Monthly Archives: November 2021

Stress affects up to 90% of people, and we know it harms our mental and physical well-being.

Stress can impact the activity and function of our genes. It does this via epigenetic changes, which turn on and off certain genes, though it doesnt change the DNA code.

But why do some people respond worse to stress, while others seem to cope under pressure?

Previous research has identified having strong social support and a sense of belonging are robust indicators of physical and mental health.

Social support means having a network you can turn to in times of need. This can come from natural sources such as family, friends, partners, pets, co-workers and community groups. Or from formal sources such as mental health specialists.

My new study, published today in the Journal of Psychiatric Research, shows for the first time that these positive effects are also observed on human genes.

Having supportive social structures buffers and even reverses some of the harmful effects of stress on our genes and health, via the process of epigenetics.

The findings suggest the DNA we are born with is not necessarily our destiny.

Read more: How chronic stress changes the brain and what you can do to reverse the damage

Our genes and our environment contribute to our health.

We inherit our DNA code from our parents, and this doesnt change during our life. Genetics is the study of how the DNA code acts as a risk or protective factor for a particular trait or disease.

Epigenetics is an additional layer of instructions on top of DNA that determines how they affect the body. This layer can chemically modify the DNA, without changing DNA code.

The term epigenetics is derived from the Greek word epi which means over, on top of.

Read more: Explainer: what is epigenetics?

This extra layer of information lies on top of the genes and surrounding DNA. It acts like a switch, turning genes on or off, which can also impact our health.

Epigenetic changes occur throughout our lives due to different environmental factors such as stress, exercise, diet, alcohol, and drugs.

For instance, chronic stress can impact our genes via epigenetic changes that in turn can increase the rate of mental health disorders such as post-traumatic stress disorder (PTSD), depression and anxiety.

New technologies now allow researchers to collect a biological sample from a person (such as blood or saliva) and measure epigenetics to better understand how our genes respond to different environments.

Measuring epigenetics at different times allows us to gain insight into which genes are altered because of a particular environment.

Read more: Extreme stress in childhood is toxic to your DNA

My study investigated both positive and negative factors that drive a persons response to stress and how this changes the epigenetic profiles of genes.

Certain groups of people are more likely to face stress as a part of their routine work, such as emergency responders, medical workers and police officers.

So, my research team and I recruited 40 Australian first year paramedical students at two points in time before and after exposure to a potentially stressful event. The students provided saliva samples for DNA and filled out questionnaires detailing their lifestyle and health at both points in time.

We investigated epigenetic changes before and after exposure to stress, to better understand:

We found stress influenced epigenetics and this in turn led to increased rates of distress, anxiety, and depressive symptoms among participants.

However, students who reported high levels of perceived social support showed lesser levels of stress-related health outcomes.

Students with a strong sense of belonging to a group, organisation, or community dealt much better with stress and had reduced negative health outcomes following exposure to stress.

Both these groups of students showed fewer epigenetic changes in genes that were altered as a result of stress.

The COVID pandemic has created heavy psychological and emotional burdens for people due to uncertainty, altered routines and financial pressures.

In Australia, the rates of anxiety, depression and suicide have soared since the start of the pandemic. One in five Australians have reported high levels of psychological distress.

The pandemic has also made us more isolated, and our relationships more remote, having a profound impact on social connections and belonging.

My study highlights how family and community support, and a sense of belonging, influence our genes and act as a protective factor against the effects of stress.

In such unprecedented and stressful times, its vital we build and maintain strong social structures that contribute to good physical and mental well-being.

See the original post:
Stress is a health hazard. But a supportive circle of friends can help undo the damaging effects on your DNA - The Conversation AU

"By establishing iHope Genetic Health, we are expanding our commitment to ensure that the benefits derived from whole-genome sequencing are available to as many people as possible, as quickly as possible, regardless of disease, geography or income," said Francis deSouza, Chief Executive Officer at Illumina. "By unlocking the power of the human genome, we can find answers for these patients where no others can, and dramatically change lives."

Through this flagship program, Illumina will enable Genetic Alliance, a global nonprofit focused on advancing genetics to benefit human health, to create networks of clinics, and laboratories equipped with the necessary genome technology to provide precision genomic diagnoses to patients suffering from rare genetic disease.As part of this program, Genetic Alliance will also partner with pharmaceutical, technology companies and care providers to support patient access to data, therapeutic interventions, and ongoing supportive care.

