From Biotics

Vitamin D for Alzheimer’s and Dementia?

Researchers from UC Davis Alzheimer’s Disease Center and Rutgers University wished to assess associations between Vitamin D (VitD) status and trajectories of change in subdomains of cognitive function. They conducted a cohort study of 382 ethnically diverse, older participants in an outpatient clinic (Feb. 2002-Aug. 2010) with baseline assessment and yearly follow-up visits. Serum 25-OHD levels were measured and categorized as deficient (< 12mg/mL), adequate (20 -49 ng/mL) or high (50 ng/mL or higher). Note: to convert to nanomoles per liter, multiply by 2.496. Subdomains of cognitive function were assessed using the Neuropsychological Assessment Scales. Associations were evaluated between 25-OHD levels (as continuous and categorical [deficient, insufficient or adequate]) and trajectories of cognitive decline. Low VitD status was associated with accelerated decline in cognitive function. According to Joshua Miller, professor in the Dept. of Pathology and Laboratory Medicine at the time the research was conducted (currently professor & chair of the Dept. of Nutritional Sciences at Rutgers University), VitD insufficiency was associated with significantly faster declines in both episodic memory and executive function performance. The researchers found that with over five years of follow-up, VitD deficient individuals experienced cognitive declines that were 2 to 3 times faster than those with adequate VitD levels.

JW Miller, et al. Vitamin D Status and Rates of Cognitive Decline in a Multiethnic Cohort of Older Adults. JAMA Neurology Publishes online Sept 142015 doi:10.1001/jama-neurol.2015.2115
Neuroscience News Sept 14, 2015

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Severe MTHFR deficiency treatment with TMG!

Researchers investigated the effect of trimethylglycine (TMG-also known as betaine) treatment on development and survival in patients with severe methylenetetrahydrofolate reductase (MTHFR) deficiency. Deficiency of (5,10)-MTHFR is a frequent remethylation disorder, and clinical consequences vary greatly depending on the degree of enzyme deficiency. Carriers of the prevalent mild thermolabile variant are at risk for moderate hyperhomocysteinemia, but do not have neurological symptoms. On the other hand, severe MTHFR is rare, and presentation is in infancy or early childhood. The inability to remethylate homocysteine to methionine induces profoundly elevated homocysteine and decreased methionine concentrations in blood. Untreated patients either die or, if they survive, exhibit severe developmental delay and a life-long dependence on care. Researchers identified 15 case reports and case series totaling 36 patients with severe MTHFR deficiency, and compared the outcomes in treated vs. untreated patients, and early vs. late-treated patients. The main outcons and measures was survival and psychomotor development. Results showed that 11 of 36 patients died (31%), all of which occurring in patients who did not receive treatment or in whom treatment was delayed. In contrast, all 5 early-treated patients survived. Additionally, psychomotor development in surviving patients receiving treatment was normal in all 5 early-treated patients, but in none of the surviving patients with delayed treatment. Researchers concluded that early treatment prevents mortality and allows normal psychomotor development in patients with severe MTHFR deficiency, highlighting the importance of timely recognition through newborn screening.

EF Diekman, et al. Survival and Psychomotor Development with Early Betaine Treatment in Patients with Severe Methylenetetrahydrofolate Reductase Deficiency. JAMA Neurol. Feb 2014, Vol 71, No. 2

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Vitamin A Directs Immune Cells to the Intestines!

We know that vitamin A deficiencies lead to increased susceptibility to disease and low concentrations of immune cells in the mucosal barrier lining the intestines. Researchers from Purdue University found that the vitamin A metabolite retinoic acid (RA), is necessary for two of the three types of innate immune cells residing in the intestine (ILC1 and ILC3) to find their proper place. Innate lymphoid cells (ILCs), which are present in barrier tissues, gather in the lymph nodes where RA activates specific receptors upon two of the three subsets, acting as homing devices for the intestines. These immune cells then travel through the circulatory system, the receptor grab onto and bind to molecules in the intestines and keep the cells in place. They need to be concentrated in mucosal barrier tissues, because they are the point of entry from many infections from bacteria, viruses and parasites. These innate immune cells reside under the epithelial cell barrier that lines the intestine in a healthy system. When a pathogen penetrates the epithelial barrier, innate immune cells respond, attacking the pathogen to keep it from penetrating farther into the tissue or reaching the bloodstream. Researchers concluded that distinct programs regulate the migration of ILC subsets to the intestine for regulation of innate immunity. Interestingly, Vitamin D has been shown to work in a similar way to guide immune cells to the skin.

MH Kin, EJ Taparowsky, CH Kim. Retinoic acid differentially regulates the migration of innate lymphoid cell subsets to the gut. Immunity Vol 43, Issue 1, p107-119, 21 July 2015
Purdue study finds vitamin A directs immune cells to the intestines. July 9, 2015. http://www.purdue.edu

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Vitamin D for Reduced Breast Density in Premenopausal Women!

