ethnic health disparities. 

“Our analysis confirms the power of the health belief model – that what you think about your disease will lead you to take action, or not, in order to advocate for yourself as a patient,” Amezcua said. “For many communities of color, there is a sense of fatalism about their ability to improve their MS, which only serves to reinforce the impact of the disease on their lives.”

Amezcua notes that previous USC studies have examined perceptions of illness, particularly MS, in the Latino population and found differences between Latinos born in the United States versus those who emigrated from other countries. Foreign born Latinos were more aligned with socio-cultural factors that made them less likely to be on treatment for MS. 

“What we learned from these studies is that education can change this,” Amezcua says, “and that perceptions are modifiable with the right intervention that promotes health literacy.”

Calling for change

Results from the study highlight the urgency of identifying new approaches to counteract the negative impact of SDOH on underrepresented populations. 

“It underscores that, when it comes to autoimmune disorders, vulnerable populations suffer from the same inequities that other chronic conditions have highlighted,” said Lourdes Baezconde-Garbanati, a co-author of the study and associate dean for community initiatives at the Keck School of Medicine.  “Going forward, we as researchers need to do a better job of including SDOH in our research models, not only to consider how they affect disease in underrepresented populations, but also to create interventions that go beyond one disease.”

About the Study

In addition to Amezcua and Baezconde-Garbanati, other authors of the study include Victor Rivera from Baylor College of Medicine; Teresa Corona Vazquez from Mexico’s National Institute of Neurology and Neurosurgery; and Annette Langer-Gould from Kaiser Permanente Southern California. 

About Keck School of Medicine

Founded in 1885, the Keck School of Medicine of USC is one of the nation’s leading medical institutions, known for innovative patient care, scientific discovery, education and community service. Medical and graduate students work closely with world-renowned faculty and receive hands-on training in one of the nation’s most diverse communities. They participate in cutting-edge research as they develop into tomorrow’s health leaders. With more than 900 resident physicians across 50 specialty and subspecialty programs, the Keck School is the largest educator of physicians practicing in Southern California.

Fibromyalgia likely the result of autoimmune problems

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Fibromyalgia likely the result of autoimmune problems
Fibromyalgia likely the result of autoimmune problems


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New research from the Institute of Psychiatry, Psychology & Neuroscience (IoPPN) at King’s College London, in collaboration with the University of Liverpool and the Karolinska Institute, has shown that many of the symptoms in fibromyalgia syndrome (FMS) are caused by antibodies that increase the activity of pain-sensing nerves throughout the body.

The results show that fibromyalgia is a disease of the immune system, rather than the currently held view that it originates in the brain.

The study, published today in the Journal of Clinical Investigation, demonstrates that the increased pain sensitivity, muscle weakness, reduced movement, and reduced number of small nerve-fibres in the skin that are typical of FMS, are all a consequence of patient antibodies.

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The researchers injected mice with antibodies from people living with FMS and observed that the mice rapidly developed an increased sensitivity to pressure and cold, as well as displaying reduced movement grip strength. In contrast, mice that were injected with antibodies from healthy people were unaffected, demonstrating that patient antibodies cause, or at least are a major contributor to the disease.

Furthermore, the mice injected with fibromyalgia antibodies recovered after a few weeks, when antibodies had been cleared from their system. This finding strongly suggests that therapies which reduce antibody levels in patients are likely to be effective treatments. Such therapies are already available and are used to treat other disorders that are caused by autoantibodies.

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Dr David Andersson, the study’s primary investigator from King’s IoPPN said “The implications of this study are profound. Establishing that fibromyalgia is an autoimmune disorder will transform how we view the condition and should pave the way for more effective treatments for the millions of people affected. Our work has uncovered a whole new area of therapeutic options and should give real hope to fibromyalgia patients.

“Previous exploration of therapies has been hampered by our limited understanding of the illness. This should now change. Treatment for FMS is focussed on gentle aerobic exercises, as well as drug and psychological therapies designed to manage pain, although these have proven ineffective in most patients and have left behind an enormous unmet clinical need.”

Current estimates suggest that at least 1 in 40 people are affected by FMS worldwide (80% of which are women) and is commonly characterised by widespread pain throughout the body, as well as fatigue (often referred to as ‘fibro fog’) and emotional distress. It most commonly develops between the ages of 25 and 55, although children can also get it.