"Since our inception in 1986, Genetic Alliance's mission has been to realize a world in which those affected by genetic disease are diagnosed and offered interventions to alleviate their suffering," said Genetic Alliance CEO, Sharon Terry. "As the mother of two children, diagnosed with a genetic condition, I can't rest until we build equitable systems to meet the needs of all who experience the diagnostic odyssey. In iHope Genetic Health we recognize the place of individuals, families, and communities to prioritize and solve the problems they face, consistent with their own values and culture."

iHopeTM Genetic Health will build upon the success of Illumina's existing iHope efforts, further extending the reach of the program and enabling clinical laboratories and care centers throughout the world to test patients impacted by rare disease and other genetic health conditions. Genetic disease affects over 300 million individuals worldwide, the vast majority of whom are children. In high income countries these patients often remain undiagnosed for up to seven years, while in low- and middle-income geographies, many families never know the cause of their child's suffering. Further enabling access will help reduce the psychological stress and loss of income that many families endure.

"The success of the Human Genome Project has revolutionized medicine by enabling treatments that precisely target disease-causing changes in DNA," said National Institutes of Health Director Francis S. Collins, M.D., Ph.D. "While the cost of genome sequencing has dropped precipitously over the past decade, it remains cost-prohibitive for many. I applaud Genetic Alliance for launching this important initiative to improve access to this life-changing technology. Access to medicine should always be a right, not a privilege."

To ensure support for patients throughout their diagnostic and care journey iHope Genetic Health will be supported by a network of disease advocacy, technology, pharmaceutical and clinical support organizations.

"We have a moral imperative to help genetic disease patients who need a diagnosis," said Ryan Taft, PhD, Illumina's iHope lead and Vice President, Scientific Research."iHope Genetic Health will change the trajectory of genomic medicine worldwide, helping patients who may have otherwise been invisible. Our vision is a genome for every patient that needs one, and a network of partners who will help them on every part of their journey to better health."

iHope Genetic Health will begin reviewing applications for clinical whole genome sequencing programs in February 2022. For more information please visit ihopegenetichealth.org.

About IlluminaIllumina is improving human health by unlocking the power of the genome. Our focus on innovation has established us as the global leader in DNA sequencing and array-based technologies, serving customers in the research, clinical and applied markets. Our products are used for applications in the life sciences, oncology, reproductive health, agriculture and other emerging segments. To learn more, visitwww.illumina.comand connect with us onTwitter,Facebook,LinkedIn,Instagram, andYouTube.

About Genetic AllianceGenetic Alliance, a nonprofit organization founded in 1986, is a leader in deploying high-tech and high-touch programs for individuals, families, and communities to transform health systems by being responsive to the real needs of people in their quest for health. The Alliance comprises 10,000 organizations, 2,000 of which are disease and patient advocacy foundations, and include community health programs, employee wellness programs, local nonprofits, religious institutions, and community-specific programs to grow and expand their reach and mission. For more information, visit geneticalliance.org.

Use of forward-looking statements This release contains forward-looking statements that involve risks and uncertainties, including the expectation for lower costs related to the storing and managing of genomic data costs. Among the important factors that could cause actual results to differ materially from those in any forward-looking statements are: (i) challenges inherent in developing and launching new products and services; (ii) our ability to successfully manage partnerships; (iii) our ability to deploy new products, services, and applications, especially in developing markets; and (iii) the acceptance by customers and other stakeholders of our newly launched products or services, which may or may not meet our and their expectations once deployed, together with other factors detailed in our filings with the Securities and Exchange Commission, including our most recent filings on Forms 10-K and 10-Q, or in information disclosed in public conference calls, the date and time of which are released beforehand. We undertake no obligation, and do not intend, to update these forward-looking statements, to review or confirm analysts' expectations, or to provide interim reports or updates on the progress of the current quarter.

Contacts For Illumina:

InvestorsBrian Blanchett858.291.6421[emailprotected]

MediaDr. Karen BirminghamEMEA: +44 7500 105665US: 646.355.2111[emailprotected]

For Genetic Alliance:[emailprotected]

SOURCE Illumina, Inc.

https://www.illumina.com

Continued here:
Illumina and Genetic Alliance Launch $120 Million Global Initiative to Increase Equity and Improve Outcomes for Families Impacted by Genetic Disease -...

web_plus145_treatment_credit-shutterstock.jpg

A new collaborative effort aims to cure HIV using a novel block-lock-excise approach and is backed by a $26.5 million grant from the National Institutes of Health. The multidisciplinary group of researchers, known as the HIV Obstruction by Programmed Epigenetics Collaboratory, is being led by scientists at Gladstone Institutes, Scripps Research, and Weill Cornell Medicine.

The biggest hurdle to curing HIV has been the viruss ability to hide a reservoir of latent copies within immune cells. Up to now most viable cure efforts have aimed at reactivating that virus reservoir in order to kill it with antiretroviral therapy an approach called shock and kill or kick and kill. Unfortunately, those approaches havent been able to wake every single copy of the latent virus (at least not without also bringing about severe side effects).

