SpectraCell Blog

Vitamin B1 and Female Fertility

Posted by SpectraCell Laboratories, Inc. on Wed, Nov 29, 2017 @ 11:00 AM

pregnant.jpegA vitamin B1 deficiency has been shown to compromise egg cell health in female mice. Even though this study was carried out on mice, the implications for human health and fertility are not lost. Scientists were interested in assessing the effect of mild and severe vitamin B1 (thiamin) deficiency on egg cells and what they found was revealing. 

Mice were fed one of two diets: normal or one lacking in vitamin B1. Not surprisingly, the vitamin B1 concentration in the ovaries of mice not given vitamin B1 was much lower than that of mice fed B1. Since the major source of cellular energy in oocytes (immature egg cells) comes from a compound (pyruvic acid) that is metabolized by a vitamin B1-dependent enzyme, researchers wanted to investigate the impact of B1 deficiency on egg cell development. 

If the vitamin B1 deficiency was “mild” (not severe enough to cause weight loss), the mice ovaries produced egg cells that were normal. However, if B1 deficiency reached severe levels, then their ovaries would produce abnormal egg cells more often: 44% of eggs from severely deficient animals were abnormal, compared to only 14% of eggs from mice with adequate B1. Furthermore, once the mice returned to a vitamin B1-containing diet, the level of abnormal egg cells dropped from 44% to 23%, suggesting that egg cell damage may occur as the cell matures but not in its immature stage. 

For more details on the cited paper, click here for a link to the abstract, “Effects of Mild and Severe Vitamin B1 Deficiencies on the Meiotic Maturation of Mice Oocytes,” published in the March 2017 issue of Nutrition and Metabolic Insights.  For a copy of the full paper, click here

Topics: micronutrients, Vitamin B1, Vitamin B1 and Fertility, Female Fertility, Vitamin B1 Deficiency

Vitamin K May Boost Performance in Athletes

Posted by SpectraCell Laboratories, Inc. on Tue, Nov 21, 2017 @ 11:00 AM

cyclist-1.jpegVitamin K is often regarded as a nutrient for improving heart health, lowering cancer risk, and increasing bone density, but it also appears to improve fitness even in healthy athletes. Like most nutrients, it seems to have quite versatile roles.

In this small study, 26 trained male and female athletes were administered placebo or vitamin K2 supplements for eight weeks while they maintained their regular exercise routines. At the beginning of the study and after eight weeks, each person completed a fitness test on an exercise machine designed to quantify their physical work load, oxygen consumption, respiratory rate, cardiac output, and heart rate.  

Vitamin K2 supplementation was associated with a 12% increase in cardiac output (volume of blood that the heart is capable of pumping per beat). The authors suggest that vitamin K2, which has previously been shown to play a role in energy metabolism (especially in tissues with high energy requirements such as skeletal muscle and heart) might be considered in healthy athletes to improve performance. 

For more details on the cited paper, click here for a link to the abstract, “Oral Consumption of Vitamin K2 for 8 Weeks Associated With Increased Maximal Cardiac Output During Exercise,” published in the July 2017 issue of Alternative Therapies in Health and Medicine. 

Topics: micronutrients, Vitamin K, Nutrition, Nutrition and Sports Performance, Vitamin K and Sports Performance, Vitamin K and Heart Health

Can We Change Our Genetic Expression with Nutrients?

Posted by SpectraCell Laboratories, Inc. on Fri, Nov 17, 2017 @ 11:30 AM

DNA Human.jpgRecent evidence suggests that the answer is yes.  Most people understand that we all have inherent genetic predispositions – some as benign as the shape of our nose and others more dangerous such as the tendency toward certain cancers.  However, as research on epigenetics grows, the ability to modulate the expression of certain genes is becoming clearer.  Epigenetics is the study of how our genetic expression is affected by factors other than changes in DNA sequence.  These factors include our environment, including what we eat, supplements we take, toxins, illnesses, even the amount of sunlight to which we are exposed. 

In this study, variations (known by geneticists as polymorphisms) in a specific gene that makes a protein called the zinc transporter 8 (ZNT8), which carries zinc into the hormone insulin, were studied. This protein ZNT8 is responsible for ensuring that pancreatic beta cells (the cells that make insulin which allows us to metabolize blood sugar) have adequate zinc available.  If cells in the pancreas do not have enough zinc, they will not function optimally which may ultimately result in higher risk of insulin resistance and the metabolic dysfunction that follows.  

When participants with the (CC) genotype ingested more zinc and omega 3 fatty acids, they lowered their risk of metabolic syndrome consequences associated with their genotype. Stated differently, people with this specific genotype (CC) responded well (in terms of improved insulin sensitivity and metabolic health) to higher levels of zinc and omega 3 fatty acids, while other genotypes (CT or TT) did not show a meaningful improvement in metabolism.  Since over-supplementation has potentially negative consequences (too much zinc can cause copper deficiency, for example), knowing your genotype may lead to more informed supplementation decisions. 

For more details, click here for a link to the abstract entitled Some dietary factors can modulate the effect of the zinc transporters 8 polymorphism on the risk of metabolic syndrome published in the May 2017 issue of Scientific Reports  (Abstract 2640).  Or read the full paper here.  (Full paper 829)

 

Adapted from July 2017 Clinical Updates.  9/27/2017.  (NLH)

Topics: micronutrients, Epigenetics, Gene Expression, Gene Expression and Nutrition, Genetic Predisposition