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The past few years have brought lots of good news for anyone who considers coffee a vice. Scientists have discovered that various compounds in coffee can help fight a number of diseases including Alzheimer’s, and now a new study is putting even more weight behind the notion that coffee is very good for you.

The work, which was published in Proceedings of the National Academy of Sciences, suggests that not only does coffee battle Parkinson’s but also another incurable brain disease called Lewy body dementia. Conducted by scientists at Rutgers, the study points to the combined effects of caffeine and a fatty acid present in coffee called EHT as potentially playing key roles in disease fighting.

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TMAO (trimethylamine N-oxide) — a gut bacteria byproduct formed during digestion—can lead to the development of cardiovascular disease, including heart attacks and strokes. TMAO is produced when gut bacteria digest choline, lecithin and carnitine, nutrients that are abundant in animal products such as red meat and liver and other animal products.


In concurrent studies, Cleveland Clinic researchers have uncovered new mechanisms that demonstrate why and how regularly eating red meat can increase the risk of heart disease, and the role gut bacteria play in that process.

The research, led by Stanley Hazen, M.D., Ph.D., builds upon showing TMAO (trimethylamine N-oxide) — a gut bacteria byproduct formed during digestion—can lead to the development of cardiovascular disease, including heart attacks and strokes. TMAO is produced when gut bacteria digest choline, lecithin and carnitine, nutrients that are abundant in animal products such as and liver and other animal products.

In a new dietary intervention study published today in the European Heart Journal, the researchers found that a rich in red meat as the primary protein source significantly increases circulating TMAO levels, compared to diets with white meat or non-meat as protein sources. The study showed chronic red meat consumption enhanced the production of TMAO by gut microbes and reduced the kidneys’ efficiency of expelling it. Both enhanced production and reduced elimination caused by a red meat diet contribute to elevation in TMAO levels, which has been linked to the development of atherosclerosis and heart disease complications.

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Of the 10 flavonoids tested, fisetin was the most potent senolytic. Acute or intermittent treatment of progeroid and old mice with fisetin reduced senescence markers in multiple tissues, consistent with a hit-and-run senolytic mechanism.


The natural product fisetin has senotherapeutic activity in mice and in human tissues. Late life intervention was sufficient to yield a potent health benefit. These characteristics suggest the feasibility to translation to human clinical studies.

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A number of therapies that directly target the aging processes are currently in human trials and could change medicine significantly in the next decade if the results are positive.

What is aging?

Aging is basically the accumulation of damage and errors caused by a collection of varied processes that harm the functions of the body through the accumulation of waste, imperfect repair, the deregulation of cellular processes, the dysfunction of the immune system, chronic inflammation, and other disorders.

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There is increasing evidence that the microbiome contributes to esophageal disease. Diet, especially fiber and fat intake, is a known potent modifier of the colonic microbiome, but its impact on the esophageal microbiome is not well described. We hypothesized that dietary fiber and fat intake would be associated with a distinct esophageal microbiome.

We collected esophageal samples from 47 ambulatory patients scheduled to undergo endoscopy who completed a validated food frequency questionnaire quantifying dietary fiber and fat intake. Using 16S high-throughput sequencing, we determined composition of the esophageal microbiome and predicted functional capacity of microbiota based on fiber and fat intake.

Among all samples, the most abundant phyla were Firmicutes (54.0%), Proteobacteria (19.0%), Bacteroidetes (17.0%), Actinobacteria (5.2%), and Fusobacteria (4.3%). Increasing fiber intake was significantly associated with increasing relative abundance of Firmicutes (p = 0.04) and decreasing relative abundance of Gram-negative bacteria overall (p = 0.03). Low fiber intake was associated with increased relative abundance of several Gram-negative bacteria, including Prevotella, Neisseria, and Eikenella. Several predicted metabolic pathways differed between highest and lowest quartile of fiber intake. Fat intake was associated with altered relative abundance of few taxa, with no alterations at the phylum level and no changes in microbiome functional composition.

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You probably learned two things about mitochondria in high school biology. First, they’re the powerhouses of the cell. Second, you can only inherit them from your mother. But a new study seems to cloud that second point.

A team of researchers from the United States, China, and Taiwan identified three unrelated families with members whose mitochondria contained DNA from both parents. While this discovery could reignite debate about the nature of inheriting mitochondrial DNA, the researchers hope it will open up new ways to treat disease.

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In order to advance innovation and keep pace with the rapidly evolving healthcare industry, the US Food and Drug Administration (FDA) is modernizing the approval process most medical device manufacturers undergo when bringing new products to market.

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D esigner therapies are treatments tailored to a specific disease, and nowhere is the need greater for new therapies than in a group of nervous system disorders, known as “neurodegenerative diseases.”

Many of these diseases are common and well-known, such as Alzheimer’s or Parkinson’s disease. However, some are very rare, genetic disorders that are the consequence of a defective gene. In all these diseases, a mutant protein that misfolds causes the degeneration and death of neurons. One effective therapeutic strategy is to prevent the rogue protein from ever being made.

Spinocerebellar ataxia type 7 (SCA7) is one such disease in which nerves in different parts of the brain, including the eye, degenerate, which leads to blindness and difficulty walking, speaking, and balancing. SCA7 is dominantly inherited — which means that you just need one bad copy of the mutation to cause disease. The disease occurs when a short section of DNA that encodes ataxin-7 gene is erroneously repeated — like a word in a book printed two or three times. In this case, three chemical units of the DNA sequence — C-A-G — are repeated over and over.

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