Vitamin D Helps Against Thyroid Autoimmunity

A paper studying the effectiveness of vitamin D replacement therapy for thyroid autoimmunity syndrome can be found here.  Abstract:

BACKGROUND:
Vitamin D was shown to be related to autoimmune thyroid diseases (AITDs) in the previous studies. We aimed to investigate the relationship between Vitamin D and thyroid autoimmunity.
MATERIALS AND METHODS:
Eighty-two patients, diagnosed with AITD by the endocrinology outpatient clinic, were included in this prospective study. All of the patients had both AITD and Vitamin D deficiency, defined as serum values <20 ng/mL. They were randomly assigned into two groups. The first group included 46 patients and the second one included 36 patients. The first group was treated with Vitamin D for 1 month at 1000 IU/day. The second group served as the control group and was not treated with Vitamin D replacement. Serum thyroid-stimulating hormone, free T4 (fT4), thyroid peroxidase antibody (TPO-Ab), thyroglobulin antibody (TgAb), and Vitamin D levels were measured at the initiation of the study and again at 1 month in all patients.
RESULTS:
Two groups were similar with regard to age, sex, and type of thyroid disease. Whereas TPO-Ab (before; 278.3 ± 218.4 IU/ml and after; 267.9 ± 200.7 IU/ml) and TgAb (before; 331.9 ± 268.1 IU/ml and after; 275.4 ± 187.3 IU/ml) levels were significantly decreased by the Vitamin D replacement therapy in group 1 (P = 0.02, P = 0.03, respectively), the evaluated parameters in the control group did not significantly change (P = 0.869, P = 0.530, respectively). In addition, thyroid function tests did not significantly change with Vitamin D replacement in two groups.
CONCLUSION:
Vitamin D deficiency may contribute to the pathogenesis of AITDs. Since supplementation of the Vitamin D decreased thyroid antibody titers in this study in Vitamin D deficient subjects, in the future Vitamin D may become a part of AITDs' treatment, especially in those with Vitamin D insufficiency. Further clinical and experimental studies are required to understand the effect of Vitamin D on AITD.

The vitamin therapy reduced levels of the thyroid antibodies that cause the problem, and this is good. Unfortunately, there was no change in actual thyroid function.  So, this is a promising initial set of findings suggesting a vitamin D link but more study is required to better understand what is going on, so as to possibly devise additional interventions that can have more optimal effects. Ideally, I believe that one would want to both decrease the antibody levels and also improve thyroid function.  

New Inroads Against Multiple Sclerosis

Read this.  Excerpts:

Medical progress against multiple sclerosis (MS) took a major leap forward in 2017 with the approval by the US Food and Drug Administration (FDA) of ocrelizumab, a drug that has shown success against 2 different forms of the disease. The year also brought further signs that it may be possible to biochemically reverse damage wrought by MS.

So, there’s a potentially effective monoclonal antibody drug, and there are possibilities of reversing the damage.  Stem cells are always useful for repair.

One of the key epidemiologic points about MS is that it has increased in frequency, and although there are now 203 genes that influence MS risk, all of these influences are very small effects, and the majority of susceptibility is not genetic and is almost certainly environmental. What in the environment is responsible for triggering MS is one of the great questions in MS research. It's unanswered but is likely to be a virus or bacterium. 

Dr Cohen:I would add that the microbe may not only be external to the person, but something in their own microbiome. It probably is not one single culprit, but many potential culprits. Or the distribution, the presence of some or absence of other microbial agents, may be what leads to susceptibility.

Once again, the microbiome.  Remember that your microbiome is influenced by diet.

Dr Hauser:It's likely that the microbiome has a substantial effect on MS in 2 ways. The first is the molecular mimicry, where some cell component of a bacterium or virus resembles a protein or substance in the brain. The second is that our microbiota influence the regulatory tone of our immune system, and that could lead to differences in the trajectory of disease after it begins. 

We don't yet know what the likely microbial culprit or culprits are. The strongest epidemiologic link to multiple sclerosis remains a late onset infection with the Epstein-Barr virus (EBV), [perhaps] the occurrence of infectious mononucleosis, but we really don’t know if EBV is causally linked or is a surrogate for some other infectious agent.

