Helicobacter pylori infection and autoimmune diseases

Posted on September 25, 2011 by Dr. Jonathan

Those managing cases of Helicobacter pylori infection (according to the World Health Organization the most common infection worldwide) should be alert to the association of Helicobacter infection and autoimmune diseases. The authors of a paper published in the journal Biomedicine & Pharmacotherapy discuss this connection, beginning with the autoimmune component of cardiovascular disease:

“In the last few years several studies have been performed on the association between H. pylori infection and a miscellany of extragastric disorders which also include autoimmune diseases. In particular, emerging evidence seems to give a potential role for H. pylori in ischaemic heart disease via a cross mimicry between antibodies against heat shock protein 65 which are produced in the consequence of infection, but which are also expressed in atherosclerotic lesions.”

They note that other autoimmune diseases have been recognized in this regard:

“In cases of healing of Sjogren syndrome and Schonlein-Henoch purpura have also been reported. A recent study, moreover, showed that eradication of H. pylori infection may be effective in the disappearance of autoimmune thrombocytopenia. Finally, a role for H. pylori has also been postulated in other autoimmune diseases such as membranous nephropathy and some acute immune polyneuropathies.”

We can also appreciate a paper just published in the journal Oral Diseases in which the authors observe:

“Helicobacter pylori (H. pylori) is a widely prevalent microbe, with between 50 and 80% of the population infected worldwide. Clinically, infection with H. pylori is commonly associated with peptic ulcer disease, but many of those infected remain asymptomatic.”

They proceed to elaborate on the implications for autoimmune disorders:

“H. pylori has evolved a number of means to affect the host immune response and has been implicated in many diseases mitigated by immune dysregulation, such as immune thrombocytopenic purpura (ITP), atrophic gastritis, and mucosa associated lymphoid tissue (MALT) lymphoma. Autoimmune diseases, such as systemic lupus erythematosus, rheumatoid arthritis, and Sjogren’s syndrome, are the result of a dysregulated host immune system which targets otherwise healthy tissues…Because of its prevalence and ability to affect human immune function, many researchers have hypothesized that H. pylori might contribute to the development of autoimmune diseases. In this article, we review the available literature regarding the role of chronic H. pylori infection in various autoimmune disease states.”

Case management of H. pylori infection requires vigilance for the possibility of an autoimmune condition, and for those suffering an autoimmune diagnosis the possibility of infection should be ruled out.

Yeast growth in the gut aggravates arthritis and allergies

Posted on September 20, 2010 by Dr. Jonathan

It is a cardinal principle in functional medicine to examine the gut in any case of autoimmune or allergic disease. No wonder, considering that 60-80% of the immune system tissue in the body is the lymphoid tissue packed around the intestines. This principle is illustrated by an interesting study recently published in the journal Medical Mycology:

“We examined whether Candida albicans gut colonization aggravates immune diseases in mice.”

The authors colonized the guts of the study animals and measured changes in contact hypersensitivity and immunoreactive arthritis. Their observations correspond to what we see in our patients:

“C. albicans gut colonization increased the incidence of allergic diarrhea, which was accompanied by gut hyperpermeability, as well as increased infiltration of inflammatory cells in the colon. Contact hypersensitivity was also exacerbated by C. albicans gut colonization, as demonstrated by increased swelling, myeloperoxidase activity, and proinflammatory cytokines in ear auricles. Furthermore, C. albicans gut colonization promoted limb joint inflammation in collagen-induced arthritis, in an animal model of rheumatoid arthritis.”

These results add to the large body of evidence for the key importance of immune regulation by microbes in the gut and the far-reaching impact of disruptions of the intestinal microbial ecology. The authors’ concluding comments apply to other gut pathogens as well:

“These findings suggest that C. albicans gut colonization in mice aggravates inflammation in allergic and autoimmune diseases, not only in the gut but also in the extra-gut tissues and underscores the necessity of investigating the pathogenic role of C. albicans gut colonization in immune diseases in humans.“

The most reliable way to investigate the microbial environment in the gut (now being used for pioneering studies of the human microbiome as well as for examination in clinical practices like ours) is DNA analysis.

Gluten sensitivity without celiac disease in the elderly: is there a concern?