The HOPE Collaboratory is taking a fundamentally different approach to targeting HIV than what everyone else has been trying, Dr. Melanie Ott, director of the Gladstone Institute of Virology and program director for the collaboratory, explained in a press statement.

The new alternative tactic, block-lock-excise, targets latent HIV without reactivating it. The inspiration for this tactic arose from the fact that researchers have found ancient viruses that are integrated into the human genome but are no longer active or viable.

The central concept behind [this] strategy is inspired by the way our cells naturally cope with the remnants of ancient retroviruses that have integrated into our genetic material during evolution, said Cedric Feschotte, one of the investigators and professor of molecular biology and genetics at Cornells College of Agriculture and Life Sciences.

Feschotte studies these so-called endogenous retroviruses, which make up about 8 percent of modern humans DNA.

Identifying which proteins are used by our immune cells to lock up endogenous retroviruses opens the way to developing new repressive molecules that can target HIV and lock it permanently, Feschotte said. The concept is exciting, and it makes sense. We want to accelerate what evolution has already achieved with thousands of relatives of HIV previously defeated and buried in every human[s] cells.

Story continues

The researchers have also found that these ancient inactive viruses are missing several elements that HIV contains. Theyve identified two elements in particular, one a sequence of DNA and the other a protein called Tat, which are necessary for latent HIV to reactivate and begin replicating again.

We have shown that blocking Tat with certain drug-like small molecules can lock HIV in its dormant stage, and this block stays in place for some time, even if antiretroviral therapy is interrupted, said Susana Valente, also a principal investigator and associate professor of immunology and microbiology at Scripps Research. With the block and lock approach, we basically want to push HIV into becoming like a harmless, ancient virus.

The pharmaceutical solution would block the Tat protein and alter the structure of the virus, making it harder for other proteins to access the HIV genes and potentially turn them on. This could prevent the virus from awakening and reactivating. That would keep HIV from returning even after someone goes off antiretroviral treatment.

The idea is not only to lock HIV so it cannot replicate without using drugs, but essentially to throw away the key, keeping it locked away forever, unable to do any more harm, Valente said.The excise part of the new approach uses recent advances in genome editing. By employing CRISPR/Cas9 genome-editing technology, researchers could delete the remnant HIV hiding in the DNA of immune cells. That would eliminate all traces of HIV and any chance of the virus rebounding.

The collaborators are drawn from 12 institutions around the globe, three pharmaceutical companies, clinical groups in Africa and Brazil providing data and samples from people living with HIV, and the San Francisco AIDS Foundation, which will bring insights and perspectives from people living with HIV.

Its absolutely key that this is a multi-institutional and multidisciplinary approach, said Gladstones Danielle Lyons, program manager for the HOPE Collaboratory. Bringing together this diverse group of people with expertise across various disciplines is what will really drive the discovery of a cure for HIV.

The HOPE Collaboratory is one of 10 groups awarded a five-year grant under the Martin Delaney Collaboratories program, the flagship program on HIV cure research at the NIH.

See original here:
Science Discovers Another Avenue That Could Lead to an HIV Cure - Yahoo News

Matthew L. Meyerson, MD, PhD, is constantly curious, both about the world and the people around him and as one of the top cancer researchers on the planet, he has a talent for elevating younger scientists, turning obstacles into discoveries, and sensing future research opportunities.

Matthew L. Meyerson, MD, PhD, is constantly curious, both about the world and the people around him. As one of the top cancer researchers on the planet, he has a talent for elevating younger scientists, turning obstacles into discoveries, and sensing future research opportunities.

Hes not afraid to try something completely different. As a freshman at Harvard University, he spent a summer on a farm, baling hay and building a cow pen the farmer called Harvard Yard. He spent his senior year in Japan, studying in a lab at Kyoto University.

That genuine sense of wonder, and wander, started when he was a child growing up in Philadelphia, Pennsylvania. Thats when Meyerson discovered the work of famed architect R. Buckminster Fuller, inventor of the geodesic dome. Fuller was a university professor emeritus at the University of Pennsylvania for the final 10 years of his life. Before his death in 1983, Fuller wrote about how technology can transform peoples lives and emphasized the role of creativity, starting in childhood.

I think its important to have a sense of wonder, and its also important to look at things and say, You know, theres always a limit to our knowledge, said Meyerson, who was named the second most influential scientist in the world in all fields of science by Thomson Reuters in 2014.

There are a lot of things that we think are true, he said. And even though theres a lot of evidence that theyre true, [the truth] ends up being different.

