Changing Your Diet Can Add 10 Years to Your Life

Everyone wants to live longer. And we’re often told that the key to doing this is making healthier lifestyle choices, such as exercising, avoiding smoking and not drinking too much alcohol. Studies have also shown that diet can increase lifespan.

This article is a repost which originally appeared on ThePrint
Laura Brown - February 20, 2022
Edited for content and readability - Images sourced from Pexels 
Study Source:

Our Takeaways:

  • An optimal diet includes more legumes (beans, peas and lentils), whole grains (oats, barley and brown rice) and nuts, and less red and processed meat.
  • Gains from changing from a western diet to the optimal diet are largest if the diet changes start early in life.
  • Eating the optimal diet from age 20 would increase life expectancy by more than a decade for women and men from the US, China and Europe.
  • At age 60, life expectancy is increased by eight years. At age 80, life expectancy is increased by almost three and a half years.

new study has found that eating healthier could extend lifespan by six to seven years in middle-aged age adults, and in young adults, could increase lifespan by about ten years.

The researchers brought together data from many studies that looked at diet and longevity, alongside data from the Global Burden of Disease study, which provides a summary of population health from many countries. Combining this data, the authors were then able to estimate how life expectancy varied with continuous changes in intake of fruit, vegetables, whole grains, refined grains, nuts, legumes, fish, eggs, dairy, red meat, processed meat and sugary drinks.

The authors were then able to produce an optimal diet for longevity, which they then compared with the typical western diet – which mostly contains high amounts of processed foods, red meat, high-fat dairy products, high-sugar foods, pre-packed foods and low fruit and vegetable intake. According to their research, an optimal diet included more legumes (beans, peas and lentils), whole grains (oats, barley and brown rice) and nuts, and less red and processed meat.

The researchers found that eating an optimal diet from age 20 would increase life expectancy by more than a decade for women and men from the US, China and Europe. They also found that changing from a western diet to the optimal diet at age 60 would increase life expectancy by eight years. For 80-year-olds, life expectancy could increase by almost three and a half years.

But given it isn’t always possible for people to completely change their diet, the researchers also calculated what would happen if people changed from a western diet to a diet that was halfway between the optimal diet and the typical western diet. They found that even this kind of diet – which they called a “feasibility approach diet” – could still increase life expectancy for 20-year-olds by just over six years for women and just over seven years for men.

These results show us that making long-term diet changes at any age may have substantial benefits to life expectancy. But the gains are largest if these changes start early in life.

Full picture?

The life expectancy estimates this study makes come from the most thorough and recent meta-analyses (a study that combines the results of multiple scientific studies) on diet and mortality.

While meta-analyses are, in many cases, the best evidence because of the amount of data analysed, they still produce assumptions with the data, which may cause important differences between studies to be ignored. It’s also worth noting that the evidence for reducing consumption of eggs and white meat was of a lower quality than the evidence they had for whole grains, fish, processed meats and nuts.

There are also a few things the study didn’t take into account. First, to see these benefits, people needed to make changes to their diet within a ten-year period. This means it’s uncertain if people may still see benefits to their lifespan if they make changes to their diet over a longer period of time. The study also didn’t take past ill-health into account, which can affect life expectancy. This means that the benefits of diet on life expectancy only reflect an average and may be different for each person depending on a variety of other factors, such as ongoing health issues, genetics and lifestyle, such as smoking, drinking alcohol and exercise.

But the evidence the researchers looked at was still robust and drawn from many studies on this subject. These findings also align with previous research which has shown that modest but long-term improvements to diet and lifestyle can have significant health benefits – including longevity.

It’s not yet entirely clear all the mechanisms that explain why diet can improve lifespan. But the optimal diet that the researchers uncovered in this study includes many foods that are high in antioxidants. Some research in human cells suggests that these substances may slow or prevent damage to cells, which is one cause of ageing. However, research in this area is still ongoing, so it’s uncertain whether antioxidants that we consume as part of our diet will have the same effect. Many of the foods included within this study also have anti-inflammatory properties, which may also delay the onset of various diseases – and the ageing process.

Of course, changing your diet completely can be difficult. But even introducing some of the foods shown to increase longevity may still have some benefit.

Calorie Restriction That Could Be Harnessed to Extend Healthy Lifespan in Humans

Decades of research has shown that limits on calorie intake by flies, worms, and mice can enhance life span in laboratory conditions. But whether such calorie restriction can do the same for humans remains unclear. Now a new study led by Yale researchers confirms the health benefits of moderate calorie restrictions in humans — and identifies a key protein that could be harnessed to extend health in humans.

This article is a repost which originally appeared on SciTechDaily
Yale University - February 20, 2022
Edited for content and readability - Images sourced from Pexels 
Source: DOI: 10.1126/science.abn6576

Our Takeaways:

  • The study observed the impact of calorie restriction to the immune and metabolic systems.
  • The thymus was analyzed – This is a gland that sits above the heart and produces T cells, a type of white blood cell and a part of the immune system. The thymus ages at a faster rate than other organs.
  • Results found that the thymus glands in participants with limited calorie intake had less fat and greater functionality after two years of calorie restriction.
  • Calorie restriction also reduced a specific protein gene PLA2G7 (a gene that impacts inflammation). Suppressing this gene in a different study protected aged mice from inflammation.

The research was based on results from the Comprehensive Assessment of Long-term Effects of Reducing Intake of Energy (CALERIE) clinical trial, the first controlled study of calorie restriction in healthy humans. For the trial, researchers first established baseline calorie intake among more than 200 study participants. The researchers then asked a share of those participants to reduce their calorie intake by 14% while the rest continued to eat as usual, and analyzed the long-term health effects of calorie restriction over the next two years.

The overall aim of the clinical trial was to see if calorie restriction is as beneficial for humans as it is for lab animals, said Vishwa Deep Dixit, the Waldemar Von Zedtwitz Professor of Pathology, Immunobiology, and Comparative Medicine, and senior author of the study. And if it is, he said, researchers wanted to better understand what calorie restriction does to the body specifically that leads to improved health.