Posted on July 19, 2010 by Dr. Jonathan

Scandinavian Journal of Gastroenterology Often tests shows anti-gliadin antibodies (AGA; gliadin is the immunoreactive component of gluten) in the absence of celiac disease but with various autoimmune conditions representing the non-celiac manifestations of gluten sensitivity. The authors of a study just published in the Scandinavian Journal of Gastroenterology explore this issue for the elderly.

“…data suggest that AGA positivity [without celiac disease] might be related to distinct disease entities such as allergy and gluten ataxia (loss of muscular coordination with unsteady movements and gait). Our aim here is to explore the clinical relevance of positive AGA in the elderly population.”

The authors correlated positive lab tests for gluten sensitivity with the incidence of depression and rheumatoid arthritis in 2815 individuals aged 52–74 years. What did their data show?

“Rheumatoid arthritis and depression were found significantly more often in AGA-positives than controls. The significance remained even when tTGA-positive and known celiac disease cases were excluded.”

Don’t forget that anti-gliadin antibody tests are not an absolute screen for gluten (or any other food) sensitivity because there are a number of factors that can suppress the expression of antibodies at the time of specimen collection. However, this study shows that if an elderly person is suffering from depression or rheumatoid arthritis the possibility of gluten sensitivity should be investigated.

Pro-inflammatory cytokines of rheumatoid arthritis reduced by Vitamin B6

Posted on July 11, 2010 by Dr. Jonathan

We’re always on the lookout for physiological agents that have the potential to calm the activity of pro-inflammatory cytokines when they are elevated in autoimmune disease. An exciting finding was reported in a paper just published in the European Journal of Clinical Nutrition:

“The purpose of this study was to investigate whether vitamin B6 supplementation had a beneficial effect on inflammatory and immune responses in patients with rheumatoid arthritis (RA).”

The control group of patients was given 5 mg/day of folic acid only while the study group was given 100 mg/day of vitamin B6 in addition for 12 weeks. Indicators of inflammation (C-reactive protein (hs-CRP), erythrocyte sedimentation rate (ESR), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α) and lymphocyte subsets were measured on day 1 (week 0) and after 12 weeks (week 12) of the intervention.

At the end of twelves the data painted this picture:

“In the group receiving vitamin B6, plasma IL-6 and TNF-α levels significantly decreased at week 12. Plasma IL-6 level remained significantly inversely related to plasma PLP (pyridoxal 5′-phosphate, B6) after adjusting for confounders.”

The bottom line conclusion is worth bearing in mind when evaluating any autoimmune disorder because underlying causal factors are similar regardless of the specific tissue under attack:

“A large dose of vitamin B6 supplementation (100 mg/day) suppressed pro-inflammatory cytokines (that is, IL-6 and TNF-α) in patients with RA.”

The autoimmune aspect of cardiovascular disease and Th17/Treg imbalance

Posted on July 9, 2010 by Dr. Jonathan

Cardiovascular disease, an inflammatory disorder, is a leading cause of death and the autoimmune component is one of the most important and in general practice, overlooked, aspects. Consider this paper published not long ago in the journal Clinical Immunology. As the authors state,

“Atherosclerosis is a chronic inflammatory disease regulated by T lymphocyte subsets.” ['T lymphocyte subsets' refers to the different categories of lymphocytes that participate in immune reactions.]

Regulatory T cells (Treg) ‘referee’ the immune response and quiet inflammation. Vitamin D is necessary for their production. Th1 refers to the lymphocytes that express the ‘innate’, cell-mediated aspect of the immune response; Th2 is the ‘adaptive’, humoral (antibody) mediated aspect. Th17 cells are a more recently recognized subtype that play a potent role in the immune system’s inflammatory attack.

“Recently, CD4+CD25+Foxp3+ regulatory T (Treg) cells and Th17 cells have been described as two distinct subsets from Th1 and Th2 cells and have the opposite effects on autoimmunity. Th17/Treg balance controls inflammation and may be important in the pathogenesis of plaque destabilization and the onset of acute coronary syndrome [ACS, including unstable angina (UA) and acute myocardial infarction (AMI)].”

The authors investigated this by assessing Th17/Treg functions by cell numbers, related cytokine secretion and their transcription factors in patients suffering from heart attacks, angina and control subjects free of heart disease. Their data made a strong impression:

“The results demonstrated that patients with ACS revealed significant increase in peripheral Th17 number, Th17 related cytokines (IL-17, IL-6 and IL-23) and transcription factor levels and obvious decrease in Treg number, Treg related cytokines (IL-10 and TGF-β1) and transcription factor (Foxp3) levels as compared with patients with SA and controls. Results indicate that Th17/Treg functional imbalance exists in patients with ACS, suggesting a potential role for Th17/Treg imbalance in plaque destabilization and the onset of ACS.”

