Fruit and vegetable intake has been associated with a reduced risk of cardiovascular disease. Quercetin and kaempferol are among the most ubiquitous polyphenols in fruit and vegetables. Most of the quercetin and kaempferol in plants is attached to sugar moieties rather than in the free form. The types and attachments of sugars impact bioavailability, and thus bioactivity.
This article aims to review the current literature on the bioavailability of quercetin and kaempferol from food sources and evaluate the potential cardiovascular effects in humans. Foods with the highest concentrations of quercetin and kaempferol in plants are not necessarily the most bioavailable sources. Glucoside conjugates which are found in onions appear to have the highest bioavailability in humans. The absorbed quercetin and kaempferol are rapidly metabolized in the liver and circulate as methyl, glucuronide, and sulfate metabolites. These metabolites can be measured in the blood and urine to assess bioactivity in human trials.
The optimal effective dose of quercetin reported to have beneficial effect of lowering blood pressure and inflammation is 500 mg of the aglycone form. Few clinical studies have examined the potential cardiovascular effects of high intakes of quercetin- and kaempferol-rich plants. However, it is possible that a lower dosage from plant sources could be effective due to of its higher bioavailability compared to the aglycone form. Studies are needed to evaluate the potential cardiovascular benefits of plants rich in quercetin and kaempferol glycoside conjugates.
A key question in biology is to understand why and how we age. Alongside this, the unprecedented gain in the average lifespan in humans, since the mid-twentieth century, has dramatically increased both the number of older people and their proportion in the population. This demographic phenomenon is changing our societal make-up, from only ~130 million being 65 years or older (~5% of the world population) in 1950, to a predicted ~1.6 billion people (~17%) by 2050.
However, the success in reducing mortality has not been matched with a reduction in chronic disease. This leads to the undesirable outcome of many years of this prolonged lifespan being spent in ill health, with an associated massive health care burden. Increasing the productivity and reducing the disease affliction in these extended years would be clearly beneficial for both the individual and society.
This aim of maximizing the “healthspan” makes obtaining accurate measures of aging-related pathology essential, to gauge its speed, decipher the changes that occur, and potentially unlock how aging acts as a disease risk factor. There is considerable population variation in the rate at which people visibly age as well as become impaired by age-related frailty and disease. Measurement of this relative “biological” aging may allow pre-emptive targeted health-promoting interventions, perhaps in a personalized and disease-specific fashion. It would also aid in testing interventions that attempt to modulate the aging process.
The cellular and molecular hallmarks of aging include changes associated with cell senescence, dysregulated nutrient sensing, and stem cell exhaustion, among others. Therefore, many biological measures, such as p16ink4a tissue levels, circulating CRP, creatinine, and fasting glucose, as well as telomere length all correlate with aging.
In this decade, we have discovered the remarkable power of epigenetic changes to estimate an individual’s age. Epigenetics encapsulates the chemical modifications and packaging of the genome that influence or indicate its activity, with strict definitions requiring inheritance through mitotic cell division. Observations of age impacting on this mechanism have been reported for more than 50 years and suggested a role in age-related disease.
However, the association between epigenetic modifications and age became most starkly apparent with the arrival of the first high-throughput arrays measuring DNA methylation. These high-resolution data enabled the construction of extremely accurate age estimators, termed “Epigenetic” or “DNA methylation clocks”.
FULL TEXT: BMC Genome Biology
Prime editing (of genes)
This video will look at the new technology to perform precise genome editing, prime editing and will look at how the method works and how it differs from the canonical CRISPR-Cas9 system.