Since previous research has shown that calorie restriction in mice can increase infections, Dixit also wanted to determine how calorie restriction might be linked to inflammation and the immune response.

“Because we know that chronic low-grade inflammation in humans is a major trigger of many chronic diseases and, therefore, has a negative effect on life span,” said Dixit, who is also director of the Yale Center for Research on Aging. “Here we’re asking: What is calorie restriction doing to the immune and metabolic systems and if it is indeed beneficial, how can we harness the endogenous pathways that mimic its effects in humans?”

Dixit and his team started by analyzing the thymus, a gland that sits above the heart and produces T cells, a type of white blood cell and an essential part of the immune system. The thymus ages at a faster rate than other organs. By the time healthy adults reach the age of 40, said Dixit, 70% of the thymus is already fatty and nonfunctional. And as it ages, the thymus produces fewer T cells. “As we get older, we begin to feel the absence of new T cells because the ones we have left aren’t great at fighting new pathogens,” said Dixit. “That’s one of the reasons why elderly people are at greater risk for illness.”

For the study, the research team used magnetic resonance imaging (MRI) to determine if there were functional differences between the thymus glands of those who were restricting calories and those who were not. They found that the thymus glands in participants with limited calorie intake had less fat and greater functional volume after two years of calorie restriction, meaning they were producing more T cells than they were at the start of the study. But participants who weren’t restricting their calories had no change in functional volume.

“The fact that this organ can be rejuvenated is, in my view, stunning because there is very little evidence of that happening in humans,” said Dixit. “That this is even possible is very exciting.”

With such a dramatic effect on the thymus, Dixit and his colleagues expected to also find effects on the immune cells that the thymus was producing, changes that might underlie the overall benefits of calorie restriction. But when they sequenced the genes in those cells, they found there were no changes in gene expression after two years of calorie restriction.

This observation required the researchers to take a closer look, which revealed a surprising finding: “It turns out that the action was really in the tissue microenvironment not the blood T cells,” Dixit said.

Dixit and his team had studied adipose tissue, or body fat, of participants undergoing calorie restriction at three time points: at the beginning of the study, after one year, and after two. Body fat is very important, Dixit said, because it hosts a robust immune system. There are several types of immune cells in fat, and when they are aberrantly activated, they become a source of inflammation, he explained.

“We found remarkable changes in the gene expression of adipose tissue after one year that were sustained through year two,” said Dixit. “This revealed some genes that were implicated in extending life in animals but also unique calorie restriction-mimicking targets that may improve metabolic and anti-inflammatory response in humans.”

Recognizing this, the researchers then set out to see if any of the genes they identified in their analysis might be driving some of the beneficial effects of calorie restriction. They honed in on the gene for PLA2G7 — or group VII A platelet activating factor acetylhydrolase — which was one of the genes significantly inhibited following calorie restriction. PLA2G7 is a protein produced by immune cells known as macrophages.

This change in PLA2G7 gene expression observed in participants who were limiting their calorie intake suggested the protein might be linked to the effects of calorie restriction. To better understand if PLA2G7 caused some of the effects observed with calorie restriction, the researchers also tracked what happened when the protein was reduced in mice in a laboratory experiment.

“We found that reducing PLA2G7 in mice yielded benefits that were similar to what we saw with calorie restriction in humans,” said Olga Spadaro, a former research scientist at the Yale School of Medicine and lead author of the study. Specifically, the thymus glands of these mice were functional for a longer time, the mice were protected from diet-induced weight gain, and they were protected from age-related inflammation.

These effects occurred because PLA2G7 targets a specific mechanism of inflammation called the NLRP3 inflammasome, researchers said. Lowering PLA2G7 protected aged mice from inflammation.

“These findings demonstrate that PLA2G7 is one of the drivers of the effects of calorie restriction,” said Dixit. “Identifying these drivers helps us understand how the metabolic system and the immune system talk to each other, which can point us to potential targets that can improve immune function, reduce inflammation, and potentially even enhance healthy lifespan.”

For instance, it might be possible to manipulate PLA2G7 and get the benefits of calorie restriction without having to actually restrict calories, which can be harmful for some people, he said.

“There’s so much debate about what type of diet is better — low carbohydrates or fat, increased protein, intermittent fasting, etc. — and I think time will tell which of these are important,” said Dixit. “But CALERIE is a very well-controlled study that shows a simple reduction in calories, and no specific diet, has a remarkable effect in terms of biology and shifting the immuno-metabolic state in a direction that’s protective of human health. So from a public health standpoint, I think it gives hope.”

David Sinclair: Extending the Human Lifespan Beyond 100 Years | Lex Fridman Podcast

David Sinclair is a geneticist at Harvard and author of Lifespan.

This Podcast is a repost which originally appeared on
Podcast notes are a repost which originally appeared on PodcastNotes
Lex Fridman Podcast #189 with David Sinclair - June 6, 2021
Edited for content and readability - Images sourced from Pexels

Key Takeaways

  • Wearables have the potential to revolutionize medicine
  • The goal is doctors being able to look at a dashboard of our body based on swabs, blood tests, and biosensors and make real-time, tailored recommendations
  • Top causes of aging: broken chromosomes, cell stress, smoking
  • Lifestyle methods to slow aging: fasting (skip 1-2 meals per day), eat more vegetables and less red meat, exercise, get good quality sleep (quality more important than quantity)


Dr. David Sinclair (@davidsinclair) is a biologist, professor of genetics at Harvard, author, and expert on aging and longevity. His research and biotech companies focus on understanding why we age and how to slow its effects.

In this episode of the Lex Fridman Podcast, Lex and guest David Sinclair discuss the determinants of why we age, solving aging, the trend of wearables and tracking health data, artificial intelligence, social perspectives of lifespan , and death, and lifestyle factors to improve lifespan.

