All People With Blue Eyes Have A Single, Common Ancestor

According to the Cleveland Clinic, up until some 10,000 years ago, it’s believed everyone in the world had brown eyes. Now, an estimated 8-10% of people in the world have blue eyes. How did that come to be? As it turns out, researchers now believe blue eyes all started with a single person who passed on a genetic mutation that spread across the world. In other words, everyone with blue eyes shares a single, common ancestor.

Back in 2008, researchers with the University of Copenhagen examined the exact genetic mutation that resulted in blue eyes all those years ago. Their research was published in the The Journal of Human Genetics. According to Science Daily, the study’s lead author, Professor Hans Eiberg, explained that humans originally had brown eyes, and a gene mutationturned off” the ability to produce brown eyes – resulting in some people having blue eyes. The press release elaborated that the affected gene, the OCA2 gene, regulates brown pigment in the eyes. If the OCA2 gene had been completely destroyed or “turned off” then the affected humans would be without any melanin in their hair, eyes, or skin color (a condition known as albinism). But with the specific mutation, the body has a limited ability to produce melanin in the iris, resulting in a blue iris, rather than a brown iris. The genetic mutation isn’t a positive or negative trait.

Mutations can affect things like freckles, balding patterns, hair color, and more“. “It simply shows that nature is constantly shuffling the human genome, creating a genetic cocktail of human chromosomes and trying out different changes as it does so,” explained Eiberg.

According to the College of Physicians of Philadelphia, researchers studied the mitochondrial DNA of individuals with blue eyes from various countries, such as Jordan, Denmark, and Turkey. The researchers found that over 97% of the blue-eyed people in the study shared a single haplotype – a grouping of genomic variants that are usually inherited. Because of this, researchers believe that the mutation is passed on genetically, meaning that everyone with blue eyes is related.

From this, we can conclude that all blue-eyed individuals are linked to the same ancestor. They inherited the same switch at the same spot in their DNA,” said Eidberg in a press release, shared in EurekaAlerta!,

Source: https://blog.thebreastcancersite.greatergood.com

Viagra Users Are 69% Less Likely to Develop Alzheimer’s

Viagra could be a useful treatment against Alzheimer’s disease, according to a US study. Alzheimer’s disease, the most common form of age-related dementia, affects hundreds of millions of people worldwide. Despite mounting numbers of cases, however, there is currently no effective treatment.

Using a large gene-mapping network, researchers at the Cleveland Clinic integrated genetic and other data to determine which of more than 1,600 Food and Drug Administration-approved drugs could be an effective treatment for Alzheimer’s disease. They gave higher scores to drugs that target both amyloid and tau – two hallmarks of Alzheimer’s – compared with drugs that targeted just one or the other.

US scientists say users of sildenafil – the generic name for Viagra – are 69% less likely to develop the form of dementia than non-users

“Sildenafil, which has been shown to significantly improve cognition and memory in preclinical models, presented as the best drug candidate,” said Dr Feixiong Cheng, the study lead.

Researchers then used a database of claims from more than 7 million people in the US to examine the relationship between sildenafil and Alzheimer’s disease outcomes by comparing sildenafil users to non-users.

They found sildenafil users were 69% less likely to develop Alzheimer’s disease than non-sildenafil users after six years of follow-up. To further explore the drug’s potential effect on Alzheimer’s disease, researchers developed a lab model that showed that sildenafil increased brain cell growth and targeted tau proteins, offering insights into how it might influence disease-related brain changes. Cheng cautioned that the study does not demonstrate a causal relationship between sildenafil and Alzhemer’s disease. Randomised clinical trials involving both sexes with a placebo control were needed to determine sildenafil’s efficacy, he said.

Dr Ivan Koychev, a senior clinical researcher at the University of Oxford, who was not involved in the study, said it was “an exciting development” because “it points to a specific drug which may offer a new approach to treating the condition”.

Prof Tara Spires-Jones, deputy director of the Centre for Discovery Brain Sciences at the University of Edinburgh, said there were several important limitations to consider. “While these data are interesting scientifically, based on this study, I would not rush out to start taking sildenafil as a prevention for Alzheimer’s disease.”

Dr Susan Kohlhaas, director of research at Alzheimer’s Research UK, said: “Being able to repurpose a drug already licensed for other health conditions could help speed up the drug discovery process and bring about life-changing dementia treatments sooner. “Importantly, this research doesn’t prove that sildenafil is responsible for reducing dementia risk, or that it slows or stops the disease. The only way to test this would be in a large-scale clinical trial measuring sildenafil effect against the usual standard of care.”

The findings were published in Nature Aging.

Source: https://www.theguardian.com/

Junk food linked to gut inflammation

Eating a Western diet impairs the immune system in the gut in ways that could increase risk of infection and inflammatory bowel disease, according to a study from researchers at Washington University School of Medicine in St. Louis and Cleveland Clinic.

The study, in mice and people, showed that a diet high in sugar and fat causes damage to Paneth cells, immune cells in the gut that help keep inflammation in check. When Paneth cells aren’t functioning properly, the gut immune system is excessively prone to inflammation, putting people at risk of inflammatory bowel disease and undermining effective control of disease-causing microbes. The findings, published in Cell Host & Microbe, open up new approaches to regulating gut immunity by restoring normal Paneth cell function.

A tiny, 3D model of the intestines formed from anti-inflammatory cells known as Paneth cells (green and red) and other intestinal cells (blue) is seen in the image above. Researchers at Washington University School of Medicine in St. Louis and Cleveland Clinic used such models, called organoids, to understand why a Western-style diet rich in fat and sugar damages Paneth cells and disrupts the gut immune system

Inflammatory bowel disease has historically been a problem primarily in Western countries such as the U.S., but it’s becoming more common globally as more and more people adopt Western lifestyles,” said lead author Ta-Chiang Liu, MD, PhD, an associate professor of pathology & immunology at Washington University. “Our research showed that long-term consumption of a Western-style diet high in fat and sugar impairs the function of immune cells in the gut in ways that could promote inflammatory bowel disease or increase the risk of intestinal infections.”

Paneth cell impairment is a key feature of inflammatory bowel disease. For example, people with Crohn’s disease, a kind of inflammatory bowel disease characterized by abdominal pain, diarrhea, anemia and fatigue, often have Paneth cells that have stopped working.

Source: https://medicine.wustl.edu/