“Learning and memory are fundamental brain functions affected by dietary and environmental factors.” The authors “show that increasing brain magnesium…leads to the enhancement of learning abilities, working memory, and short- and long-term memory…”

Facilitation (the pathways become more efficient) and long-term potentiation (the synapses become more efficient) are the means by which learning and memory are ’sculpted’ in the brain. The authors go on to conclude:

“Our findings suggest that an increase in brain magnesium enhances both short-term synaptic facilitation and long-term potentiation and improves learning and memory functions.”

Though they used a novel form, it’s the magnesium in the brain, not the form, that does the job. This is another item added to the long list of reasons to keep your magnesium up. The next time you suffer a leg or foot cramp remember—this may be affecting your brain too.

Consider this study that was published in the journal GUT, An International Journal of Gastroenterology and Hepatology. The authors investigated how nitric oxide is part of the intestinal inflammatory reaction reaction to gluten, and how it relates to the white blood cell response. They noted this in their conclusion:

“Mucosal activation of neutrophils and eosinophils [white blood cells] precedes pronounced enhancement of mucosal NO [nitric oxide] production after rectal wheat gluten challenge in patients with coeliac disease. Some of our coeliac patients displayed signs of an inflammatory reaction, as measured by NO and granulocyte markers, after rectal corn gluten challenge.”

So it depends on the individual. The more serious your condition the more important it is to check yourself for corn sensitivity with the immunological ‘gold standard’—a properly managed elimination-provocation protocol.

We are also bereft of a perfectly decisive indication  for oats because rare individuals can react, though this study published in the Scandinavian Journal of Gastroenterology indicates that most celiac patients can tolerate them. First the authors note that…

“We have…identified three adult coeliac disease patients who developed a flare of active coeliac disease after ingestion of oats, which suggests that oats might not be entirely innocent in coeliac disease.”

They set out to compare the immune response to oats and wheat by comparing production of the main intestinal antibody (IgA) that participates in the reaction. Although other immune activity was observed,…

“No significant differences were found in IgA against oats in oats-eating and non-oats-eating coeliac disease patients.”

Their conclusion:

“Ingestion of oats does not cause increased levels of IgA against oats in adult coeliac disease patients on a gluten-free diet. The findings support the notion that most adult coeliac disease patients can tolerate oats.”

Note the “most”. And even if you are not sensitive to oats, it is important to be sure that they are certified gluten-free. Otherwise they can be contaminated with gluten during storage, transport, processing and packaging.

What about blood tests for food allergies? Too many variables influence antibody tests for them to give a reliable indication. If you have a serious condition with an autoimmune basis, it’s best to consult with a functional medicine practitioner who can  help you through an elimination-provocation protocol (eliminating and re-introducing foods), and who knows how to use objective lab tests to profile your immune imbalance.

“the influence of coffee and caffeine consumption on atrial fibrillation (AF) in hypertensive patients…with regard to spontaneous conversion of arrhythmia.”

Spontaneous conversion is when the heart rhythm normalizes on its own. Along the way they made some interesting observations:

“Coffee consumption was higher in normotensive (normal blood pressure) patients. High coffee consumers were more frequent in normotensive patients compared with hypertensive patients. On the other hand, the intake of caffeine was similar in hypertensive and normotensive patients, owing to a higher intake in hypertensive patients from sources other than coffee. Within normotensive patients, we report that non-habitual and low coffee consumers showed the highest probability of spontaneous conversion, whereas, within hypertensive patients, moderate but not high coffee consumers had the lowest probability of spontaneous conversion.”

Interestingly, their data show that if you have high blood pressure, more coffee is better for normalizing atrial fibrillation. Their conclusion:

“Coffee and caffeine consumption influence spontaneous conversion of atrial fibrillation. Normotensive non-habitual coffee consumers are more likely to convert arrhythmia within 48h from the onset of symptoms. Hypertensive patients showed a U-shaped relationship between coffee consumption and spontaneous conversion of AF, moderate coffee consumers were less likely to show spontaneous conversion of arrhythmia.”

“…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.

“Gluten sensitivity typically presents as celiac disease, a chronic, autoimmune-mediated, small-intestinal disorder. Neurological disorders occur with a frequency of up to 10% in these patients. However, neurological dysfunction can also be the sole presenting feature of gluten sensitivity.”