Host: Lex Fridman (@lexfridman)

Book: Lifespan: Why We Age and Why We Don’t Have To by David Sinclair

Artificial Intelligence & Immortality

  • We live in a time we can leverage data to have the pieces of the life of people we can gather using technology, beyond just written books
  • AI makes it possible to bring back people that we love in some way and in essence achieve immortality
  • AI can be used to build experience, thoughts, speech
  • AI uses in aging: generate biological clocks, predict protein folding, assemble genomes, predict longevity in mouse in response to stimuli, diagnosing a virus

David Sinclair Interest And Predictions On Wearables

  • Wearables represent the merging of machines and humans  
  • Wearables help us collect biological data about our bodies
  • We can use data to keep ourselves in optimal shape
  • “Picture a future where you’re monitored constantly so you wouldn’t have a heart attack, you’d know that was coming.” – David Sinclair
  • It’s feasible that wearables and similar technology will indicate what antibiotic or medication to take, what to eat, etc. – and augment physicians who would just need to sign off on the protocol
  • COVID-19 accelerated biological technologies & medical advances
  • There will be day doctor’s use wearable technology to send patients home for monitoring instead of keeping them in the hospital
  • Wearables will revolutionize medicine – it can collect data which can be used to predict sickness, diagnose disease


  • InsideTracker: David Sinclair co-founded a company that creates personalized and actionable plans to help people optimize their bodies through nutrition, supplements, and lifestyle
  • Connects scientific papers to individual data and make recommendations for lifestyle
  • InsideTracker leverages hundreds of thousands of human data points and thousands of scientific articles to create a formula of what works and what doesn’t for your body
  • Recommendation of food and nutrition was better than leading drug at treating type 2 diabetes
  • Soon, the current model of medicine is going to outdated as machines and data will know us better than our doctor
  • “We wouldn’t drive a car without a dashboard so why would doctors do the same?” – David Sinclair

How And Why We Age

  • Aging is both a feature and bug of evolution
  • We only need to live as long as we need to in order to replace ourselves – some breed slowly and build a body that lasts, some breed quickly and die quickly
  • We can do better at aging
  • Hallmarks of aging include: loss of telomeres, senescent cells, loss of energetics
  • Defining factor of aging: preservation of information and loss of entropy
  • “Loss of information in our bodies is a root cause of aging.” – David Sinclair
  • We have information regulator genes in our bodies – upregulation could preserve health
  • Information in cells = DNA and epigenome
    • DNA is usually intact in animals and humans over time
    • Epigenome: regulators of genetic information
  • Question of importance: is there a repository of information in the body to restore from?
  • Antagonistic pleiotropy: a system built to keep us alive when we’re young but has damaging effects later in life
  • Causes of aging: (1) broken chromosomes and (2) cell stress – smoking also dramatically accelerates biological age
    • It’s hard to repair something that’s constantly breaking: we have 1000 chromosome breaks per day – the break is recognized by proteins and is usually fixed but not always
  • You can slow down aging using three embryonic genes to reset the age of tissues to a certain point – but if you don’t do it right it can cause tumors  

Data Sharing In Biology

  • “We’re living through what’s going to be seen as one of the biggest revolutions in human health through the gathering of data about our bodies.” – David Sinclair
  • Ultimately, we’re all going to be monitored
  • There will be a reversal where blamed will be assigned for not collecting data
  • Decisions are made based on very few tests when we have the opportunity to collect more
  • Consumer health is going in the direction of the patient having access to better data than the doctor (through private lab tests, biotech companies, etc.)
  • Doctors are becoming excited and interested about seeing and using privately collected patient data to make more informed decisions
  • The U.S. currently spends 17% of GDP on healthcare – we can save money by monitoring using wearables and prevention
  • Ideally, we can create a system where we can share data as we’d like and keep what we wouldn’t

Lifestyle Methods To Slow Aging

  • Fasting is one of the oldest ways to improve health – we need to optimize how long and the frequency
  • “If there’s one thing I can recommend to anybody to slow down aging it’s to skip a meal or two a day.” – David Sinclair
  • Note: David Sinclair is a big fan of one meal a day; the carnivore diet has made Lex feel really good
  • When you eat seems to be more important than what you eat
  • Data says plant-based foods are better than meat-based foods
    • People who live longer tend to eat Mediterranean diets with little red meat
    • High meat consumption stimulates mTor
    • Could take rapamycin to counteract effects of meat
    • Meat produces immediate health benefits (muscle, energy) but potentially at the expense of long term effects
  • Eat a diet full of leafy greens, avoid spikes in sugar, possibly explore supplementing with resveratrol
  • Exercise clearly extends longevity
  • You don’t need much exercise to get great benefit – exercise aerobically a few times per week (even 10 minutes) and lift weights a few times per week
  • Sleep is critical for longevity to avoid premature aging and adverse health outcomes
  • Sleep quality seems to matter more than quantity
  • The brain is the center for longevity so we have to take care of stress levels, mental health

Data Collection Methods

  • We’ll likely work to moving away from blood draws for data
  • Currently: swab and ship to the lab to test hormones, stress levels, blood glucose, etc.
  • In the next 10 years: spit on paper and stick in a machine for analysis
  • Home tests are really easy and scalable if they can become democratized (price reduced)

Realistic Goals Of Lifespan

  • If you start eating cleaner in your 20s, that has been shown to improve lifespan in animal models
  • If you are in your 20s, aim to reach 100
  • There’s no maximum limit to human lifespan

Death & Denial

  • We seem to draw meaning from life being rooted in our existence – most of us find it distressing to face our own mortality
  • All living beings have evolved to want to live and survive
  • It’s possible we evolve to naturally deny aging because we need to use our energy and focus for innovation and life instead of death
  • It might be easier to be lazy if you are immortal

Note: Wearable Oura ring was referred to multiple times throughout the show

Researchers discover a wound-healing repair in gut diseases

An international team led by the Case Western Reserve University School of Medicine has discovered novel properties of the protein Gasdermin B that promotes repair of cells lining the gastrointestinal tract in people with chronic inflammatory disorders like Crohn’s disease and ulcerative colitis.

