Eating broccoli is the key to good eyesight and curbing loss of vision, a new study claims.
The green vegetable contains a compound called indole-3-carbinol (I3C).
During tests, researchers have found a highly potent concentration of the property could be used to treat age-related macular degeneration, the leading cause of vision loss.
To reap the benefits, one would have to eat ‘an unreasonable amount of broccoli’, the team at Buck Institute concede – about 10 times the recommended helping.
But the researchers hope their study could lead to the discovery of related molecules to develop targeted treatment for sight-loss.
Eat your way to good eyes: A study claims broccoli contains a key compound that activates a detoxifying receptor protein in the retina.
That receptor protein is crucial to preventing age-related maculur degeneration
It is the latest piece of good press for broccoli: recent studies have also touted the vegetable as preventative treatment for lymphoma, metastatic cancer, breast cancer and prostate cancer.
In eyes, I3C activates AhR, a receptor protein which drives chemical detoxification in the retina.
AhR declines with age, but it is crucial for keeping eyes clear and healthy.
Previous studies show that AhR-deficient mice develop a condition which looks extremely similar to AMD.
Buck faculty and lead author Arvind Ramanathan, PhD, decided to try boosting AhR using broccoli’s I3C.
But he knew there was a challenge – I3C is weak activator of AhR.
So he did a virtual search on a publicly-available database of millions of compounds to find ones with the same properties.
His team found 2,2?-aminophenyl indole (2AI).
2AI has the same chemical makeup as I3C, but it is ten times more potent and would bind to AhR with more strength.
Age-related maculur degeneration (AMD) is the leading cause of vision-loss.
These two images (pictured) demonstrate the impact.
Left is an eye with normal sight.
Right is an eye with AMD ‘2AI prevented cell death in the retinas of mice that were exposed to light stress,’ said Buck faculty and co-senior author Deepak Lamba, MBBS, PhD, who is developing stem-cell based therapies for degenerative eye diseases.
‘Our next step is to study the functional outcomes of treatment with 2AI, something I am eager to do because environmental stress is the major contributor to age-related vision loss.
The study’s results also suggests people should eat foods rich in omega-7 palmitoleic acid, such as nuts, fish, dairy and vegetable oils.
Injecting palmitoleic acid into mice had protective effects on their retinal cells.
Alzheimer’s risk may be detectable from age 18
Researchers have developed a genetic risk score that they say could pinpoint which adults are at risk of developing Alzheimer’s disease decades before symptoms arise.
Researchers suggest a higher polygenic risk score may indicate a higher risk of Alzheimer’s.
Elizabeth C Mormino, PhD of Massachusetts General Hospital in Charlestown, and colleagues reveal how they used the score to identify possible indicators of Alzheimer’s disease (AD) in healthy adults as young as 18.
AD is one of the most devastating and challenging diseases of our time, affecting more than 5 million adults in the United States, with this number expected to triple over the next 30 years.
The study authors note that the pathophysiologic processes of AD are believed to occur for at least a decade before symptoms of the condition appear.
“Given that current clinical trials are testing whether therapies can slow memory and thinking decline among people at risk for the disease, it is critical to understand the influence of risk factors before symptoms are present,” says Mormino.
While the exact causes of AD remain unclear, it is thought that genetics play a role.
For example, studies have shown that people who possess a form of the APOE gene – known as APOE e4 – are at increased risk of the disease.
“In addition to the APOE gene, to date 21 common genetic variants have been associated with AD in large genome-wide association study meta-analyses,” say the authors.
For their study, the researchers created a so-called polygenic risk score.
They did so by analyzing the genomes of 166 adults with dementia and 1,026 adults without dementia.
They developed scores based on whether the adults – who were an average age of 75 – possessed a number of genetic variants associated with increased risk of AD.
The researchers also analyzed the participants for a number of markers of AD, including decline in thinking and memory, volume of the hippocampus – the brain region associated with memory – and clinical progression of AD.
Additionally, the researchers applied the polygenic risk score to 1,322 healthy adults aged 18-35 and assessed the volume of their hippocampus, in order to establish whether there is a link between the two.
Among older adults who were free of dementia, the team found a higher polygenic risk score was an indicator of worse memory and a smaller hippocampus at study baseline; the risk score accounted for 2.
3 percent of the variance in memory and 2 percent of hippocampal volume variance.
Furthermore, during the 3-year study period, the researchers found that a higher polygenic risk score could be associated with increased decline in longitudinal memory and executive function among older adults, as well as greater clinical AD progression.
The team also found the polygenic risk score could be linked to overall clinical progression of AD.
Of 194 older adults who had normal cognitive functioning at study baseline, 15 developed mild cognitive impairment (MCI) or AD over 3 years, while 143 of 332 older participants who had MCI at the start of the study developed AD during the 3-year follow-up.
Overall, the researchers found that each increase in standard deviation of polygenic risk was represented by a 1.
6-times greater risk of clinical AD progression.
Among the younger study participants, the researchers found a higher polygenic risk score could be linked to smaller hippocampal volume; the risk score accounted for around 0.
2 percent of hippocampal volume variance.
The team says this finding indicates that genetic risk for AD is not specific to processes that occur in late.