Gary’s Daily Health News - Vol. 5

Drinking sufficient water could prevent heart failure

National Heart, Lung, and Blood Institute (US), 24 Aug 2021

Staying well hydrated throughout life could reduce the risk of developing heart failure, according to research presented at ESC Congress 2021.1

“Our study suggests that maintaining good hydration can prevent or at least slow down the changes within the heart that lead to heart failure,” said study author Dr. Natalia Dmitrieva of the National Heart, Lung, and Blood Institute, part of the National Institutes of Health, Bethesda, US. “The findings indicate that we need to pay attention to the amount of fluid we consume every day and take action if we find that we drink too little.”

Recommendations on daily fluid intake vary from 1.6 to 2.1 litres for women and 2 to 3 litres for men. However, worldwide surveys have shown that many people do not meet even the lower ends of these ranges.2 Serum sodium is a precise measure of hydration status: when people drink less fluid, the concentration of serum sodium increases. The body then attempts to conserve water, activating processes known to contribute to the development of heart failure.

Dr. Dmitrieva said: “It is natural to think that hydration and serum sodium should change day to day depending on how much we drink on each day. However, serum sodium concentration remains within a narrow range over long periods,3 which is likely related to habitual fluid consumption.”

This study examined whether serum sodium concentration in middle age, as a measure of hydration habits, predicts the development of heart failure 25 years later. The researchers also examined the connection between hydration and thickening of the walls of the heart's main pumping chamber (left ventricle) – called left ventricular hypertrophy – which is a precursor to heart failure diagnosis.

The analysis was performed in 15,792 adults in the Atherosclerosis Risk in Communities (ARIC) study. Participants were 44 to 66 years old at recruitment and were evaluated over five visits until age 70 to 90.

Participants were divided into four groups based on their average serum sodium concentration at study visits one and two (conducted in the first three years): 135–139.5, 140–141.5, 142–143.5, and 144–146 mmol/l. For each sodium group, the researchers then analysed the proportion of people who developed heart failure and left ventricular hypertrophy at visit five (25 years later).

Higher serum sodium concentration in midlife was associated with both heart failure and left ventricular hypertrophy 25 years later. Serum sodium remained significantly associated with heart failure and left ventricular hypertrophy after adjusting for other factors related to the development of heart failure: age, blood pressure, kidney function, blood cholesterol, blood glucose, body mass index, sex and smoking status. Every 1 mmol/l increase in serum sodium concentration in midlife was associated with 1.20 and 1.11 increased odds of developing left ventricular hypertrophy and heart failure, respectively, 25 years later.

The risks of both left ventricular hypertrophy and heart failure at age 70 to 90 began to increase when serum sodium exceeded 142 mmol/l in midlife.

Dr. Dmitrieva said: “The results suggest that good hydration throughout life may decrease the risk of developing left ventricular hypertrophy and heart failure. In addition, our finding that serum sodium exceeding 142mmol/l increases the risk of adverse effects in the heart may help to identify people who could benefit from an evaluation of their hydration level. This sodium level is within the normal range and would not be labelled as abnormal in lab test results but could be used by physicians during regular physical exams to identify people whose usual fluid intake should be assessed.”

 

High cholesterol fuels cancer by fostering resistance to a form of cell death

Most cancer cells die under the stress of metastasis, but cholesterol fuels a process that makes them impervious to stress-induced cell death

Duke University, August 24, 2021

Chronically high cholesterol levels are known to be associated with increased risks of breast cancer and worse outcomes in most cancers, but the link has not been fully understood.

In a study appearing online Aug. 24 in the journal Nature Communications, a research team led by the Duke Cancer Institute has identified the mechanisms at work, describing how breast cancer cells use cholesterol to develop tolerance to stress, making them impervious to death as they migrate from the original tumor site.

“Most cancer cells die as they try to metastasize -- it’s a very stressful process,” said senior author Donald P. McDonnell, Ph.D., professor in the departments of Pharmacology and Cancer Biology and Medicine at Duke University School of Medicine. “The few that don’t die have this ability to overcome the cell’s stress-induced death mechanism. We found that cholesterol was integral in fueling this ability.”

McDonnell and colleagues built on earlier research in their lab focusing on the link between high cholesterol and estrogen-positive breast and gynecological cancers. Those studies found that cancers fueled by the estrogen hormone benefitted from derivatives of cholesterol that act like estrogen, stoking cancer growth.

But a paradox emerged for estrogen-negative breast cancers. These cancers are not dependent on estrogens, but high cholesterol is still associated with worse disease, suggesting a different mechanism might be at work.

In the current study using cancer cell lines and mouse models, the Duke researchers found that migrating cancer cells gobble cholesterol in response to stress. Most die.

But in the what-doesn’t-kill-you-makes-you-stronger motif, those that live emerge with a super-power that makes them able to withstand ferroptosis, a natural process in which cells succumb to stress. These stress-impervious cancer cells then proliferate and readily metastasize.

The process appears to be used not only by ER-negative breast cancer cells, but other types of tumors, including melanoma. And the mechanisms identified could be targeted by therapies.

“Unraveling this pathway has highlighted new approaches that may be useful for the treatment of advanced disease,” McDonnell said. “There are contemporary therapies under development that inhibit the pathway we’ve described. Importantly, these findings yet again highlight why lowering cholesterol -- either using drugs or by dietary modification -- is a good idea for better health.”

 

Drinking green tea may be protective against Alzheimer disease

Anhui Agricultural University, August 23, 2021

The following information was released by the Chinese Academy of Sciences:

Chinese scientists have found that drinking green tea may help prevent Alzheimer's disease, Science and Technology Daily reported Monday.

With population aging deepening, neurodegenerative diseases, including Alzheimer's disease, are showing rapid high incidence rates.

Scientists from Anhui Agricultural University and the University of Science and Technology of China have revealed that green tea could help reduce synaptic damage and improve learning and memory.

The study provides a theoretical basis for revealing the mechanism of preventing Alzheimer's disease by drinking tea and its further application.

The study was recently published in the journal Molecular Nutrition and Food Research. 

 

 

Effects of one month of Common Yoga Protocol practice appear to be mediated by the angiogenic and neurogenic pathway: A pilot study

Post Graduate Institute of Medical Education and Research (India), August 19, 2021

 

To examine the molecular effects of mindful activities such as yoga and meditation. Common Yoga Protocol includes asanas, pranayama and meditation practice. Markers of angiogenesis and neurogenesis were analyzed before and after one month of Common Yoga Protocol practice in healthy adults.

Study participants

64 healthy individuals within the age of 18–60 years were recruited for this one month yoga intervention study. The participants were assessed for biochemical parameters including Fasting Sugar and Lipid profile. The molecular markers of neurogenesis (i.e. Brain derived Neurotropic Factor, BDNF) and Angiogenesis (i.e. Vascular Endothelial Growth Factor, VEGF and Angiogenin) along with Amyloid β (marker related to neuro-degenerative diseases) were assessed. All the assessments were made at baseline and after one month of the intervention.

Results

After one month of CYP practice High Density Lipoprotein (HDL) levels increased significantly (p