This article is a repost which originally appeared on ScienceDaily

Case Western Reserve University - February 7, 2022
Edited for content and readability - Images sourced from Pexels 
Source: DOI: 10.1016/j.cell.2021.12.024

Our Takeaways:

  • Gasdermins are a type of proteins that cause cell death
  • Gasdermin B is an exception – instead it keeps the gastrointestinal tract healthy
  • Future therapies investigating Gasdermin B could produce effective wound-healing of the lungs, skin and other organs

The new findings, recently published in the journal, Cell, are significant because the impact of Gasdermin B (GSDMB) on healing epithelium — a type of body tissue that lines the organs that have direct contact with the external environment — will play a key role in research on wound formation and designing novel therapeutics to enhance wound repair, said Theresa Pizarro, lead study author and the Louis Pillemer Professor of Experimental Pathology at the School of Medicine. In addition to medical school colleagues on campus, researchers included scientists from Cleveland Clinic, Texas, England and Greece.

Gasdermin B

Gasdermins are a family of proteins known to cause pyroptosis — a type of cell death usually triggered by infections and inflammation that contributes to conditions like ulcerative colitis and Crohn’s disease.

Within that protein family, Gasdermin B (GSDMB), unlike other gasdermin proteins, doesn’t cause pyroptosis, especially in epithelial cells, but instead contributes to keeping the gastrointestinal tract healthy — a significant discovery for the development of future therapeutic treatments.

Previous research has shown that individuals carrying genetic variations of Gasdermin B have an increased risk of developing inflammatory disorders like asthma or inflammatory bowel disease (IBD).

“Little was known regarding the mechanisms of how this occurred,” Pizarro said. “In our studies, we uncovered the functional consequences of these GSDMB genetic variants.”

“So, although IBD patients may produce higher levels of GSDMB when they have disease flares,” she said, “the GSDMB protein produced by the genetic variants interferes with the ability of epithelial cells to regenerate and form a healthy barrier critical to healing, for example, in ulcers of patients with ulcerative colitis.”

The study

The scientists analyzed samples from Crohn’s disease and ulcerative colitis patients using state-of-the-art techniques, such as single-cell RNA sequencing, CRISPR/Cas9 and epithelial organoid cultures. Results confirmed substantial increases of GSDMB in biopsies of those with IBD, particularly ulcerative colitis, when compared to levels of GSDMB found in healthy individuals.

The findings unexpectedly showed the lack of epithelial cell death due to GSDMB; instead, this increased level led to:

  • Proliferation, or the growth of new cells;
  • Migration, or the movement of cells;
  • And decreased adhesion dynamics — the attractive forces between cells and other surfaces that affect motility.

Together, these processes promote restoration of the epithelial layer and effective wound-healing, Pizarro said.

“Future therapies targeting gasdermin B are not necessarily restricted to IBD or other chronic inflammatory states of the gastrointestinal tract,” Pizarro said, “but also have far-reaching implications for effective wound-healing of the lungs, skin and other organs interfacing with the external environment that require maintenance of an efficient epithelial barrier.”

Pizarro credited “this groundbreaking discovery on the collaborative and concerted efforts from immunologists, gastroenterologists, cell biologists and bioinformaticians from around the world,” including from Oxford University, University of Athens, Baylor College of Medicine, UT Southwestern and her colleagues at Cleveland Clinic Lerner Research Institute and Case Western Reserve.

How mRNA and DNA vaccines could soon treat cancers, HIV, autoimmune disorders and genetic diseases

The idea of using genetic material to produce an immune response has opened up a world of research and potential medical uses far out of reach of traditional vaccines. Deborah Fuller is a microbiologist at the University of Washington who has been studying genetic vaccines for more than 20 years. We spoke to her about the future of mRNA vaccines.

Below are excerpts from that conversation which have been edited for length and clarity.

This article is a repost which originally appeared on The Conversation
Deborah Fuller - January 6, 2022
Edited for content and readability - Images sourced from Pexels 

Our Takeaways:

  • Nucleic acid vaccines are based on the idea that DNA makes RNA and then RNA makes proteins.
  • These vaccines are effective at inducing a T cell response.
  • For cancer, the goal is to make your body better able to recognize the very specific neoantigens the cancer cell has produced and destroy it.
  • For autoimmune disorders, the vaccine would suppress the T Cells to keep the immune system from attacking myelin

How long have gene-based vaccines been in development?

This type of vaccine has been in the works for about 30 years. Nucleic acid vaccines are based on the idea that DNA makes RNA and then RNA makes proteins. For any given protein, once we know the genetic sequence or code, we can design an mRNA or DNA molecule that prompts a person’s cells to start making it.

When we first thought about this idea of putting a genetic code into somebody’s cells, we were studying both DNA and RNA. The mRNA vaccines did not work very well at first. They were unstable and they caused pretty strong immune responses that were not necessarily desirable. For a very long time DNA vaccines took the front seat, and the very first clinical trials were with a DNA vaccine.

But about seven or eight years ago, mRNA vaccines started to take the lead. Researchers solved a lot of the problems – notably the instability – and discovered new technologies to deliver mRNA into cells and ways of modifying the coding sequence to make the vaccines a lot more safe to use in humans.

Once those problems were solved, the technology was really poised to become a revolutionary tool for medicine.

What makes nucleic acid vaccines different from traditional vaccines?

Most vaccines induce antibody responses. Antibodies are the primary immune mechanism that blocks infections. As we began to study nucleic acid vaccines, we discovered that because these vaccines are expressed within our cells, they were also very effective at inducing a T cell response. This discovery really prompted additional thinking about how researchers could use nucleic acid vaccines not just for infectious diseases, but also for immunotherapy to treat cancers and chronic infectious diseases – like HIV, hepatitis B and herpes – as well as autoimmune disorders and even for gene therapy.

How can a vaccine treat cancers or chronic infectious diseases?

T cell responses are very important for identifying cells infected with chronic diseases and aberrant cancer cells. They also play a big role in eliminating these cells from the body.

