In The News: August 2017

In a double-blind trial employing women with polycystic ovary syndrome (PCOS), supplementation with CoQ10 resulted in lower glucose, insulin, insulin resistance, and total and LDL cholesterol compared with a placebo group that did not receive CoQ10.*

Dr. Zatollah Asemi and colleagues randomized 60 women with PCOS to receive 100 mg of CoQ10 or a placebo daily for 12 weeks. Blood samples collected before and after the treatment period were evaluated for serum lipid levels and markers of insulin metabolism.

Among CoQ10-supplemented participants, acne and hair loss, which are prominent features of PCOS, were reduced by the end of the trial compared with the placebo group. Women in the CoQ10 group had lower fasting plasma glucose, serum insulin and insulin resistance. Total cholesterol and LDL cholesterol were also reduced.

Editor’s Note: Abnormal lipids affect an estimated 70% of women with PCOS and insulin resistance is estimated to affect between 50% and 75%. In previous research, Dr. Asemi and colleagues found that 100 mg of CoQ10 per day in subjects with metabolic syndrome improved markers of insulin metabolism.

A recent study detailed findings that point to a potential benefit for every-other-day fasting in the treatment of the most common form of childhood leukemia.*

Cheng Cheng Zhang and his associates at the University of Texas Southwestern Medical Center found that alternate-day fasting inhibited the initiation of B cell as well as T cell acute lymphoblastic leukemia and reversed their progression in rodent models with the malignancy. Fasting was not, however, effective in acute myeloid leukemia, which occurs more frequently in adults.

“Strikingly, we found that in models of T cell acute lymphoblastic leukemia, a regimen consisting of six cycles of one day of fasting followed by one day of feeding completely inhibited cancer development,” Dr. Zhang reported. “Mice in the [acute lymphoblastic leukemia] model group that ate normally died within 59 days, while 75% of the fasted mice survived more than 120 days without signs of leukemia.”

Editor’s Note: “It will be important to determine whether [acute lymphoblastic leukemia] cells can become resistant to the effects of fasting,” Dr. Zhang remarked. “It also will be interesting to investigate whether we can find alternative ways that mimic fasting to block [acute lymphoblastic leukemia] development.”

Vitamin D deficiency has been found to play a central role in the development of metabolic syndrome—a group of risk factors that increases your risk for heart disease, stroke, and diabetes.*

For 18 weeks, Dr. Yuan-Ping Han and colleagues gave mice a control diet supplemented with a sufficient amount of vitamin D3, a vitamin D-deficient control diet, a high-fat diet supplemented with vitamin D3, or a high-fat diet that was deficient in vitamin D. The team found that a high-fat diet by itself is not sufficient to induce insulin resistance and fatty liver disease, but that “a second hit,” in the form of vitamin D deficiency, is required.

It was demonstrated that a high-fat diet alters gut bacteria, which contributes to elevated glucose and fatty liver. This imbalance is aggravated by a lack of vitamin D, which results in decreased production of antimicrobial molecules called defensins that are needed to maintain healthy flora.

“Based on this study, we believe that keeping vitamin D levels high…is beneficial for prevention and treatment of metabolic syndrome,” said coauthor Stephen Pandol of Cedars-Sinai Medical Center. “A sufficient dietary vitamin D supplement can partially but significantly antagonize metabolic syndrome caused by high-fat diet in mice.”

Editor’s Note: In animals that received high fat, vitamin D deficient diets, oral administration of synthetic defensin improved intestinal bacteria balance.

An article in JAMA Otolaryngology-Head & Neck Surgery reports an association between iron deficiency anemia and hearing loss.*

Kathleen Schieffer, BS, and colleagues evaluated data from 305,339 men and women between the ages of 21 and 90 who visited Penn State Milton S. Hershey Medical Center during 2011-2015 and had information available concerning serum ferritin and hemoglobin levels. Iron deficiency anemia was determined by low serum ferritin levels and low hemoglobin levels that were determined according to age and sex-defined values.

Hearing loss identified during past visits was categorized as conductive (associated with the bones of the middle ear), sensorineural, or combined loss (conductive and/or sensorineural loss, deafness or loss due to unspecified causes). Subjects who had iron deficiency anemia had 82% higher odds of being diagnosed with sensorineural hearing loss and a greater than two-fold increased risk of combined hearing loss.

Editor’s Note: The authors note that only one artery supplies blood to the cochlea of the ear, and that low hemoglobin levels that impair the blood’s oxygen-carrying capacity can lead to ischemia in this area.

Nicotinamide may have promising beneficial use in the treatment of early-stage Parkinson’s disease.*

In a recent study, L. Miguel Martins and colleagues focused on fruit flies with a mutation, PINK1, that results in a condition similar to human Parkinson’s disease. The flies were fed a diet supplemented with nicotinamide, which is a precursor to nicotinamide adenine dinucleotide (NAD+), a coenzyme needed for the generation of energy in cells’ mitochondria. NAD+ also helps protect neurons from degeneration.

Flies with the PINK1 mutation that received nicotinamide had fewer faulty mitochondria and less neuron loss compared to those that did not receive the vitamin. Preventing depletion of NAD+ in the brain resulted in healthier mitochondria, greater neuron survival, and longer life.

“The results suggest that in familial Parkinson’s, available NAD+ is critical for keeping mitochondria in shape and the disease at bay,” Dr. Martins concluded.

Editor’s Note: “Parkinson’s disease occurs when dopaminergic neurons in a part of the brain called the substantia nigra are lost,” Dr. Martins explained. “This can happen for a variety of reasons, but in some hereditary cases, the main problem is unhealthy mitochondria—the organelles that power the cell.”

“Mutations in genes such as PINK1 prevent cells from clearing out the defective powerhouses,” he continued. “When they accumulate, neurons can’t get enough energy and die. The faulty mitochondria also release toxic molecules that damage their genes encoded by DNA.”