Antibodies directed toward transglutaminase in the gut are a well-known diagnostic feature of celiac disease. These investigators have identified another member of the transglutaminase family:

“…a novel neuronal transglutaminase isozyme and investigated whether this enzyme is the target of the immune response in patients with neurological dysfunction.” They found that “Whereas the development of anti-transglutaminase 2 IgA is linked with gastrointestinal disease, an anti-transglutaminase 6 IgG and IgA response is prevalent in gluten ataxia, independent of intestinal involvement.”

(Ataxia is loss of the ability to coordinate muscle movement, especially as it appears with difficulty walking.) Their conclusion:

“Antibodies against transglutaminase 6 can serve as a marker…to identify a subgroup of patients with gluten sensitivity who may be at risk for development of neurological disease.“

If you are gluten sensitive, you can have neurological disease without celiac involvement.

“Higher RDW values were strongly associated with an increased risk of death…Even when analyses were restricted to nonanemic participants or to those in the reference range of RDW (11%-15%) without iron, folate, or vitamin B12 deficiency, RDW remained strongly associated with mortality. The prognostic effect of RDW was observed in both middle-aged and older adults for multiple causes of death.”

Two weeks later the another paper was published in the same journal on the same topic that begins with this observation:

“Red blood cell distribution width (RDW), an automated measure of red blood cell size heterogeneity (eg, anisocytosis) that is largely overlooked, is a newly recognized risk marker in patients with established cardiovascular disease (CVD).”

They set out to investigate

“the association of RDW with all-cause mortality and with CVD, cancer, and chronic lower respiratory tract disease mortality in 15,852 adult participants.”

Their conclusion:

“Higher RDW is associated with increased mortality risk in this large, community-based sample, an association not specific to CVD.”

Another paper just published in The Journals of Gerontology confirms these findings with an analysis of seven community-based studies of older adults. Their conclusion:

“RDW is a routinely reported test that is a powerful predictor of mortality in community-dwelling older adults with and without age-associated diseases.”

This paper just published in the journal Diabetes Care reports on the link between RDW, metabolic syndrome and cardiovascular disease: “A possible explanation for the observed association between RDW and MetS is that high RDW reflects an underlying inflammatory state that leads to impaired erythrocyte (red blood cell) maturation and anisocytosis (size variation), as suggested previously (1–3). In fact, MetS exacerbates oxidative and inflammatory stress in obese adults, which is a potential mechanism for the increased cardiovascular risk in this condition.”

And as you would expect, the European Journal of Heart Failure recently published a study on heart failure that compares RDW with N-terminal brain natriuretic peptide (NT-proBNP) in which the authors conclude:

“Red cell distribution width is a readily available test in the HF-population with similar independent prognostic power to NT-proBNP across the first to third quartiles. Prognostic models in HF (heart failure) should include RDW.”

And the ‘plot thickens’. In this paper published in the journal Digestive Diseases and Sciences the investigators observe:

“Impaired iron absorption or increased loss of iron was found to correlate with disease activity and markers of inflammation in inflammatory bowel disease (IBD). Red cell distribution width (RDW) could be a reliable index of anisocytosis with the highest sensitivity to iron deficiency.”

Their compelling conclusion:

“Among the laboratory tests investigated, including fibrinogen, CRP, ESR, and platelet counts…analysis indicated RDW to be the most significant indicator of active UC [ulcerative colitis]. For CD [Crohn's disease], CRP was an important marker of active disease.”

Lastly, you’ll appreciate the broadest statement yet about the value of this inexpensive and readily available marker. In a recent paper published in the Archives of Pathology & Laboratory Medicine. The authors begin by chiming in with the neighborhood chorus:

“A strong independent association has been recently observed between elevated red blood cell distribution width (RDW) and increased incidence of cardiovascular events;”

but they aim to

“assess whether RDW is associated with plasma markers of inflammation.”

Their conclusion:

“To our knowledge, our study demonstrates for the first time a strong, graded association of RDW with hsCRP and ESR independent of numerous confounding factors.”

In other words, RDW is inexpensive, easily obtained, and a powerful marker for inflammation in general, the common denominator of most chronic disease.

Here’s the ‘take home’ message (if you’ve gotten this far): If you have almost any blood work done at all it’s likely to include RDW automatically. Make good use of it, keeping in mind that laboratory reference ranges do not reflect the latest research and your doctor may not be aware of this. Functional medicine doctors want RDW to be no more than 13%.