When a cell becomes cancerous, it starts producing neoantigens. In normal cases, the immune system detects these neoantigens, recognizes that something’s wrong with the cell and eliminates it. The reason some people get tumors is that their immune system isn’t quite capable of eliminating the tumor cells, so the cells propagate.

With an mRNA or DNA vaccine, the goal is to make your body better able to recognize the very specific neoantigens the cancer cell has produced. If your immune system can recognize and see those better, it will attack the cancer cells and eliminate them from the body.

This same strategy can be applied to the elimination of chronic infections like HIV, hepatitis B and herpes. These viruses infect the human body and stay in the body forever unless the immune system eliminates them. Similar to the way nucleic acid vaccines can train the immune system to eliminate cancer cells, they can be used to train our immune cells to recognize and eliminate chronically infected cells.

What is the status of these vaccines?

Some of the very first clinical trials of nucleic acid vaccines happened in the 1990s and were for cancer, particularly for melanoma.

Today, there are a number of ongoing mRNA clinical trials for the treatment of melanoma, prostate cancer, ovarian cancer, breast cancer, leukemia, glioblastoma and others, and there have been some promising outcomes. Moderna recently announced promising results with its phase 1 trial using mRNA to treat solid tumors and lymphoma

There are also a lot of ongoing trials looking at cancer DNA vaccines, because DNA vaccines are particularly effective in inducing T cell responses. A company called Inovio recently demonstrated a significant impact on cervical cancer caused by human papilloma virus in women using a DNA vaccine.

Can nucleic acid vaccines treat autoimmune disorders?

Autoimmune disorders occur when a person’s immune cells are actually attacking a part of the person’s own body. An example of this is multiple sclerosis. If you have multiple sclerosis, your own immune cells are attacking myelin, a protein that coats the nerve cells in your muscles.

The way to eliminate an autoimmune disorder is to modulate your immune cells to prevent them from attacking your own proteins. In contrast to vaccines, whose goal is to stimulate the immune system to better recognize something, treatment for autoimmune diseases seeks to dampen the immune system so that it stops attacking something it shouldn’t. Recently, researchers created an mRNA vaccine encoding a myelin protein with slightly tweaked genetic instructions to prevent it from stimulating immune responses. Instead of activating normal T cells that increase immune responses, the vaccine caused the body to produce T regulatory cells that specifically suppressed only the T cells that were attacking myelin.

Any other applications of the new vaccine technology?

The last application is actually one of the very first things that researchers thought about using DNA and mRNA vaccines for: gene therapy. Some people are born missing certain genes. The goal with gene therapy is to supply cells with the missing instructions they need to produce an important protein.

A great example of this is cystic fibrosis, a genetic disease caused by mutations in a single gene. Using DNA or an mRNA vaccine, researchers are investigating the feasibility of essentially replacing the missing gene and allowing someone’s body to transiently produce the missing protein. Once the protein is present, the symptoms could disappear, at least temporarily. The mRNA would not persist very long in the human body, nor would it integrate into people’s genomes or change the genome in any way. So additional doses would be needed as the effect wore off.

Research has shown that this concept is feasible, but it still needs some work.

Study suggests Vitamin D and fish oil supplements may help prevent autoimmune disease

Taking daily vitamin D and fish oil supplements may help protect older adults from developing autoimmune disorders such as rheumatoid arthritis, psoriasis, thyroid diseases and polymyalgia rheumatica, an inflammatory disease that causes muscle pain and stiffness in the shoulders and hips, a new study found.

This article is a repost which originally appeared on CNN
Sandee LaMotte - January 27, 2022
Edited for content and readability - Images sourced from Pexels 
Source: doi:

Our Takeaways:

  • The body makes vitamin D when the skin is exposed to sunshine, and consuming fortified food and beverages.
  • People (aged 50+) taking 2,000 IU of vitamin D3 for over five years had a 22% lower rate of confirmed autoimmune diagnoses.
  • Taking both vitamin D and omega-3 fatty acid supplements, versus the placebo, decreased autoimmune disease by about 30%.
  • You should always talk to your doctor first before starting a new regimen.

People age 50 and older taking 2,000 IU (International Units) of vitamin D3 for over five years had a 22% lower relative rate of confirmed autoimmune diagnoses, said study author Dr. Karen Costenbader, a professor of medicine at Harvard Medical School in the division of Rheumatology, Inflammation and Immunity and the director of the lupus program at Brigham and Women’s Hospital in Boston.

That dosage is two to three times the recommended daily dose of vitamin D for adults, which is 600 IU for people up to 69 years old and 800 IU for those age 70 and up, according to the National Institutes of Health.

Once people had been taking vitamin D for at least two years, the prevention rate from autoimmune disorders rose to 39%, according to the study, published Wednesday in the journal BMJ.

The study also found a possible link between taking 1,000 milligrams of omega-3 fatty acid (fish oil) and a reduction in autoimmune disorders, but the association was not statistically significant until possible cases of autoimmune disease — not just confirmed cases — were factored into the analysis.However, the study did find that taking both vitamin D and omega-3 fatty acid supplementsversus the placebo alone, decreased autoimmune disease by about 30%.

Vitamin D toxicity

People should not just run out and start popping vitamin D pills to boost their chances of avoiding autoimmune disease, Costenbader warned, as there are significant consequences to taking too much of the supplement.

Unlike water-soluble vitamins, which the body can easily eliminate, vitamin D is stored in the fat cells of the body and can build up to toxic levels, leading to bone pain and kidney damage.Because the body makes vitamin D when the skin is exposed to sunshine, and milk and other foods like cereals are often fortified with vitamin D, many experts say healthy, younger people are not likely to require vitamin D supplements, especially in amounts over the recommended level of 600 IU/day.

Levels do drop in older age, but “I would say everybody should talk to their doctor first before taking 2000 international units of vitamin D on top of whatever else you’re taking,” Costenbader said. “And there are certain health problems such as kidney stones and hyperparathyroidism (a rise in calcium levels), where you really shouldn’t be taking extra vitamin D.”

