April 2018 – Vol. 12, Issue 4


 

In This Issue…                                                                            

·        CoQ10 shows promise as first-line treatment for heart disease prevention

·        This supplement may reduce cravings for alcohol

·        How much is too much when it comes to vitamin D mega-doses?

·        Aggressive supplementation with vitamins B5 and B7 overcomes faulty genes that cause intestinal inflammation, study suggests

·        Cellular levels of vitamin B1 may influence the progression of Huntington’s disease

 


 

CLINICAL UPDATE – CoQ10 shows promise as first-line treatment for heart disease prevention
            The benefit of coenzyme Q10 in combination with pharmacological treatment, especially statins, for heart disease prevention has been well studied in the past.  However, a team of researchers in China wanted to find out whether treating people with dyslipidemia, often referred to – albeit somewhat inaccurately, as “high cholesterol” – with coenzyme Q10 (and only coenzyme Q10) would lower heart disease risk.  The people studied were dyslipidemic,  meaning they all had lipoprotein and cholesterol metabolism issues, but none were being treated with cholesterol or blood sugar control-controlling medications.
            101 patients were included in the study and were given 120mg CoQ10 or placebo daily for six months.  After the first 3 months, CoQ10 but not placebo lowered blood pressure.  Not surprisingly, since CoQ10 is such a potent antioxidant, it also increased antioxidant capacity in patients taking it.  In fact, CoQ10 is also known as ubiquinone (oxidized form) and ubiquinol (reduced form) since it is so ubiquitous throughout the body as it is in almost every cell that undergoes any metabolic process.  Consequently, areas in the body that have very high energy requirements such as muscle and cardiac tissue, have very high coenzyme Q10 requirements. 
            After another 3 months of supplementation with coQ10, blood pressure was lowered even more.  Plus, compared to placebo, CoQ10 lowered triglycerides, lowered low-density lipoprotein cholesterol and decreased at least one parameter of blood sugar regulation (called HOMA-IR for homeostatis model assessment of insulin resistance index).  Because the CoQ10 supplementation positively affected several biomarkers for cardiovascular health, they concluded that CoQ10 is “a potential candidate for the primary prevention of CVD.”
           (Journal of Clinical Lipidology, April 2018)
           
LINK to ABSTRACT Treatment of coenzyme Q10 for 24 weeks improves lipid and glycemic profile in dyslipidemic individuals.

 

CLINICAL UPDATE – This supplement may reduce cravings for alcohol
            NAC (N-acetylcysteine) is an antioxidant supplement that is known in part for its role in helping liver detoxification, particularly as a precursor to the very powerful antioxidant glutathione, which is crucial for its role in metabolizing chemicals – alcohol, medications, food additives – via liver detoxification pathways.  Previous evidence suggests NAC can benefit people with substance abuse disorders but its role in alcohol abuse is less clear.
            In this randomized, double-blind trial of 277 chronic marijuana users, participants were given either placebo or 1200 mg N-acetyl cysteine twice daily, which is a relatively large dose compared to most over-the-counter supplementation recommendations. The people in the trial were actively stopping marijuana use, but they agreed to document alcohol use as well.  It should be noted that they were not actively in a program to stop using alcohol.  Instead, they simply agreed to make notes as to how much alcohol they consumed and in what time period they consumed it (i.e. whether they were binge-drinking versus social drinking). 
            After 12 weeks, the authors noted that the people taking the NAC supplement drank alcohol in lesser amounts and less often, regardless of whether or not they were successful in stopping marijuana use.  Specifically, the authors concluded that NAC “may be effective at reducing consumption of alcohol by ∼30% among treatment-seeking adults.”
          (Drug and Alcohol Dependence, April 2018)
         
LINK to ABSTRACT The effect of N-acetylcysteine on alcohol use during a cannabis cessation trial.

 

 CLINICAL UPDATE – How much is too much when it comes to vitamin D mega-doses?
            According to this recent trial on teenagers, even a monthly mega-dose of 150,000 IU of Vitamin D is not too much.  The small trial included 26 adolescents that were divided into three groups:  Group 1 took 50,000 IU of vitamin D3 in a single oral dose once a month.  Group 2 took 50,000 IU of vitamin D3 in three oral doses over the course of a month (for a total monthly dose of 150,000 IU).  Group 3 took placebo pills.  The above dosages continued for 12 months.
            Serum Vitamin D was measured four times – at baseline, 3, 6 and 12 months.  At the end of the yearlong study, one person was still vitamin D deficient of the16 people taking vitamin D who completed the study.  Of the ten people taking placebo, six remained deficient in vitamin D after the yearlong study.   In addition, for the groups taking 50,000 IU and 150,000 IU of vitamin D3 every month, their blood levels were 30% and 54% higher than those taking placebo.  Specifically, the highest dose group (Group 2) had serum Vitamin D levels of 76 nmol/L.  Group 1 had 65 nmol/L serum vitamin D levels and Group 3 (placebo) had 50 nmol/L serum vitamin D levels.
            Since adverse events reported were minor, the authors of this study conclude that even a dose as high as 150,000 IU monthly for an entire year can safely and effectively correct vitamin D deficiency in adolescents.  Although they don’t explicitly suggest this dosage routinely, the data can help practitioners tailor vitamin D dosage requirements in their patients.
          (European Journal of Clinical Nutrition, April 2018)
          