High breast density has been identified as a strong risk factor for breast cancer. Researchers tested the association between vitamin D intake, but not circulating vitamin D levels, and mammographic breast density among women. They conducted a cross-sectional study of 165 screening mammography patients at Nashville General Hospital’s Breast Health Center. Dietary and total (dietary plus supplementation) vitamin D, and calcium intakes were estimated by the AFFQ and blood samples were analyzed for 25(OH)D3. Average percent breast density for the left and right beast combined was estimated from digitized films. After statistical adjustment for age, race and body mass index, the result revealed there were significant trends of decreasing breast density with increasing vitamin D and calcium intake among premenopausal (but not postmenopausal) women.

AM Fair, et al. Increased vitamin D and calcium intake associated with reduced mammographic breast density among premenopausal women. Nutrition Research. Published online July 31, 2015

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Melatonin for GERD?

Melatonin is a hormone produce by the pineal gland and enterochromaffin cells which control sleep and gastrointestinal motility. Low melatonin levels lead to gastroesophageal reflux disease (GERD). Most patients with GERD have a sleep disorder, and low melatonin levels are a main cause of insomnia. It has an inhibitory action on gastric acid secretion and seems to control the lower esophageal sphincter.(1) Additionally, melatonin has been found to protect the gastrointestinal mucosa from oxidative damage caused by reactive oxygen species in different experimental ulcer models, where is has been shown to prevent acute ethanol-induced gastric injury from ethanol-induced via its antioxidant activity.(2) Another clinical study showed oral melatonin has a role in the prevention of GERD, and is effective in relieving epigastric pain and heartburn.(3)

1) J Dulce, et al. Which is the best choice for gastroesophageal disorders: Melatonin or proton pump inhibitors. World J Gastrointest Pharmcol Ther. 2010 Oct 6, 1(5): 102-106
2) D.Bilici, et al. Melatonin Prevents Ethanol-Induced Gastric Mucosal Damage Possibly Due to Its Antioxidant Effect. Digestive Diseases and Sciences. Apr 2002, Vol. 47, Issue 4. Pp 856-861.
3) TS Kandil, et al. The potential therapeutic effect of melatonin in Gastro-Esophageal Reflux Disease. BMC Gastroenterol. 2010 Jan 18;10:7. doi: 10.1186/1471-230X-10-7.

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Vitamin D for gut microbiome and GI function?

Vitamin D is known for its effects on bone mineralization, inflammatory processes and immunomodulatory properties, which positively influences human health, but in-vivo data on its effects on human gut microbiome are missing. Researchers conducted an open-label, interventional pilot study to investigate the effects of oral vitamin D3 on the human mucosa-associated and stool microbiome as well as CD8+ T cells in healthy volunteers. Sixteen participants were endoscopically examined to access a total of 7 sites, and researchers sampled stomach, small bowel, colon, and stools before and after 8 weeks of vitamin D3 supplementation. Weeks 1-4 participants took a weekly dose representing 140 IU/Kg body weight per day up to a max of 68,600 IU/week (9,800 IU/day). The following 4 weeks they took half the amount (70 IU/Kg body weight per day up to 34,300 IU/week (4,900 IU/day). Supplementation changed the gut microbiome in the upper GI tract (gastric corpus, antrum and duodenum). Researchers found a decreased relative abundance of Gammaproteobacteria including Pseudomonas spp., Escherichia/Shigella spp. and increased bacterial richness. No major changes occurred in the terminal ileum, appendiceal orifice, ascending colon, and sigmoid colon or in stool, but the CD8+ T cell fraction was significantly increased in the terminal ileum. They concluded that vitamin D3 modulates the gut microbiome of the upper GI tract which might explain its positive influence on GI diseases such as inflammatory bowel disease or bacterial infections. Local effects demonstrate pronounce regional differences in the response of the GI microbiome to external factors.

M Bashir, et al. Effects of high doses of vitamin D3 on mucosa-associated gut microbiome vary between regions of the human gastrointestinal tract. Eur J Nutr. 2015 Jul 1. [Epub ahead of print]

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Consume More Potassium to Reduce Blood Pressure?

In order to evaluate the efficacy of daily potassium intake on decreasing blood pressure in non-medicated normotensive or hypertensive patients, researchers conducted a meta-analysis of 15 randomized controlled trials. A total of 917 patients without antihypertensive medication were seleIn order to evaluate the efficacy of daily potassium intake on decreasing blood pressure in non-medicated normotensive or hypertensive patients, researchers conducted a meta-analysis of 15 randomized controlled trials. A total of 917 patients without antihypertensive medication were selected for the meta-analysis. Potassium supplementation resulted in the reduction of systolic blood pressure (SBP) and diastolic blood pressure (DBP) across the board, though the effect was found to be greater in hypertensive patients. Meta-regression analysis showed that both increased daily potassium excretion and decreased sodium-to-potassium ratio were associated with blood pressure reduction. Researchers concluded that potassium supplementation is associated with reduction of blood pressure in patients who are not on antihypertensive medication, and the effect is significant in hypertensive patients.cted for the meta-analysis. Potassium supplementation resulted in the reduction of systolic blood pressure (SBP) and diastolic blood pressure (DBP) across the board, though the effect was found to be greater in hypertensive patients. Meta-regression analysis showed that both increased daily potassium excretion and decreased sodium-to-potassium ratio were associated with blood pressure reduction. Researchers concluded that potassium supplementation is associated with reduction of blood pressure in patients who are not on antihypertensive medication, and the effect is significant in hypertensive patients.

