Volume 17 • Number 7 • July 2016

My home state of Utah is wrestling with THC and CBD oil issues. Many here wish to legalize their medical use because there is ample evidence that they can help with some neurologic problems such as seizures. Utah is quite conservative as you know, so for the reddest state in the Union to debate this issue signals that Americans have reached a tipping point on their views concerning drugs AND pharmaceuticals.

In my opinion hidden economic and political agendas are at play, but, I won’t torment you with what I have found reading widely, which I advise you to do yourself. You would not nor should you believe what I have to say about this problem. However, I have included articles in this newsletter that validate the use of non pharmaceutical interventions that help with a variety of neurological problems.

Hugo Rodier, MD

BRAIN UPDATE

Psilocybin may be safe, effective for treatment-resistant severe depression, small study suggests

Reuters (5/17, Kelland) reports that psilocybin found in psychedelic mushrooms may be safe and effective for alleviating treatment-resistant severe depression, the findings of a small study (5/17) published online May 17 in The Lancet Psychiatry suggest. All 12 patients in the study who took psilocybin in capsule form demonstrated a decrease in depressive symptoms for at least 21 days.

The New York Daily News (5/17, Pesce) reports, “Three months after, seven (58%) were still better, although five did show some degree of relapse.” The study’s senior author explained that psilocybin “targets the serotonin receptors in the brain, just as most antidepressants do, but it has a very different chemical structure to currently available antidepressants, and acts faster than traditional antidepressants.”

Nutrition for depression and dementia

American Psychiatric Association (APA) 2016 Annual Meeting. There is increasing evidence regarding the crucial role that diet plays in brain health, particularly in the areas of depression and dementia. Key nutrients include long-chain omega 3 fatty acids, magnesium, calcium, fiber, and vitamins B1, B9, B12, D, and E.

Yoga, meditation may help minimize cognitive problems that often precede Alzheimer’s, study suggests

The Huffington Post (5/10, Brenoff) reports that “a three-month course of yoga and meditation helped minimize the cognitive and emotional problems that often precede Alzheimer’s disease and other forms of dementia,” research involving people aged 55 and older suggests. The 25-participant study published online May 10 in the Journal of Alzheimer’s Disease revealed that “practicing yoga was even more beneficial for managing mild cognitive impairment than the memory enhancement exercises that have thus far been considered the gold standard.”

A lack of B vitamins is associated with faster brain aging

Individuals with increased levels of circulating homocysteine have faster rates of brain changes associated with aging than other people, whereas higher levels of vitamin B12 are associated with slower rates of brain aging, published online April 27 in JAMA Psychiatry.

VINEGAR’S MANY BENEFITS

I hope you are at least using vinegar for cooking. After reading this you may use it for many health conditions. Several of my patients drink a few teaspoonfuls each day with great results. It has been shown to help with diabetes (this article’s focus,) mood issues, heart disease, reflux, stomach ulcers, arthritis, and kidney problems. But, all you may remember after studying the references below is that it can help you lose weight.