Dr Andreas Goebel, the study’s principle clinical investigator from the University of Liverpool said, “When I initiated this study in the UK, I expected that some fibromyalgia cases may be autoimmune. But David’s team have discovered pain-causing antibodies in each recruited patient. The results offer amazing hope that the invisible, devastating symptoms of fibromyalgia will become treatable.”

Professor Camilla Svensson, the study’s primary investigator from Karolinska Institute said, “Antibodies from people with FMS living in two different countries, the UK and Sweden, gave similar results, which adds enormous strength to our findings. The next step will be to identify what factors the symptom-inducing antibodies bind to. This will help us not only in terms of developing novel treatment strategies for FMS, but also of blood-based tests for diagnosis, which are missing today.

Dr Craig Bullock, Research Discovery and Innovations Lead at Versus Arthritis said “Fibromyalgia affects millions of people in the UK and can have a devastating impact on quality of life. It causes pain all over the body, fatigue, disturbed sleep and regular flare-ups where symptoms get even worse.

“Fibromyalgia is a particularly difficult condition to diagnose and manage because its causes are unknown. This research shows that antibodies found in human blood can cause fibromyalgia-like symptoms in mice, suggesting that these antibodies play a crucial role in the condition. Further research is needed but this offers hope to the millions of people with fibromyalgia that an effective treatment could be found in the relatively near future.”

Do COVID-19 Vaccines Work for Immuno-suppressed People? [Israel Pfizer BNT162b2 Effectiveness Study]

Do COVID-19 Vaccines Work for Immunosupprssed People? [Israel Pfizer  BNT162b2 Effectiveness Study] - YouTube


Do COVID-19 vaccines work for immunosuppressed people? Given that vaccines work by inducing an immune response, will people taking immunosuppressive drugs benefit from the vaccines? What is the effectiveness compared to the general population? This study on the Pfizer Vaccine in Israel answers this question and breaks down data into different age groups.


Genetic tools help identify a cellular culprit for type 1 diabetes

By mapping its genetic underpinnings, researchers at University of California San Diego School of Medicine have identified a predictive causal role for specific cell types in type 1 diabetes, a condition that affects more than 1.6 million Americans.

The findings are published in the May 19, 2021 online issue of Nature.

Type 1 diabetes is a complex autoimmune disease characterized by the impairment and loss of insulin-producing pancreatic beta cells and subsequent hyperglycemia (high blood sugar), which is damaging to the body and can cause other serious health problems, such as heart disease and vision loss. Type 1 is less common than type 2 diabetes, but its prevalence is growing. The U.S. Centers for Disease Control and Prevention projects 5 million Americans will have type 1 diabetes by 2050. Currently, there is no cure, only disease management.

The mechanisms of type 1 diabetes, including how autoimmunity is triggered, are poorly understood. Because it has a strong genetic component, numerous genome-wide association studies (GWAS) have been conducted in recent years in which researchers compare whole genomes of persons with the same disease or condition, searching for differences in the genetic code that may be associated with that disease or condition.

In the case of type 1 diabetes, identified at-risk variants have largely been found in the non-coding regions of the genome. In the Nature study, senior author Kyle Gaulton, PhD, an assistant professor in the Department of Pediatrics at UC San Diego School of Medicine, and colleagues integrated GWAS data with epigenomic maps of cell types in peripheral blood and the pancreas. Epigenomic mapping details how and when genes are turned on and off in cells, thus determining the production of proteins vital to specific cellular functions.

Specifically, researchers performed the largest-to-date GWAS of type 1 diabetes, analyzing 520,580 genome samples to identify 69 novel association signals. They then mapped 448,142 cis-regulatory elements (non-coding DNA sequences in or near a gene) in pancreas and peripheral blood cell types.

“By combining these two methodologies, we were able to identify cell type-specific functions of disease variants and discover a predictive causal role for pancreatic exocrine cells in type 1 diabetes, which we were able to validate experimentally,” said Gaulton.

Pancreatic exocrine cells produce enzymes secreted into the small intestine, where they help digest food.

Co-author Maike Sander, MD, professor in the departments of Pediatrics and Cellular and Molecular Medicine at UC San Diego School of Medicine and director of the Pediatric Diabetes Research Center, said the findings represent a major leap in understanding the causes of type 1 diabetes. She described the work as “a landmark study.”

“The implication is that exocrine cell dysfunction might be a major contributor to disease. This study provides a genetic roadmap from which we can determine which exocrine genes may have a role in disease pathogenesis.”