“…account for only a small fraction of cases, and do not easily explain key clinical and epidemiological features.” He further states that “Indirect evidence for an environmental contribution to autism comes from studies demonstrating the sensitivity of the developing brain to external exposures such as lead, ethyl alcohol and methyl mercury. But the most powerful proof-of-concept evidence derives from studies specifically linking autism to exposures in early pregnancy – thalidomide, misoprostol, and valproic acid; maternal rubella infection; and the organophosphate insecticide, chlorpyrifos.”

The author concludes by summarizing:

“Children today are surrounded by thousands of synthetic chemicals. Two hundred of them are neurotoxic in adult humans, and 1000 more in laboratory models. Yet fewer than 20% of high-volume chemicals have been tested for neurodevelopmental toxicity. I propose a targeted discovery strategy focused on suspect chemicals, which combines expanded toxicological screening, neurobiological research and prospective epidemiological studies.”

Many of you reading this may already know that I am using laboratory tools to objectively assess for toxic exposure and metabolism, along with evidence-based physiological interventions that protect and support the capacity of the body to break down and eliminate these ubiquitous poisons.

“…on immediate word recall and delayed word recall, both groups of MDMA users recalled significantly less words than controls. Animal research has shown that MDMA can lead to serotonergic neurodegeneration, particularly in the hippocampus and frontal cortex…these data are consistent with other findings of memory decrements in recreational MDMA users, possibly caused by serotonergic neurotoxicity.”

“the relationship between habitual sleep disturbances and the incidence of type 2 diabetes.”

The authors analyzed 10 studies that included 107,756 male and female participants. Their clear-cut conclusion:

“Quantity and quality of sleep consistently and significantly predict the risk of the development of type 2 diabetes. The mechanisms underlying this relation may differ between short and long sleepers.”

The mechanisms include hormone dysregulation, low-grade chronic inflammation, and gastroesophageal reflux disease (GERD; see earlier post on how medication can worsen this association). For help with sleep disorders there are sound functional medicine resources that address the biological component, cognitive behavioral methods (see recent post about internet-based CBT for insomnia), and neurotherapies including neurofeedback and brain wave entrainment tools.

Here we have a study just published in the European Journal of Pharmacology showing the effect of resveratrol in a model of ulcerative colitis, “a nonspecific inflammatory disorder characterized by oxidative and nitrosative stress, leucocyte infiltration and upregulation of inflammatory mediators.” The authors note that “Resveratrol is a polyphenolic compound found in grapes and wine, with multiple pharmacological actions, mainly anti-inflammatory, antioxidant, antitumour and immunomodulatory activities.” They documented the positive effect of resveratrol on a number inflammatory signalling pathways, and observed that the “resveratrol group significantly attenuated the clinical signs such as loss of body weight, diarrhea and rectal bleeding improving results from disease activity index and inflammatory score.” Their conclusion: The “resveratrol diet represents a novel approach to the treatment of chronic intestinal inflammation.”

Here is a paper published in the Journal of Agriculture and Food Chemistry that describes a beneficial effect not only on inflammation and tissue damage with colitis but also on the gut flora from even very small doses of resveratrol. In addition to that, they observed “Resveratrol significantly protected the colonic mucosa architecture, reduced body weight loss, diminished the induced anemia and reduced systemic inflammation markers, colonic mucosa prostaglandin E2, cycloxygenase-2, prostaglandin E synthase and nitric oxide levels.” Their conclusion: “These results reinforce the concept of resveratrol as a dietary beneficial compound in intestinal inflammation at doses possibly attainable with resveratrol-enriched nutraceuticals.”

One more paper, published in the Journal of Investigative Surgery, documents the beneficial effect of resveratrol on healing after colon surgery. The authors defined their task: “Since anastomotic [connecting two severed tubular parts] healing possesses paramount importance to prevent complications in colorectal surgery, the present study is aimed to evaluate the effect of RSV on the healing of experimental left colonic anastomoses.” Their findings and disclosure: “Histopathological analysis revealed that RSV (resveratrol) administration leads to a better anastomotic healing…Although the precise cellular mechanisms by which RSV enhances anastomotic wound healing is not clear, stimulation of neovascularization (new blood vessels), generation of collagen synthesis, inhibition of overinflammation, and restriction of oxidative injury seems to be of paramount importance.”