  1. Johnston CS, Gaas CA. Vinegar: medicinal uses and antiglycemic effect. MedGenMed. 2006;8:61.
  2. US Food and Drug Administration. CPG Sec. 525.825 Vinegar, Definitions – Adulteration with Vinegar Eels. March 1995. http://www.fda.gov/ICECI/ComplianceManuals/CompliancePolicyGuidanceManual/ucm074471.htm Accessed March 19, 2016.
  3. O’Keefe JH, Gheewala NM, O’Keefe JO. Dietary strategies for improving post-prandial glucose, lipids, inflammation, and cardiovascular health. J Am Coll Cardiol. 2008;51:249-255. Abstract
  4. Ebihara K, Nakajima A. Effect of acetic acid and vinegar on blood glucose and insulin responses to orally administered sucrose and starch. Agric Biol Chem. 1988;52:1311-1312.
  5. Brighenti F, Castellani G, Benini L, et al. Effect of neutralized and native vinegar on blood glucose and acetate responses to a mixed meal in healthy subjects. Eur J Clin Nutr. 1995;49:242-247. Abstract
  6. Liljeberg H, Bjorck I. Delayed gastric emptying rate may explain improved glycemia in healthy subjects to a starchy meal with added vinegar. Eur J Clin Nutr. 1998;64:886-893.
  7. Johnston CS, Buller AJ. Vinegar and peanut products as complementary foods to reduce postprandial glycemia. J Am Diet Assoc. 2005;105,1939-1942.
  8. Leeman M, Ostman E, Bjorck I. Vinegar dressing and cold storage of potatoes lowers postprandial glycaemic and insulinaemic responses in healthy subjects. Eur J Clin Nutr. 2005;59:1266-1271. Abstract
  9. Hlebowicz J, Darwiche G, Björgell O, Almér LO. Effect of apple cider vinegar on delayed gastric emptying in patients with type 1 diabetes mellitus: a pilot study. BMC Gastroenterol. 2007;7:46.
  10. Mitrou P, Raptis AE, Lambadiari V, et al. Vinegar decreases postprandial hyperglycemia in patients with type 1 diabetes. Diabetes Care. 2010;33:e27.
  11. Liatis S, Grammatikou S, Poulia KA, et al. Vinegar reduces postprandial hyperglycaemia in patients with type II diabetes when added to a high, but not to a low, glycaemic index meal. Eur J Clin Nutr. 2010;64:727-732. Abstract
  12. Mitrou P, Petsiou E, Papakonstantinou E, et al. The role of acetic acid on glucose uptake and blood flow rates in the skeletal muscle in humans with impaired glucose tolerance. Eur J Clin Nutr. 2015;69:734-739. Abstract
  13. Mitrou P, Petsiou E, Papakonstantinou E, et al. Vinegar consumption increases insulin-stimulated glucose uptake by the forearm muscle in humans with type 2 diabetes. J Diabetes Res. 2015;2015:175204.
  14. van Dijk JW, Tummers K, Hamer HM, van Loon LJ. Vinegar co-ingestion does not improve oral glucose tolerance in patients with type 2 diabetes. J Diabetes Complications. 2012;26:460-461. Abstract
  15. Darzi J, Frost GS, Montaser R, et al. Influence of the tolerability of vinegar as an oral source of short-chain fatty acids on appetite control and food intake. Int J Obes (Lond). 2014;38:675-681. Abstract
  16. Lhotta K, Höfle G, Gasser R, Finkenstedt G. Hypokalemia, hyperreninemia and osteoporosis in a patient ingesting large amounts of cider vinegar. Nephron. 1998;80:242-243. Abstract
  17. Gambon DL, Brand HS, Veerman EC. [Unhealthy weight loss. Erosion by apple cider vinegar]. Ned Tijdschr Tandheelkd. 2012;119:589-591. Abstract
  18. Petsiou E, Mitrou PI, Raptis SA, Dimitriadis GD. Effect and mechanisms of action of vinegar on glucose metabolism, lipid profile, and body weight. Nutr Rev. 2014;72:651

http://www.healingdaily.com/experts.gif PLASTIC PROBLEMS

Do you believe everything industry tells you?

Here is some of the evidence that two key ingredients in plastic, Phthalates to make them softer, and BPA to make them more transparent (I wish the industry were more transparent) are not so good for you. The latter is also used as a dental sealant, and in aluminum cans to keep the metal from getting into our food. Not funny.

J. Environ Health Perspect; 2016DOI:10.1289/ehp.1509760 Urinary Phthalate Metabolite Concentrations and Reproductive Outcomes among Women Undergoing in Vitro Fertilization: Results from the EARTH Study. Urinary concentrations of DEHP metabolites were inversely associated with oocyte yield, clinical pregnancy, and live birth following ART.

Bisphenol A Exposure Disrupts Neurotransmitters Through Modulation of Transaminase Activity in the Brain of Rodents J. Endocrinology 2016;157(5), pp. 1736–1739
Bisphenol A Induces Fatty Liver by an Endocannabinoid-Mediated Positive Feedback Loop J. Endocrinology 2016;157(5), pp. 1751–1763
Chronic Exposure to Bisphenol A Affects Uterine Function During Early Pregnancy in Mice J. Endocrinology 2016;157(5), pp. 1764–1774

THE GUT-LIVER AXIS

This is a reprint of a full article on Medscape. Most patients have a problem in this area which then affects EVERY aspect of their health.

The term “gut-liver axis” is used to describe the close relationship that is established between the gut and liver, beginning in the very early stages of fetal life.[1] The quantitative and qualitative variations in the bacteria that compose the gut microbiota may actively contribute to the pathogenesis of several liver diseases, including nonalcoholic fatty liver disease (NAFLD), alcoholic steatohepatitis, and cirrhosis.[2]

Obesity is a major risk factor for NAFLD in children, and there is evidence that the gut microbiota can directly influence body weight in several ways:

  • Affecting the proportion of calories obtained from the intestinal contents;
  • Contributing to increased intestinal permeability through loss of epithelial barrier integrity;
  • Increasing bacterial translocation into the systemic circulation and allowing more hepatic access for ethanol and bacterial endotoxins such as lipopolysaccharide, which triggers nuclear factor-κB-mediated proinflammatory cytokine production; and
  • Promoting development of insulin resistance in the host.[3]

The gut microbiota meets the definition for a tissue organ based on complexity and behavior because it is able to manage the entire framework of metabolic activities associated with the network of microbial communities. Therefore, the well-characterized gut-liver axis might correctly be considered the gut-microbiota-liver network owing to the high degree of interconnectedness between the microbiota and host.[4] Recently developed systems biology approaches are able to integrate gut microbiota targeted-metagenomics, metabolomics, and clinical phenomics parameters into a multilayered system of “integrated-omics” data.[5]

The aim of this study was to investigate the structural and functional role of the gut microbiota in the onset and progression of pediatric NAFLD by evaluating the fecal gut microbiome of patients with NAFLD, nonalcoholic steatohepatitis (NASH), or obesity in terms of the phylome and metabolome, compared with healthy children.