The body attacks itself

Costenbader’s study analyzed 25,871 men and women age 50 and older who were participating in VITAL, a randomized, double-blind, placebo-controlled research study designed to see whether taking daily dietary supplements of vitamin D3 (2000 IU) or omega-3 fatty acids (1,000 mg of Omacor fish oil) would reduce the risk for developing cancer, heart disease and stroke in people with no prior history of these illnesses.That trial showed no benefits from the extra supplementation in preventing either cardiovascular disease or cancer. Because prior research has shown both vitamin D and omega-3 fatty acids derived from seafood can have a positive effect on inflammation and immunity in autoimmune disorders, Costenbader decided to use the same trial to investigate whether the supplements might prevent such diseases.

Autoimmune disease occurs when the body’s natural defense system suddenly sees normal cells as invaders and begins destroying those cells by mistake. In rheumatoid arthritis, for example, the immune system attacks the lining of joints, creating inflammation, swelling and pain. With psoriasis, overactive T-cells — which are among the body’s best defenders — cause inflammation that creates raised, scaly patches on the skin.In Type 1 diabetes, the body’s defenders destroy the insulin-producing cells of the pancreas. There’s even some evidence to show that inflammation throughout the body might be part of the progression of Type 2 diabetes. Autoimmune disorders can develop at any stage of life but do appear more among older adults, particularly women, Costenbader said.

More research needed

To date, no large randomized clinical trials (considered the gold standard of research) had investigated whether fish oil and vitamin D could actually prevent the development of autoimmune diseases.

“This is the first direct evidence in older adults that taking vitamin D or omega-3 fatty acids — or a combination — for five years reduces autoimmune disease incidence, with more pronounced effect after two years of supplementation,” Costenbader said.At five years into the research, the study could not tease apart which of the 80 or more autoimmune diseases might benefit most from vitamin D and fish oil supplements, Costenbader said, but research is continuing. The study is now in its seventh year, she said. and more data should be released in the future.

How the timing of dinner and genetics affect individuals’ blood sugar control

Eating dinner close to bedtime, when melatonin levels are high, disturbs blood sugar control, especially in individuals with a genetic variant in the melatonin receptor MTNR1B, which has been linked to an elevated risk of type 2 diabetes. The high melatonin levels and food intake associated with late eating impairs blood sugar control in carriers of the MTNR1B genetic risk variant through a defect in insulin secretion

This article is a repost which originally appeared on ScienceDaily
Massachusetts General Hospital - January 25, 2022
Edited for content and readability - Images sourced from Pexels 
Source: DOI: 10.2337/dc21-1314

Our Takeaways:

  • The melatonin receptor-1b gene (MTNR1B) has been linked with an elevated risk of type 2 diabetes.
  • Late dinner timing resulted in lower insulin levels and higher blood sugar levels for the entire group
  • People with the MTNR1B gene had higher blood sugar levels than those without this genetic variant.

Blood sugar control, which is impaired in individuals with diabetes, is affected by various factors — including the timing of meals relative to sleep as well as levels of melatonin, a hormone primarily released at night that helps control sleep-wake cycles. In research published in Diabetes Care, a team led by investigators at Massachusetts General Hospital (MGH), Brigham and Women’s Hospital (BWH) and the University of Murcia in Spain conducted a clinical trial to look for connections between these two factors.

“We decided to test if late eating that usually occurs with elevated melatonin levels results in disturbed blood sugar control,” says senior author Richa Saxena, PhD, a principal investigator at the Center for Genomic Medicine at MGH.

For the randomized crossover study that included 845 adults from Spain, each participant fasted for eight hours and then for the next two evenings had first an early meal and then a late meal relative to their typical bedtime. The investigators also analyzed each participant’s genetic code within the melatonin receptor-1b gene (MTNR1B) because previous research has linked a variant (called the G-allele) in MTNR1B with an elevated risk of type 2 diabetes.

“In natural late eaters, we simulated early and late dinner timing by administering a glucose drink and compared effects on blood sugar control over two hours,” explains Saxena. “We also examined differences between individuals who were carriers or not carriers of the genetic variant in the melatonin receptor.”

The team found that melatonin levels in participants’ blood were 3.5-fold higher after the late dinner. The late dinner timing also resulted in lower insulin levels and higher blood sugar levels. (This connection makes sense because insulin acts to decrease blood sugar levels.) In the late dinner timing, participants with the MTNR1B G-allele had higher blood sugar levels than those without this genetic variant.

“We found that late eating disturbed blood sugar control in the whole group. Furthermore, this impaired glucose control was predominantly seen in genetic risk variant carriers, representing about half of the cohort,” says lead author Marta Garaulet, PhD, a professor of physiology and nutrition in the Department of Physiology at the University of Murcia.

Experiments revealed that the high melatonin levels and carbohydrate intake associated with late eating impairs blood sugar control through a defect in insulin secretion.

“Our study results may be important in the effort towards prevention of type 2 diabetes,” says co-senior author Frank A.J.L. Scheer, PhD, MSc, director of the Medical Chronobiology Program at BWH. “Our findings are applicable to about a third of the population in the industrialized world who consume food close to bedtime, as well as other populations who eat at night, including shift workers, or those experiencing jetlag or night eating disorders, as well as those who routinely use melatonin supplements close to food intake.”

The authors note that for the general population, it may be advisable to abstain from eating for at least a couple of hours before bedtime. “Genotype information for the melatonin receptor variant may further aid in developing personalized behavioral recommendations,” says Saxena. “Notably, our study does not include patients with diabetes, so additional studies are needed to examine the impact of food timing and its link with melatonin and receptor variation in patients with diabetes.”

Men Prone To Worry and Anxiety May Develop Heart Disease and Diabetes Risk Factors at Younger Ages

Middle-aged men who are anxious and worry more may be at greater biological risk for developing heart disease, stroke, and type 2 diabetes, also called cardiometabolic disease, as they get older, according to new research published today in the Journal of the American Heart Association, an open access journal of the American Heart Association.