That’s also useful to know, and another avenue to explore for prevention of therapy, mostly the former.

Salt, Microbiota, and High Blood Pressure

A high salt diet can alter gut microbiota, which in turn induces certain immune cells that can contribute to autoimmunity leading to, among other problems, high blood pressure.  This finding provides more evidence foe the link between diet, gut microbiota, and altered human health, and also demonstrates a novel mechanism whereby a high salt diet contributed to hypertension.  Abstract:

A Western lifestyle with high salt consumption can lead to hypertension and cardiovascular disease. High salt may additionally drive autoimmunity by inducing T helper 17 (TH17) cells, which can also contribute to hypertension. Induction of TH17 cells depends on gut microbiota; however, the effect of salt on the gut microbiome is unknown. Here we show that high salt intake affects the gut microbiome in mice, particularly by depleting Lactobacillus murinus. Consequently, treatment of mice with L. murinus prevented salt-induced aggravation of actively induced experimental autoimmune encephalomyelitis and salt-sensitive hypertension by modulating TH17 cells. In line with these findings, a moderate high-salt challenge in a pilot study in humans reduced intestinal survival of Lactobacillus spp., increased TH17 cells and increased blood pressure. Our results connect high salt intake to the gut-immune axis and highlight the gut microbiome as a potential therapeutic target to counteract salt-sensitive conditions.

Inflammation Memory

By The original uploader was Samir at English Wikipedia - Transferred from en.wikipedia to Commons., CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=2107303

Here is an interesting study that suggests a form of “inflammation memory” exists.  Therefore, in epithelial stem cells that have already been exposed to acute inflammation there is a molecular “memory” of the event, which enables a more rapid response for subsequent inflammatory exposures.   While this has some benefits in dealing with the immediate need for a response to certain stimuli, this increased sensitivity may contribute to autoimmune diseases and cancer.  From the preventive and therapeutic angle, it is therefore important to study.  Abstract:

The skin barrier is the body's first line of defence against environmental assaults, and is maintained by epithelial stem cells (EpSCs). Despite the vulnerability of EpSCs to inflammatory pressures, neither the primary response to inflammation nor its enduring consequences are well understood. Here we report a prolonged memory to acute inflammation that enables mouse EpSCs to hasten barrier restoration after subsequent tissue damage. This functional adaptation does not require skin-resident macrophages or T cells. Instead, EpSCs maintain chromosomal accessibility at key stress response genes that are activated by the primary stimulus. Upon a secondary challenge, genes governed by these domains are transcribed rapidly. Fuelling this memory is Aim2, which encodes an activator of the inflammasome. The absence of AIM2 or its downstream effectors, caspase-1 and interleukin-1β, erases the ability of EpSCs to recollect inflammation. Although EpSCs benefit from inflammatory tuning by heightening their responsiveness to subsequent stressors, this enhanced sensitivity probably increases their susceptibility to autoimmune and hyperproliferative disorders, including cancer.

Microbiotic Importance

By Darryl Leja, NHGRI - http://www.genome.gov/dmd/img.cfm?node=Photos/Graphics&id=85320, Public Domain, https://commons.wikimedia.org/w/index.php?curid=29534265

Here is a review once again stressing the importance of the microbiota for human health, concentrating on immune system effects that influence “host response to infection, vaccination and cancer, as well as susceptibility to autoimmune and neurodegenerative disorders."  Abstract:

The study of the intestinal microbiota has begun to shift from cataloging individual members of the commensal community to understanding their contributions to the physiology of the host organism in health and disease. Here, we review the effects of the microbiome on innate and adaptive immunological players from epithelial cells and antigen-presenting cells to innate lymphoid cells and regulatory T cells. We discuss recent studies that have identified diverse microbiota-derived bioactive molecules and their effects on inflammation within the intestine and distally at sites as anatomically remote as the brain. Finally, we highlight new insights into how the microbiome influences the host response to infection, vaccination and cancer, as well as susceptibility to autoimmune and neurodegenerative disorders.