LINK to ABSTRACT The optimal dosage regimen of vitamin D supplementation for correcting deficiency in adolescents: a pilot randomized controlled trial.

  

CLINICAL UPDATE – Aggressive supplementation with vitamins B5 and B7 overcomes faulty genes that cause intestinal inflammation, study suggests
            In this provocative animal study, scientists stopped the function of a specific gene (which is also referred to as a “gene knockout”) in mice called the SLC5A6 gene.  The SLC family of genes contains the instructions to make proteins called solute carrier (SLC) proteins, which are proteins found in cell membranes that help transport various things across the cell membrane. 
           In this study, the gene that was “knocked out” (i.e. removed) was the gene that makes SMVT (sodium-dependent multivitamin transporter) which is a protein that carries vitamins B5 (also called pantothenic acid) and vitamin B7 (also called biotin) across the intestinal epithelium and into the bloodstream for use by the body.   When this gene is removed, the animal experiences severe inflammation, particularly in the gastrointestinal tract which becomes permeable and unable to maintain proper barrier integrity, ultimately leading to premature death.
            Once the gene was “knocked out” and scientists confirmed the consequences of removing it (intense gastrointestinal damage), they proceeded to aggressively supplement female mice with vitamin B5 and B7.  Then these mice became pregnant and continued to receive aggressive supplementation of vitamins B5 and B7.  The offspring, who did not have the gene and therefore could not manufacture the protein necessary to absorb vitamin B5 and B7, were also given supplemental vitamin B5 and B7.   Even though these mice did not have the gene, and therefore the protein, that is critical for normal growth and a functioning gastrointestinal tract, the aggressive supplementation of the corresponding vitamins prevented these gastrointestinal problems from occurring.  
            In other words, the scientists confirmed two things: (1) that both vitamin B5 and biotin play an important role in maintaining normal intestinal integrity and health and (2) that even if a potentially severe genetic defect exists, targeted repletion may overcome its clinical manifestation. 
          (American Journal of Physiology and Cell Physiology, April 2018)
          
LINK to ABSTRACT Biotin and pantothenic acid over-supplementation to conditional SLC5A6 KO mice prevents the development of intestinal mucosal abnormalities and growth defects.

  

CLINICAL UPDATE – Cellular levels of vitamin B1 may influence the progression of Huntington’s disease
            Huntington’s disease is a relatively rare disease that occurs when a person has altered expression of a specific gene called the huntingtin gene.  The presence of this mutated gene initiates the synthesis of an altered protein (similarly called the mutated huntingtin protein, or mHTT) that damages nerve cells in the brain over time.  The disease progresses over the course of several years and clinically manifests as gradually worsening mental, emotional and physical dysfunction, to the point of total incapacity.
            In this experiment, scientists studied the effect of supplemental vitamin B1 (thiamine) on B lymphocytes (white blood cells) that carried the mutated Huntington gene and compared them to normal B lymphocytes that did not carry the mutated gene, which served as the control.  The scientists supplemented vitamin B1 on the two sets of cells and compared the following: (1) cell growth rates, (2) vitamin B1 intake into the cell, (3) genetic profile of 27 different thiamine related genes and (4) the enzyme activity of several B1-dependent proteins.
            They found that supplemental vitamin B1 stimulated more of an increase in growth in the mutated Huntington gene cells than the control cells, suggesting the Huntington cells had a higher requirement for vitamin B1. In addition, vitamin B1 intake, and therefore intracellular levels, was increased in the Huntington cells compared to control.  Enzyme activity did not differ between cell types, but the expression of genes related to B1-dependent energy metabolism did differ between the control and mutated cell groups.
             Vitamin B1 is known for its role in energy metabolism and deficiency has been linked to a several neurological syndromes such as Alzheimer’s disease and Wernicke encephalopathy, which suggests it may play a role in Huntington’s disease.  Although this study was done in vitro (in test tubes), the increased expression of B1-related genes upon supplementation of B1 suggests intracellular vitamin B1 levels may play an important role in the manifestation of this enigmatic disease.
            (Advances in Clinical and Experimental Medicine, August 2017)
           
LINK to ABSTRACT Role of thiamine in Huntington's disease pathogenesis: In vitro studies.    
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