This article is a repost which originally appeared on SciTechDaily

The American Heart Association - January 24, 2022
Edited for content and readability - Images sourced from Pexels
Source: DOI: 10.1161/JAHA.121.022006

Our Takeaways:

  • Heart disease and Type 2 diabetes developed earlier in life among those who reported more feelings of worry or being overwhelmed.
  • The study suggests that men prone to worry and anxiety may need to pay extra attention to cardiometabolic disease risk factors, such as maintaining a healthy weight and taking blood pressure or cholesterol medicines, if needed.
  • The findings also suggest that treating anxiety disorders may lower cardiometabolic disease risk.

“While the participants were primarily white men, our findings indicate higher levels of anxiousness or worry among men are linked to biological processes that may give rise to heart disease and metabolic conditions, and these associations may be present much earlier in life than is commonly appreciated – potentially during childhood or young adulthood,” said Lewina Lee, Ph.D., lead author of the study, an assistant professor of psychiatry at Boston University School of Medicine, and an investigator and clinical psychologist at the National Center for Posttraumatic Stress Disorder at the U.S. Department of Veterans Affairs, both in Boston.

To track the relationship between anxiety and cardiometabolic disease risk factors over time, the investigators analyzed data on participants in the Normative Aging Study, which is a longitudinal study of aging processes in men, founded at the U.S. Veterans Affairs outpatient clinic in Boston in 1961. The study includes both veterans and non-veterans. This analysis included 1,561 men (97% white), who were an average age of 53 years in 1975. The men completed baseline assessments of neuroticism and worry and did not have cardiovascular disease or cancer at that time. A personality inventory assessed neuroticism on a scale of 0–9. In addition, a worry assessment tool asked how often they worried about each of 20 items, with 0 meaning never and 4 meaning all the time.

“Neuroticism is a personality trait characterized by a tendency to interpret situations as threatening, stressful and/or overwhelming. Individuals with high levels of neuroticism are prone to experience negative emotions – such as fear, anxiety, sadness and anger – more intensely and more frequently,” said Lee. “Worry refers to our attempts at problem-solving around an issue whose future outcome is uncertain and potentially positive or negative. Worry can be adaptive, for example, when it leads us to constructive solutions. However, worry can also be unhealthy, especially when it becomes uncontrollable and interferes with our day-to-day functioning.”

After their baseline assessment, the men had physical exams and blood tests every 3-5 years until they either died or dropped out of the study. The research team used follow-up data through 2015. During follow-up visits, seven cardiometabolic risk factors were measured: systolic (top number) blood pressure; diastolic (bottom number) blood pressure; total cholesterol; triglycerides; obesity (assessed by body mass index); fasting blood sugar levels; and the erythrocyte sedimentation rate (ESR), a marker of inflammation.

A risk factor for cardiometabolic disease was considered in the high-risk range if the test results for the risk factor was higher than the cut-point established by national guidelines, or if the participant was taking any medicines to manage that risk factor (such as cholesterol-lowering medications). Cut points for ESR as a risk factor are not standardized, so the participant was ranked as high-risk if they were in the top 25% of those tested. Each participant was assigned a risk factor count score, one point for each of the seven risk factors classified as high-risk. The men were then stratified based on whether they did or did not develop six or more high-risk factors during the follow-up period.

“Having six or more high-risk cardiometabolic markers suggests that an individual is very likely to develop or has already developed cardiometabolic disease,” said Lee.

The researchers found:

  • Between ages 33 to 65, the average number of cardiometabolic high-risk factors increased by about one per decade, averaging 3.8 risk-factors by age 65, followed by a slower increase per decade after age 65.
  • At all ages, participants with higher levels of neuroticism had a greater number of high-risk cardiometabolic factors.
  • Higher neuroticism was associated with a 13% higher likelihood of having six or more cardiometabolic disease risk factors, after adjusting for demographic characteristics (such as income and education) and family history of heart disease.
  • Higher worry levels were associated with a 10% higher likelihood of having six or more cardiometabolic disease risk factors after adjusting for demographic characteristics.

“We found that cardiometabolic disease risk increased as men aged, from their 30s into their 80s, irrespective of anxiety levels, while men who had higher levels of anxiety and worry consistently had a higher likelihood of developing cardiometabolic disease over time than those with lower levels of anxiety or worry,” Lee said.

The researchers did not have data on whether participants had been diagnosed with an anxiety disorder. Standard evidence-based treatment for anxiety disorders includes psychotherapy or medication, or a combination of the two.

“While we do not know whether treatment of anxiety and worry may lower one’s cardiometabolic risk, anxious and worry-prone individuals should pay greater attention to their cardiometabolic health. For example, by having routine health check-ups and being proactive in managing their cardiometabolic disease risk levels (such as taking medications for high blood pressure and maintaining a healthy weight), they may be able to decrease their likelihood of developing cardiometabolic disease,” said Lee.

It is unclear to what extent the results of this analysis are generalizable to the public since the study participants were all male and nearly all white. In addition, although participants were followed for four decades, they were middle-aged when the study began.

“It would be important for future studies to evaluate if these associations exist among women, people from diverse racial and ethnic groups, and in more socioeconomically varying samples, and to consider how anxiety may relate to the development of cardiometabolic risk in much younger individuals than those in our study,” Lee said.

Proteins could be key to long and healthy life

Developing drugs that target these proteins could be one way of slowing the ageing process, according to the largest genetic study of ageing.

This article is a repost which originally appeared on The University of Edinburgh
The University of Edinburgh - January 24, 2022
Edited for content and readability - Images sourced from Pexels

Our Takeaway:

  • 2 proteins are identified to have significant negative effects across ageing measures.
  • Individuals with raised levels these 2 proteins (LPA & VCAM1), are less likely to live longer lives.
  • High levels of LPA can increase the risk of atherosclerosis. Heart disease and stroke is also possible.
  • VCAM1 helps with blood clotting and the immune response and increases when it has detected an infection.
  • Studies are being done to lower these proteins when elevated.

As we age, our bodies begin to decline after we reach adulthood, which results in age-related diseases and death. This latest research investigates which proteins could influence the ageing process.