In other words, the inflammatory process of cardiovascular disease that culminates in the rupture of a vulnerable plaque, which is the precipitating event for a heart attack, expresses this Th17/Treg functional imbalance.

You may have read earlier posts discussing oxidized LDL (ox-LDL) as a fundamental feature of cardiovascular disease and a valuable laboratory marker. This fascinating paper published recently in the journal Biochemical and Biophysical Research Communications that reports on the relationship between ox-LDL and Th17/Treg balance.

“Oxidized low-density lipoprotein (ox-LDL) is an instrumental factor in atherogenesis…CD4+CD25+ regulatory T (Treg) cells and Th17 cells, subsets of T-helper cells, play important roles in peripheral immunity and their imbalance leads to the development of tissue inflammation and autoimmune diseases…To explore the shift of Th17/Treg balance in ACS [acute coronary syndrome] patients and the effect of ox-LDL on the balance, we examined the frequencies of Th17 and Treg cells, key transcription factors and relevant cytokines in patients with AMI [acute myocardial infarction = heart attack], UA [unstable angina], stable angina (SA) and controls.”

What did their data show about the connection between these immune cells and inflammatory cardiovascular disease?

“Our study demonstrated that ACS patients have shown a significant increase of Th17 frequency, RORγt expression and serum Interleukin 17 (IL-17), and a obvious decline of Treg frequency, Foxp3 expression, suppressive function, and serum IL-10. Serum ox-LDL positively correlated with the frequency of Th17 cells and negatively correlated with the frequency of Treg cells…. Treg and Th17 cells from ACS patients were significantly more susceptible to ox-LDL-mediated alterations.“

Take a moment to appreciate the profound significance of this for the evaluation and treatment of cardiovascular disease. Cholesterol levels can be high in the absence of CVD, but when it is damaged by oxidation it somehow participates in the inflamed lesions of the vessel wall that are the basic characteristic of condition…

“Th17/Treg numerical and functional imbalance exists in ACS patients, and ox-LDL has a direct effect on Th17/Treg imbalance which may contribute to the occurrence of ACS.”

How else might Th17/Treg imbalance manifest in cardiovascular disease? A study published this year in the Scandinavian Journal of Immunology reveals its role in idiopathic dilated cardiomyopathy, a fairly common cause of heart failure (the enlarged heart fails to pump properly).

“To assess whether Treg/Th17 balance was broken in patients with idiopathic dilated cardiomyopathy (DCM). We studied 25 patients who were diagnosed as idiopathic DCM (18 men and seven women, mean age 35.6 ± 5.2) and 25 normal persons (18 men and seven women, mean age 33.8 ± 4.9). Then, we detected Treg/Th17 functions on different levels including cell frequencies, related cytokine secretion and key transcription factors in patients with idiopathic DCM and controls.”

What did their data show?

“The results demonstrated that patients with idiopathic DCM revealed significant increase in peripheral Th17 number, Th17-related cytokines (IL-17, IL-6, IL-23) and transcription factor (RORγt) levels and obvious decrease in Treg number, Treg-related cytokines (TGF-β1 and IL-10) and transcription factor (Foxp3) levels when compared to normal persons. Results indicated that Treg/Th17 functional imbalance existed in patients with idiopathic DCM, suggesting a potential role for Treg/Th17 imbalance in the development of idiopathic DCM.”

We can also see that this is a mechanism promoting adverse cardiovascular events when uric acid increases in the bloodstream, such as when people undergo dialysis, from a paper published not long ago in the journal Nephrology.

“Adverse cardiovascular events resulting from accelerated atherosclerosis are the leading cause of mortality in uraemic patients on maintenance haemodialysis (MHD). Chronic inflammation due to antigen-specific responses is an important factor in the acceleration of atherosclerosis...The aim of the present study was to assess the Treg/Th17 pattern in uraemic patients on MHD and to explore the significance of Treg/Th17 imbalance in the development and outcome of acute cardiovascular events.”