Binia A, Jaeger J, Ju Y, Singh A, Zimmermann D. Daily potassium intake and sodium-to-potassium ratio in the reduction of blood pressure: a meta-analysis of randomized controlled trials. J Hypertens. 2015 Aug;33(8): 1509-20. doi: 10.1097/HJH.0000000000000611.

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Resveratrol for Hepatic Metaflammation and NLRP3 activation!

It is known that resveratrol regulates NAD bioavailability and sirtuin-related metabolism which relates to aging, metabolic syndrome and non-alcoholic liver disease. Recent studies have demonstrated that resveratrol inhibits NLRP3 inflammasome activation and ameliorates hepatic metaflammation. Aberrant activation of the NLRP3 inflammasome often causes inflammatory diseases including gout. Resveratrol has been shown to inhibit the accumulation of acetylated α-tubulin-mediated spatial arrangement of mitochondria and their subsequent contact with the endoplasmic reticulum (ER). In a rodent model of progressive IgA nephropathy, resveratrol mitigated glomerular proliferation, glomerular sclerosis, and glomerular inflammation. These findings were associated with decreased renal mononuclear leukocyte infiltration, reduced superoxide anion levels, and inhibited renal NLRP3 inflammasome activation. In another rodent study, researchers investigated the effects of resveratrol on hepatic metaflammation in a model of high-fat (HF) diet-induced obesity. The HF diet resulted in aggravated hepatic inflammation, impaired glucose control, and increased serum and liver TG levels. Administration of resveratrol significantly improved glucose control, serum and liver TC contents, and reduced the levels of the pro-inflammatory markers. These improvements were accompanied by alterations in sirtuin pathway and NLRP3 inflammasome activation.

T Misawa, et al. Resveratrol inhibits the acetylated α-tubulin-mediated assembly of the NLRP3-inflammasome. Int Immunol. 2015 Apr 7 online.
YP Chang, et al. Resveratrol inhibits NLRP3 inflammasome activation by preserving mitochondrial integrity and augmenting autophagy. J Cell Physiol. 2015 Jul;230(7): 1567-79. Doi: 10.1002/jcp.24903.
SJ Yang, Y Lim. Resveratrol ameliorates hepatic metaflammation and inhibits NLRP3 inflammasome activation. Metabolism Clinical and Experimental 2014 May Vol. 63. Issue 5, pg 693-701.

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Green Tea Catechin (EGCG) for Cognition?

It is know that stress induces reactive oxygen species (ROS) and causes alterations in brain cytoarchitecture and cognition. The green tea catechin epigallocatechin-3-gallate (EGCG) possesses significant antioxidative properties able to protect against oxidative damage. Using a rodent model, investigators studied the impact of stress on locomotor activity, learning and memory. Results indicated that locomotor activity was decreased, and learning and memory were impaired in stressed rats (SRs). EGCG treatment was able to prevent decreased locomotor activity, and improve learning and memory in SRs. EGCG treatment was also able to reduce the increased oxidative status in SRs hippocampi. Results suggest a positive therapeutic effect of EGCG in treating stress-induced impairment of learning and memory.

Soung HS, et al. (-)Epigallocatechin-3-gallate decreases the stress-induced impairment of learning and memory in rats. Neurosci Lett. 2015 Jun 27. Pii: S0304-3940(15)00478-4. doi: 10.1016/j.neulet.2015.06.035. [Epub ahead of print]

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Chondroitin Sulfates for Osteoarthritis; the research says yes!

A group from the Cochrane Library set out to evaluate the benefit and harm of oral chondroitin for treating osteoarthritis compared with placebo, or a comparator oral medication including, but not limited to NSAIDs, analgesics, opioids, and glucosamine or other “herbal” medications. They conducted an intervention review of forty-three randomized controlled trials including 4,962 participants treated with chondroitin and 4,148 participants given placebo or another control. The majority of trials were for knee osteoarthritis (OA). Trial durations varied from 1 month to 3 years. Not only was the use of oral chondroitin safe, it had a lower risk of serious adverse events than controls. Those with OA who took chondroitin had less pain based on standard WOMAC measurements, scored better on Lequesne’s Index (a combination index of pain and physical function, indicating quality of life), and had less reduction in minimum joint space width than those who took placebo.

JA Singh, S Noorbalooch, R MacDonald, LJ Maxwell. Chondroitin for osteoarthritis. The Cochrane Library Published online: 28 Jan 2015

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