Many complex and related factors determine the rate at which we age and die, and these include genetics, lifestyle, environment and chance. The study sheds light on the part proteins play in this process.


Some people naturally have higher or lower levels of certain proteins because of the DNA they inherit from their parents. These protein levels can, in turn, affect a person’s health.

University of Edinburgh researchers combined the results of six large genetic studies into human ageing – each containing genetic information on hundreds of thousands of people,

Among 857 proteins studied, researchers identified two that had significant negative effects across various ageing measures.

People who inherited DNA that causes raised levels of these proteins were frailer, had poorer self-rated health and were less likely to live an exceptionally long life than those who did not.

Protein roles

The first protein, called apolipoprotein(a) (LPA), is made in the liver and thought to play a role in clotting. High levels of LPA can increase the risk of atherosclerosis – a condition in which arteries become clogged with fatty substances. Heart disease and stroke is a possible outcome.

The second protein, vascular cell adhesion molecule 1 (VCAM1), is primarily found on the surfaces of endothelial cells – a single-cell layer that lines blood vessels. The protein controls vessels’ expansion and retraction – and function in blood clotting and the immune response.

Levels of VCAM1 increase when the body sends signals to indicate it has detected an infection, VCAM1 then allows immune cells to cross the endothelial layer (a thin membrane that lines the inside of the heart and blood vessels), as seen for people who have naturally low levels of these proteins.

Improved ageing

The researchers say that drugs used to treat diseases by reducing levels of LPA and VCAM1 could have the added benefit of improving quality and length of life.  

One such example is a clinical trial that is testing a drug to lower LPA as a way of reducing the risk of heart disease.

There are currently no clinical trials involving VCAM1, but studies in mice have shown how antibodies lowering this protein’s level improved cognition during old age.

The findings have been published in the journal Nature Aging.

Drinking Coffee: Study Finds Both Beneficial and Harmful Short-Term Health Effects

This article is a repost which originally appeared on SciTechDaily
Edited for content and readability - Images sourced from Pexels

Key Points:

  • A randomized trial to study caffeinated coffee consumption among 100 volunteers for two weeks found both potentially beneficial and harmful short-term health consequences of drinking coffee.
  • When participants were randomly assigned to drink coffee, they were more physically active, yet they also had an increased number of abnormal heartbeats and slept less compared to when they were randomly assigned to avoid all caffeine.

Drinking caffeinated coffee appears to have both beneficial and harmful short-term health effects: increased abnormal heartbeats, increased physical activity, and reduced sleep duration, according to research that was presented at American Heart Association’s Scientific Sessions 2021.

“Coffee is the most commonly consumed beverage in the world, yet its health effects remain uncertain,” said study author Gregory Marcus, M.D., M.A.S., associate chief of cardiology for research and endowed professor of atrial fibrillation research at the University of California, San Francisco. “While the majority of long-term observational studies have suggested multiple potential benefits of drinking coffee, this is the first randomized trial to investigate the real-time, physiologic consequences of coffee consumption.”

Marcus and colleagues enrolled 100 adult volunteers, and they were assigned to wear continuously recording ECG devices (to track heart rhythm), wrist-worn devices to track physical activity and sleep; and continuous glucose monitors to track blood sugar levels for two weeks. The participants were an average age of 38 years, 51% were women and 48% were white. Researchers also obtained DNA saliva samples from the participants to assess genetic variants that may affect caffeine metabolism.

Participants were then randomly assigned to either avoid or consume coffee for no more than two consecutive days each for 14 consecutive days. Coffee and espresso consumption were recorded in real time via a “time stamp button” on the ECG monitor, and researchers tracked trips to coffee shops with geotracking. In addition, participants completed daily questionnaires to detail how much coffee they had consumed every morning.

The analysis found that coffee consumption was associated with a 54% increase in premature ventricular contractions, a type of abnormal heartbeat originating in the lower heart chambers reported to feel like a skipped heartbeat. In contrast, drinking more coffee was associated with fewer episodes of supraventricular tachycardia, an abnormally rapid heart rhythm arising from the upper heart chambers.

Consuming coffee was consistently associated with more physical activity as well as less sleep. Specifically:

  • Participants who consumed coffee logged more than 1,000 additional steps per day compared to days when they did not drink coffee.
  • On the days participants drank coffee, they had 36 fewer minutes of sleep per night according to their Fitbit devices.
  • Drinking more than one coffee drink more than doubled the number of irregular heartbeats arising from the heart’s lower chambers.
  • Each additional cup of coffee consumed was associated with nearly 600 more steps per day and 18 fewer minutes of sleep per night.
  • There were no differences in continuously recorded glucose measured when the study participants consumed versus avoided coffee.

These findings were corroborated by analyses of adherence to their randomization assignment and amplified when more versus less coffee was consumed.

“More physical activity, which appears to be prompted by coffee consumption, has numerous health benefits, such as reduced risks of Type 2 diabetes and several cancers, and is associated with greater longevity,” Marcus said. “On the other hand, reduced sleep is associated with a variety of adverse psychiatric, neurologic and cardiovascular outcomes. More frequent abnormal heartbeats from the upper heart chambers influence risk of atrial fibrillation, and more frequent abnormal beats from the lower chambers, or ventricles, increase the risk of heart failure. These results highlight the complex relationship between coffee and health.”

The study participants with genetic variants associated with faster caffeine metabolism exhibited more abnormal heart beats originating in the ventricles, or PVCs, when more caffeinated coffee was consumed. The slower an individual metabolized caffeine based on their genetics, the more sleep they lost when they drank caffeinated coffee.

The investigators also sought to determine if changes in exercise or sleep influenced coffee’s effects on abnormal heart rhythms, and no such association was identified.

Marcus noted that because coffee was randomly assigned to the study participants, cause-and-effect can be inferred. These observations were made during repeated assessments of days when coffee was consumed versus when it was not for each study participant, eliminating concerns regarding differences in individual-level characteristics as an explanation for these results.