Their findings offer fascinating insight into the link between uric acid and cardiovascular inflammation:

“Patients with uraemia exhibited an obvious imbalance of Treg/Th17 function when compared to the normal control group, displaying increased peripheral Th17 frequency, Th17-related cytokines (interleukin [IL]-17, IL-6 and IL-23) and RORγt mRNA levels. These patients also displayed decreased Treg frequency, Treg-related cytokines (IL-10, transforming growth factor-β1) and Foxp3 mRNA levels…It was also observed that the imbalance of Treg/Th17 was not only consistent with the cardiovascular disease but also correlated with a microinflammatory state.”

Clinicians and patients should bear their concluding point in mind:

“This Th17/Treg imbalance might act synergistically with microinflammation on immune-mediated atherosclerosis and contribute to the high incidence of adverse cardiovascular events.”

Clinical & Experimental Immunology I would like to note the evidence that Th17/Treg imbalance also plays a role in autoimmune disease associated with organ transplantation since a case this year involving autoimmune attack on the nerves regulating the heartbeat followed by another autoimmune inflammatory reaction to the pacemaker (Dressler’s syndrome). The authors of a paper published in Clinical and Experimental Immunology state:

“…it can be proposed that skewing of responses towards Th17 or Th1 and away from Treg may be responsible for the development and/or progression of AD [autoimmune disease] or acute transplant rejection in humans. Blocking critical cytokines in vivo, notably IL-6, may result in a shift from a Th17 towards a regulatory phenotype and induce quiescence of AD or prevent transplant rejection…”

They sum up their extensive review by concluding:

“Interleukin 17 is a pleiotropic cytokine with multiple proinflammatory functions that is likely to be involved in either the causation or progression of inflammatory diseases and transplant rejection in humans. Regulatory T cells are an anti-inflammatory lineage of T cells… It is possible that acute flares of autoimmune diseases or acute episodes of transplant rejection may be explained by a change in the relative dominance of these pathways…”

What resources can we turn to for correcting Th17/Treg imbalances? A fascinating paper just published in the European Journal of Immunology explains how the proinflammatory cytokine IL-6 (Interleukin-6) is a regulator of Th17/Treg.

“IL-6 is a pleiotropic cytokine involved in the physiology of virtually every organ system. Recent studies have demonstrated that IL-6 has a very important role in regulating the balance between IL-17-producing Th17 cells and regulatory T cells (Treg). The two T-cell subsets play prominent roles in immune functions: Th17 cell is a key player in the pathogenesis of autoimmune diseases and protection against bacterial infections, while Treg functions to restrain excessive effector T-cell responses.”

The authors explain the pivotal role played by IL-6 in determining the relative balance of autoimmune inflammation-promoting Th17 versus the anti-inflammatory Treg cells:

“IL-6 induces the development of Th17 cells from naïve T cells together with TGF-β; in contrast, IL-6 inhibits TGF-β-induced Treg differentiation. Dysregulation or overproduction of IL-6 leads to autoimmune diseases such as multiple sclerosis (MS) and rheumatoid arthritis (RA), in which Th17 cells are considered to be the primary cause of pathology.”

Their conclusion offers a welcome insight in that we have evidence-based physiological interventions that act to regulate IL-6:

“Given the critical role of IL-6 in altering the balance between Treg and Th17 cells, controlling IL-6 activities is potentially an effective approach in the treatment of various autoimmune and inflammatory diseases.”

Further evidence for the pivotal role of IL-6 in regulating T17 and Treg balance is found in an interesting paper published in the journal Mucosal Immunology that points out the same process in inflammatory bowel disease:

“T helper (Th)17 cells have been shown to play a role in the pathogenesis of inflammatory and autoimmune diseases including inflammatory bowel diseases (IBD). It is now well established that although transforming growth factor (TGF)-beta alone induces FoxP3+ regulatory T (Treg) cells, TGF-beta and interleukin (IL)-6, acting in concert, induce differentiation of mouse naive T cells into Th17.”

Going a step further, they were able to discern that IL-6 can act alone in promoting the development of Th17 cells:

“We found that upon activation, Treg cells induce CD4+CD25- naive T cells or Treg cells themselves to differentiate into Th17 in the presence of IL-6 alone without exogenous addition of TGF-beta.”

