June 2017 – Vol. 11, Issue 6

In This Issue...                                                                       

  • When it comes to bone health, a comprehensive look at vitamin status may be key
  • Zinc supplementation early in life is not without consequence
  • Vitamin D augments the benefits of exercise
  • Omega-3 fatty acids help offset the cancer-inducing properties of insulin
  • A lymphocyte’s ability to communicate is linked to healthy aging


CLINICAL UPDATE – When it comes to bone health, a comprehensive look at vitamin status may be key
In this case control study, blood was drawn on 116 patients upon admission to a hospital for hip fracture plus 73 non-hospitalized patients who served as a control group.   Several vitamins – vitamin A, C, E, B6, B12 and B9 (folic acid) – were measured. In addition, levels of the bone-building vitamins D and K were evaluated plus two proteins involved in bone formation: osteocalcin – a vitamin K dependent  protein important in the bone mineralization process and alkaline phosphatase (ALP)  – a protein that aids in the early stages of bone mineralization but that may contribute to arterial calcification over time.
          The researchers discovered that not only were the well known “bone nutrients” – vitamin D and K – related to bone health but other vitamins – A, C, E and B6 – had an impact as well.  Higher levels of these vitamins were correlated to higher levels of the bone building protein osteocalcin.  Further, higher levels of these vitamins correlated to lower levels of ALP, a protein that may calcify arteries.  They concluded that low vitamin A, C and E are associated with an increased risk of hip fracture, which suggesting that  a comprehensive assessment of several vitamins, versus one or two “well researched” ones may provide a superior perspective on bone health.
          (Clinical Nutrition, April 2017)
LINK to ABSTRACT Micronutrients and the risk of hip fracture: case-control study.


CLINICAL UPDATE – Zinc supplementation early in life is not without consequence
Although research suggests zinc deficiency during pregnancy and infancy can increase the risk of disease later in life, this study suggests that zinc supplementation may also pose risks.  In this animal study, pregnant rats were given three different amounts of zinc during gestation:  (1) a zinc deficient diet, (2) a zinc adequate diet and (3) a zinc supplemented diet.  Their food contained vastly different levels of the mineral:   3 mg, 35 mg and 180 mg of zinc in their food respectively.  In other words, the zinc supplemented diet had over 5 times the amount of zinc as the zinc-adequate diet, which in turn had over 10 times the amount of zinc as the zinc deficient diet.
          When the pregnant rats gave birth, their female babies were fed the same diets.  Then after a couple of months, the female offspring were exposed to a powerful carcinogen and put on the same zinc-adequate diet. After 6 months, the rats were inspected for tumors.  Interestingly, the group fed supplemental zinc, which was 60 times the amount of zinc given to group 1 and five times the amount given to group 2,  had more tumors than the others.  In addition, the expression of several genes was altered in the rats given the most zinc, making the mice that got too much zinc more susceptible to developing breast tumors. 
          This study illustrates that micronutrient deficiency and excess can both have negative implications with respect to physiological development.  Especially in the case of zinc, in which excess supplementation may induce a deficiency in other micronutrients (copper, for example), the importance of targeted supplementation with specific emphasis on correcting known deficiency – versus blind supplementation – cannot be underestimated.
          (Journal of Nutritional Biochemistry, June 2017)
          LINK to ABSTRACT
Early-in-life dietary zinc deficiency and supplementation and mammary tumor development in adulthood female rats.


CLINICAL UPDATE – Vitamin D augments the benefits of exercise
In order to study the effects of vitamin D and exercise on metabolism, researchers studied female rats that were given high, moderate or low doses of vitamin D and a controlled exercise regimen.  After two months, their metabolic efficiency was measured by looking at blood sugar, insulin and a protein called peroxisome proliferator-activated receptor (PPAR)  that regulates fat storage and glucose metabolism. Vitamin D increased the expression of the PPAR gene that produces this fat-regulating protein, thus magnifying the beneficial effect that physical exercise had on fat metabolism and energy.  Conversely, a vitamin D deficiency may decrease this fat-burning protein and exacerbate the negative effects of a sedentary lifestyle.
          (Nutrition, April 2017)
          LINK to ABSTRACT
Vitamin D increases PPARγ expression and promotes beneficial effects of physical activity in metabolic syndrome.




CLINICAL UPDATE – Omega-3 fatty acids help offset the cancer-inducing properties of insulin
Elevated levels of the hormone insulin, which is released in response to blood sugar increases, have been linked to breast cancer in previous research and are considered a risk factor in obese people that may induce breast tumor formation.  This study evaluated the effect that omega 3 fatty acids have on insulin-induced growth of breast cancer cells and it shows that omega 3 fatty acids actually blunt the cancerous effects of chronically elevated insulin in breast tissue. 
          This is how it works:  when breast cells are exposed to insulin over time, their method of communicating from cell to cell becomes dysfunctional and consequently, cells send the wrong “cellular signals” for controlling growth, leading to tumor formation.  Omega 3 fatty acids attenuate this insulin-induced cellular communication breakdown which ultimately helps protect the breast cells from cancer.
          (Nutrition Research, June 2017)
LINK to ABSTRACT Omega-3 free fatty acids attenuate insulin-promoted breast cancer cell proliferation.




CLINICAL UPDATE – A lymphocyte’s ability to communicate is linked to healthy aging
As medical focus on healthy aging gains popularity, research into potential biomarkers for aging have also gained attention.  A recent study on white blood cells in mice sheds light on the concept of cellular aging.  When lymphocytes (a type of immune cell) are stimulated to increase, the cells in young subjects were very highly regulated and their genetic expression was tightly coordinated via very specific communication pathways between cells.  As the cells aged, their ability to communicate was compromised such that the cells essentially lost the ability to signal how and what genes should be expressed.  In other words, aging decreases the ability of lymphocytes to respond appropriately to instructions from other cells.  Since lymphocytes are responsible for strong immunity against both external pathogens and endogenous tumor cells, the loss of lymphocyte’s ability to respond to cellular signals may be a novel biomarker for aging.
          (Science, March 2017)
          LINK to ABSTRACT
Aging increases cell-to-cell transcriptional variability upon immune stimulation.
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