AUGUST 2015 - Volume 2015, Issue 08

In This Issue….

  • Carnitine and CoQ10 reduced chemotherapy-induced fatigue
  • Vitamin K helps pancreas rebuild cells
  • Meta-analysis concludes vitamin E reduces this inflammatory protein
  • Review paper debunks the cholesterol hypothesis of heart disease
  • Is Alzheimer’s really type 3 diabetes?
  • New study explains mechanism behind dangers of oxidized LDL


CLINICAL UPDATE – Carnitine and CoQ10 reduced chemotherapy-induced fatigue
57 women with breast cancer who were undergoing chemotherapy and experiencing cancer related fatigue were given either regular care or supplemented with coenzyme Q10 and carnitine daily for three weeks. Fatigue levels were measured using standardized scoring systems. After three weeks, changes in the worst level of fatigue were significantly different between groups, leading researchers to conclude that the coenzyme Q10 and carnitine supplement “may control moderate-severe cancer related fatigue in breast cancer patients.” (Supportive Care in Cancer, June 2015)

Efficacy and safety of an amino acid jelly containing coenzyme Q10 and L-carnitine in controlling fatigue in breast cancer patients receiving chemotherapy: a multi-institutional, randomized, exploratory trial (JORTC-CAM01).



CLINICAL UPDATE – Vitamin K may help pancreas rebuild cells
In this novel study, diabetes was induced by streptozotocin, a chemical that is very damaging to pancreatic beta cells. When treated with vitamin K, the animals in the study demonstrated significantly less oxidative damage to the pancreatic tissue. In fact, treatment with vitamin K prevented pancreatic cell death associated with streptozotocin, which occurs in type 1 diabetes. Additionally, vitamin K enhanced insulin secretion to the point where blood glucose normalized in the subjects that actually had type 1 diabetes induced by the drug. Researchers concluded that their results point to the possibility of “therapeutic use of this vitamin in stimulating islet cell proliferation/ regeneration.” (Nutrition, January 2015)

LINK to ABSTRACT Vitamin K1 alleviates streptozotocin-induced type 1 diabetes by mitigating free radical stress, as well as inhibiting NF-κB activation and iNOS expression in rat pancreas.



CLINICAL UPDATE – Meta-analysis concludes vitamin E reduces this inflammatory protein
A telling marker of chronic inflammation – C-reactive protein – has been very strongly linked to chronic disease, particularly cardiovascular disease and aging. In this meta-analysis, twelve trials on the effect of vitamin E supplementation (mainly tocopherols) on CRP levels were included. With a pooled average reduction over all trials of 0.62 mg/L in the serum levels of CRP, the results suggest that vitamin E can reduce CRP levels in the blood. (European Journal of Clinical Nutrition, August 2015)

LINK to ABSTRACT Effect of vitamin E supplementation on serum C-reactive protein level: a meta-analysis of randomized controlled trials.



CLINICAL UPDATE – Review paper debunks the cholesterol hypothesis of heart disease
Although the link between dietary cholesterol and heart disease and stroke has been questioned for years, a newly published review paper lends credence to the idea that dietary cholesterol does not cause cardiovascular disease. In summary, forty studies that included over 361,000 people were reviewed and authors found that “dietary cholesterol was not statistically significantly associated with any coronary artery disease, ischemic stroke or hemorrhagic stroke.” In addition, the authors noted that dietary cholesterol did not change triglyceride levels or VLDL (very low density lipoprotein) levels.

This study suggests that conventional cholesterol testing is misleading at best, and quite possibly a very common cause of pharmacological overtreatment. The review supports lipoprotein particle measurement as a more clinically relevant diagnostic tool than standard cholesterol testing. (American Journal of Clinical Nutrition, June 2015)

LINK to ABSTRACT Dietary cholesterol and cardiovascular disease: a systematic review and meta-analysis.


CLINICAL UPDATE – Is Alzheimer’s really type 3 diabetes?
In this study, 150 normal cognitive functioning men (mean age = 60 years old) that were at risk for Alzheimer’s due to family history were evaluated for glucose uptake into various areas of the brain. In addition, their blood was evaluated for insulin resistance and they also underwent a serious of cognitive tests.

Researchers found that insulin resistance, which is known to undermine glucose uptake into muscle, was also associated with impaired glucose uptake into the brain, which ultimately impaired memory (immediate and delayed) in this group of men. (Journal of the American Medical Association Neurology, July 2015)

LINK to ABSTRACT Association of Insulin Resistance with Cerebral Glucose Uptake in Late Middle-Aged Adults at Risk for Alzheimer Disease.


CLINICAL UPDATE – New study explains mechanism behind dangers of oxidized LDL
Oxidized LDL (low density lipoprotein) has long been considered a risk factor for both cardiovascular disease and cancer and a new study sheds light on why this occurs. Researchers demonstrated that oxidized LDL actually affects the methylation of genes – a chemical process that can affect whether or not certain genes are expressed. Specifically, a gene called microRNA-210, which is turned on in the presence of oxidized LDL, produces a protein that is heavily implicated in cancer biology. (Oncotarget, June 2015)

Oxidized low-density lipoprotein is a common risk factor for cardiovascular diseases and gastroenterological cancers via epigenomical regulation of microRNA-210.