Another clue to some of the therapies we can use is suggested by a study published in the Journal of Immunology on the ability of retinoic acid (RA), a metabolite of Vitamin A, to inhibit the expression of IL-6. The authors first observe:

“The de novo generation of Foxp3+ regulatory T (Treg) cells in the peripheral immune compartment and the differentiation of Th17 cells both require TGF-β, and IL-6 and IL-21 are switch factors that drive the development of Th17 cells at the expense of Treg cell generation.”

The authors elucidate the pathways by which Treg can be promoted and IL-6 inhibited by retinoic acid (RA):

“Herein we show that RA enhances TGF-β signaling…and this results in increased Foxp3 [Treg] expression even in the presence of IL-6 or IL-21. RA also inhibits the expression of IL-6R{alpha}…and thus inhibits Th17 development. In…experimental autoimmune encephalomyelitis…RA suppresses the disease very efficiently by inhibiting proinflammatory T cell responses, especially pathogenic Th17 responses.”

Their conclusion is well worth keeping in mind when we are researching a treatment plan for the autoimmune component of cardiovascular disease or any other autoimmune condition:

“These data not only identify the signaling mechanisms by which RA can affect both Treg cell and Th17 differentiation, but they also highlight that in vivo during an autoimmune reaction, RA suppresses autoimmunity mainly by inhibiting the generation of effector Th17 cells.”

Nervous system regulation of inflammation, cytokines, and heart rate variability

Posted on May 27, 2010 by Dr. Jonathan

As readers here know, inflammation is a fundamental factor in chronic disease and accelerated aging (neurodegeneration). A functional approach to treatment requires an objective understanding of how this system is working for each patient. Here are several of the many studies that illustrate how nervous system function and inflammation can be evaluated with heart rate variability (HRV) analysis and cytokine (‘messenger molecules’ of inflammation) levels.

Shock The practical focus is on restoring parasympathetic nervous system (PNS) activity which inhibits inflammation. (PNS resources decline with disease, stress and age resulting in a state of ‘sympathetic nervous system dominance’.) This paper just published in the journal Shock shows how autonomic nervous system activity (sympathetic and parasympathetic) as measured by HRV corresponds to inflammatory cytokine activity, in this case when stimulated by endotoxins (poisons produced by bacterial infections):

“Autonomic inputs from the sympathetic and parasympathetic nervous systems, as measured by heart rate variability (HRV), have been reported to correlate to the… responses to infectious challenge… In addition, parasympathetic/vagal activity has been shown experimentally to exert anti-inflammatory effects via attenuation of splanchnic tissue TNF-α [cytokine] production. We sought… to determine if baseline HRV parameters correlated with endotoxin-mediated circulating cytokine responses.”

They documented a strong correspondence regardless of gender, body mass index and resting heart rate:

“…we found a significant correlation of several baseline HRV parameters…on TNF-α release after endotoxin exposure.”

This is not a new observation. An interesting study published a few years ago in the journal Psychosomatic Medicine documents the HRV expression of autonomic activity in response to an inflammatory challenge and its correspondence to cytokine production. They begin by noting that:

“…the autonomic nervous system plays a key role in regulating the magnitude of immune responses to inflammatory stimuli. Signaling by the parasympathetic system inhibits the production of proinflammatory cytokines by activated monocytes/macrophages and thus decreases local and systemic inflammation.”

They examined the relationship of HRV to lipopolysaccharide-induced production of the inflammatory cytokines interleukin (IL)-1ß, IL-6, tumor necrosis factor (TNF)-{alpha}, and IL-10. What did the data show?

“Consistent with animal findings, higher derived estimates of vagal activity measured during paced respiration* were associated with lower production of the proinflammatory cytokines TNF-{alpha} and IL-6…These associations persisted after controlling for demographic and health characteristics, including age, gender, race, years of education, smoking, hypertension, and white blood cell count.”

Their conclusion has profound implications for the biological mechanism by which stress causes inflammation:

“These data provide initial human evidence that vagal activity is inversely related to inflammatory competence, raising the possibility that vagal regulation of immune reactivity may represent a pathway linking psychosocial factors to risk for inflammatory disease.”

How might this show up in heart disease? This paper published not long ago in the journal Brain, Behavior, and Immunity investigates the links between HRV, inflammatory cytokines, coronary heart disease and depression:

“Studies show negative correlations between heart rate variability (HRV) and inflammatory markers [less variability = more inflammation]…We investigated links between short-term HRV and inflammatory markers in relation to depression in acute coronary syndrome (ACS) patients.”