Study Summary

In the study by Del Chierico and colleagues, 61 children and adolescents, ranging in age from 7 to 16 years, were recruited from the Hepato-Metabolic Disease Unit of the Pediatric Hospital Bambino Gesù in Rome during 2013. The patients were stratified by diagnosis of NAFLD (n=27), NASH (n=26), or obesity (n=8) and matched in a case-control fashion to healthy control children (n=54) with an overlapping age range who were enrolled at the hospital’s Human Microbiome Unit.

The investigators found that the most abundant operational taxonomic units at a phylum level in all patients were Firmicutes, followed by Bacteroidetes, Proteobacteria, Actinobacteria, Verrucomicrobia, and Tenericutes.

In children with NAFLD, compared with controls, Actinobacteria were significantly increased, and Bacteroidetes were reduced. Bacteroidaceae and Bacteroides were reduced in patients with NAFLD and NASH and increased in obese patients compared with controls. Overall, children with NAFLD had increased levels of Blautia, Bradyrhizobium, Anaerococcus, Peptoniphilus, Propionibacterium acnes, Dorea, and Ruminococcus and reduced proportions of Oscillospira and Rikenellaceae compared with control children.

In the group with NASH, lower levels of Oscillospira were associated with higher abundance of Dorea and Ruminococcus and higher levels of 2-butanone, 4-methyl-2-pentanone compared with control children. Remarkably, Oscillospira was significantly less abundant in patients with NAFLD and NASH and in those who were obese compared with the control children.

In the complex scenario of NAFLD, the interrelated enterotype (enterogradient)-metabotype framework of the gut microbiota appears to contribute to a signature change during disease onset and progression. In particular, the combination of a low abundance of Oscillospira with high levels of 2-butanone may be a specific gut microbiota metagenomics and metabolomics-based profile for liver steatosis in children. The high relative abundance of Lachnospiraceae, Ruminococcus, and Dorea observed in pediatric patients with NASH suggests that changes in the gut microbiota are associated with disease severity.

These findings might inform development of a specific metabolic diagnostic profile of steatosis and suggest a first-line probiotic candidate for treating NAFLD, with potential use of Oscillospira delivered orally or instilled directly into the gut.

Moreover, the investigators suggest that following a hypothesis-driven process of data integration rather than a data-driven approach could allow the generation of enterogradient models of the NAFLD microbiota. Interpretation of these models would allow clinical evidence to inform the selection of outlier subjects and features during model generation. In other diseases, gut microbiota models may actually work in an opposite fashion, possibly as a result of “stronger” gut microbiota profiling. This way of thinking opens new avenues in the novel concept of disease phenotype related to the host-microbiota interplay.[6]

  1. Llorente C, Schnabl B. The gut microbiota and liver disease. Cell Mol Gastroenterol Hepatol. 2015;1:275-284.
  2. Mehal WZ. The gut-liver axis: a busy two-way street. Hepatology. 2012;55:1647-1649. Abstract
  3. Vajro P, Paolella G, Fasano A. Microbiota and gut-liver axis: their influences on obesity and obesity-related liver disease. J Pediatr Gastroenterol Nutr. 2013;56:461-468. Abstract
  4. Burcelin R, Serino M, Chabo C, et al. Metagenome and metabolism: the tissue microbiota hypothesis. Diabetes Obes Metab. 2013;15 Suppl 3:61-70. Abstract
  5. Del Chierico F, Gnani D, Vernocchi P, et al. Meta-omic platforms to assist in the understanding of NAFLD gut microbiota alterations: tools and applications. Int J Mol Sci. 2014;15:684-711. Abstract
  6. Putignani L, Dallapiccola B. Foodomics as part of the host-microbiota-exposome interplay. J Proteomics. 2016 Apr 26. [Epub ahead of print]

 

Hugo Rodier, MD is an integrative physician based in Draper, Utah who specializes in healing chronic disease at the cellular level by blending proper nutrition, lifestyle changes, & allopathic practices when necessary.

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Information on this blog is provided for informational purposes only and is not intended as a substitute for the advice provided by your physician or other healthcare professional. You should not use the information on this blog for diagnosing or treating a health problem or disease, or prescribing any medication or other treatment. These statements have not been evaluated by the Food and Drug Administration. Please consult your health care practitioner with any questions or concerns you may have.