They measured C-reactive protein (CRP), interleukin-6 (IL-6, a cytokine), depression symptoms and heart rate variability determinants of autonomic function. What did their data show?

“…all HRV measures were negatively and significantly associated with both inflammatory markers…HRV independently accounted for at least 4% of the variance in CRP in the depressed, more than any factor except BMI.”

Interestingly, they also noted that:

“Relationships between measures of inflammation and autonomic function are stronger among depressed than non-depressed cardiac patients. Interventions targeting regulation of both autonomic control and inflammation may be of particular importance.”

The research of another group published in the Journal of Critical Care used sepsis as their model.

“The aim of the study was to investigate possible associations between different heart rate variability (HRV) indices and various biomarkers of inflammation in 45 septic patients.”

They examined the correlation between HRV, C-reactive protein, and the cytokines interleukin 6 and interleukin 10:

“Our data suggest that low HRV and sympathovagal balance during septic shock are associated with both an increased hyperinflammatory and antiinflammatory response.”

The antiinflammatory response corresponds to high HRV and interleukin-10, the cytokine that is also increased by vitamin D.

Journal of Internal Medicine How can we reduce inflammation by increasing HRV and reducing inflammatory cytokines? There are numerous methods; one is to increase cholinergic activity in the nervous system (parasympathetic activity mediated by the neurotransmitter acetylcholine). We can increase this with natural precursor support for acetylcholine. This study published recently in the Journal of Internal Medicine shows the connection between vagal parasympathetic function (as shown by HRV), inflammatory cytokines, cholinergic activity and rheumatoid arthritis:

“The central nervous system regulates innate immunity in part via the cholinergic anti-inflammatory pathway, a neural circuit that transmits signals in the vagus nerve that suppress pro-inflammatory cytokine production…Vagus nerve activity is significantly suppressed in patients with autoimmune diseases, including rheumatoid arthritis (RA). It has been suggested that stimulating the cholinergic anti-inflammatory pathway may be beneficial to patients…”

They found that increasing cholinergic signaling in stimulated whole blood cultures suppressed cytokine production in rheumatoid arthritis patients whose vagal activity was deficient:

“These findings suggest that it is possible to pharmacologically target the α7nAChR dependent control of cytokine release in RA patients with suppressed vagus nerve activity.”

In a functional medicine practice, of course, we use natural acetylcholine precursors.

This is a drop in the bucket, but here’s one more fascinating paper published recently in the journal Brain, Behavior, and Immunity that shows how acetylcholine activity in the brain (the upper level of autonomic regulation) controls systemic cytokine levels through vagal function:

“The excessive release of cytokines by the immune system contributes importantly to the pathogenesis of inflammatory diseases. Recent advances in understanding the biology of cytokine toxicity led to the discovery of the “cholinergic anti-inflammatory pathway,” defined as neural signals transmitted via the vagus nerve that inhibit cytokine release…Vagus nerve regulation of peripheral functions is controlled by brain nuclei and neural networks…Here we report that brain acetylcholinesterase activity controls systemic and organ specific TNF [cytokine] production during endotoxemia.”

They demonstrated that inhibiting the breakdown of acetylcholine† markedly reduced proinflammatory serum TNF levels through the resulting increasing vagus nerve signaling which prevented inflammatory damage. What do they conclude from their research?

“These findings show that inhibition of brain acetylcholinesterase [that breaks down acetylcholine] suppresses systemic inflammation through a central…mediated and vagal…dependent mechanism. Our data also indicate that a clinically used centrally-acting acetylcholinesterase inhibitor† can be utilized to suppress abnormal inflammation to therapeutic advantage.”

* There are numerous therapies to reduce inflammation by increasing parasympathetic function. Breathing is a powerful stimulus to the autonomic nervous system. We train breathing with biofeedback while simultaneously monitoring for CO2 (capnography) and coherence in HRV to hit the physiological “sweet spot”.

† Agents that inhibit the breakdown of neurotransmitters including reuptake inhibitors do not restore the body’s ability to make its own. Precursor therapy provides the natural ingredients that have been depleted or are insufficient to meet genetic needs so neurotransmitters can be increased naturally.

How important is Vitamin D for autoimmune disease?

Posted on March 9, 2010 by Dr. Jonathan

It’s hard to overemphasize the importance. Consider this paper published in Nature Reviews Rheumatology in which the authors assert that the…

“…immunoregulatory and anti-inflammatory properties” of vitamin D can be used for the “control of autoimmune diseases.”

They note that…

“…Epidemiological evidence indicates a significant association between vitamin D deficiency and an increased incidence of several autoimmune diseases,”

Which include…

“a variety…from rheumatoid arthritis to systemic lupus erythematosus, and possibly also multiple sclerosis, type 1 diabetes, inflammatory bowel diseases, and autoimmune prostatitis.”

(Extra highlight for autoimmune prostatitis because very few are aware how common this is.) Of great practical importance is their observation that…

“The net effect of the vitamin D system on the immune response is an enhancement of innate immunity coupled with multifaceted regulation of adaptive immunity.”

We are awash in studies on vitamin D, here’s one more for good measure. This paper, recently published in the journal Psychoneuroendocrinology, focuses on its use in the treatment of autoimmune disease that attacks the brain and nervous system. The authors begin by noting that…

“It has been known for more than 20 years that vitamin D exerts marked effects on immune and neural cells…it has been shown that diminished levels of vitamin D…is a risk factor for various brain diseases.”

They further state that…

“…vitamin D has been found to be a strong candidate risk-modifying factor for Multiple Sclerosis (MS)…”

And proceed to..

“…assess how vitamin D imbalance may lay the foundation for a range of adult disorders, including brain pathologies (Parkinson’s disease, epilepsy, depression) and immune-mediated disorders (rheumatoid arthritis, type I diabetes mellitus, systemic lupus erythematosus or inflammatory bowel diseases).”

These are some of the reasons why I always screen for vitamin D sufficiency.

Resistance exercise necessary for weight management and metabolic control

Posted on January 23, 2010 by Dr. Jonathan

Diabetes Care Aerobic exercise, especially if performed in an interval fashion (see earlier posts) is very good, but don’t leave out the high-intensity resistance (“strength”) training for improving body composition which, of course, depends on metabolic control. This timely paper recently published in the journal Diabetes Care confirms that high-intensity resistance exercise does something that other forms of exercise don’t. Adiponectin is hormone critical for burning rather than storing fat; higher levels are better. The investigators found that “Adiponectin concentration increased after 12 h and remained elevated for 24 h only in the high-intensity group.” They go on to conclude: “Resistance exercise does increase REE and adiponectin in an intensity-dependent manner for as long as 48 and 24 h, respectively, in overweight elderly individuals. It appears that resistance exercise may represent an effective approach for weight management and metabolic control…” [REE = resting energy expenditure]

By the way, if you are suffering from rheumatoid arthritis or another inflammatory disorder is it safe and effective for you to do high-intensity resistance training? According to this study published in the journal Arthritis Care & Research, the answer is yes. The investigators set out “To confirm, in a randomized controlled trial (RCT), the efficacy of high-intensity progressive resistance training (PRT) in restoring muscle mass and function in patients with rheumatoid arthritis (RA).” Their conclusion: “In an RCT, 24 weeks of PRT proved safe and effective in restoring lean mass and function in patients with RA…PRT should feature in disease management.”

Adverse events are common with steroids

Posted on December 6, 2009 by Dr. Jonathan

This meta-analysis of data retrieved from 28 studies comprising 2382 patients was just published in the journal Annals of the Rheumatic Diseases. The important thing to note is that “High rates of adverse events were reported in high-qualitystudies with short follow-up” for low to medium doses. (All patients received prednisilone.) Rates of adverse events were especially high with inflammatory bowel disease, but significant also for the rheumatic diseases included in the study. This highlights one of the advantages of the functional medicine approach that minimizes dependence on steroids by addressing the underlying immune system dysfunction.

Family history of autoimmune disease and autism linked

Posted on November 12, 2009 by Dr. Jonathan

This interesting study evaluated data from 689,196 children from 1993 to 2004. The investigators observed: “Increased riskof ASDs was observed for children with a maternal history ofrheumatoid arthritis and celiac disease. Also, increased riskof infantile autism was observed for children with a familyhistory of type 1 diabetes.” [ASD = autistic spectrum disorders] This will not surprise Lapis Light patients who are aware of the vulnerability of the brain to autoimmune driven inflammation.