In Meyersons office at Dana-Farber Cancer Institute, his desk is covered with photos of friends and his family, including his wife, Sandra Meyerson, a primary care pediatrician also on the Harvard Medical School faculty, and their 4 children, Sophia, 30; Olivia, 27; Jacob, 25; and Phoebe, 20. On the wall is artwork from his sister-in-law, a drawing of what looks like a tree but is actually a set of lungs, reflecting his work on the genetics of human lung carcinomas.

Im not so sure Biz Markie isnt not one of the dopest to ever grip the mic.

Meyerson received his MD in 1993 and PhD in 1994 from Harvard University. Prior to joining Dana-Farber in 1998, he completed a residency in clinical pathology at Massachusetts General Hospital and a research fellowship with the legendary Robert Weinberg, PhD, at Whitehead Institute in Cambridge, Massachusetts. In the early 1980s, Weinberg discovered the first human cancer-causing gene, the RAS oncogene. By 1986, he and his team also isolated the first known tumor-suppressor gene, the retinoblastoma gene. And in 1997, Meyerson and Christopher M. Counter, PhD, identified the telomerase catalytic subunit gene.

From 2006 through 2015, Meyerson was a principal investigator for The Cancer Genome Atlas (TCGA), a landmark program aimed at comprehensive cancer genome characterization. TCGA was a joint effort of the National Cancer Institute (NCI) and the National Human Genome Research Institute based at the Broad Institute of Massachusetts Institute of Technology and Harvard. He served as cochair of the lung cancer disease working group, and his projects have identified many mutated genes in lung cancer.

He says that his work on lung cancer mutations in the EGFR gene has been his most impactful discovery to date. EGFR mutations occur mostly in nonsmokers who develop lung cancer, helping investigators understand why the disease develops in what should be a low-risk population.

Like many discoveries, Meyerson says it kind of happened by good fortune. In 2003, he was working with fellow Harvard researchers William Sellers, MD, and Bruce E. Johnson, MD, the 2018 Giants of Cancer Care award winner trying to identify mutations in lung cancer that could be targeted therapeutically.

They had lung cancer samples from a group of Japanese patients including women who had lung cancer but werent smokers. It turned out half of them had the EGFR mutation. Further studies with Sellers, Johnson and Pasi A. Jnne, MD, PhD, this years Giants of Cancer Care award winner in the lung cancer category, showed that those with the mutation responded well to therapy.

There was already a drug out theregefitinib [Iressa], an EGFR inhibitorbut people didnt really know what patients it worked on or why it worked, Meyerson said. The study really answered the question and helped us target therapy.

It led to much improved EGFR inhibitors, and it led to this whole wave of discovery in lung cancer. There are now literally dozens of targeted inhibitors that are in use for lung cancer and more coming all the time. So it was just a huge impact on the field.

Research in lung cancer has expanded since Meyerson first started in the field in the late 1990s. He says he was frustrated by the stigma of the disease and the limited number of treatments available. Now, because more patients survive, theres more support for research.

The people who really push for research in the field are the survivors. They know about the disease, they know how bad it is, and theyre still here, he said.

Although most of Meyersons research has been in lung cancer, his lab has also studied microbes that cause human cancer. Comparing the genomes from 9 colon tumors with normal tissue from the same patient led to a major discovery in 2011: colorectal cancer tissue contains high levels of several types of bacteria, most notably Fusobacterium nucleatum. Now Meyerson and colleagues are trying to understand whether these bacteria cause colon cancer as part of the NCI/ Cancer Research UKs Cancer Grand Challenges.

Meyerson is also excited about his labs work on telomeres and mortal and immortal cells, a project that spans all types of cancer. In normal cells, telomeres protect the DNA from mutating and eventually stop the cell from dividing. But mutations in cancer cells occur outside the gene that controls how much of the telomerase enzyme is made. Although this discovery is 25 years old, there still isnt a drug that inhibits that mutation. Yet.

My lab has [started working] on a project in this area, [so] Im hoping that will change in the next few years, he said.

Meyerson started working in a laboratory while still in high school and says he thought doing research would be easierthat hed start working on something and figure it out. He learned, instead, that doing scientific research is like constructing a skyscraper.

If you look at building a skyscraper, most of the time is spent digging out and structuring and shoring up the foundation. And then when you actually erect the steel frame, it goes really fast, he said. Research is like that; youve got to do a huge amount of preparation before you actually answer a scientific question.

You might have to build the experimental system, or if its a human disease, you have to collect the patient samples. And sometimes thats weeks or months, but sometimes its years. Sometimes it takes many years.That balance and the need for all the prep work, that was a surprise to me.

As a student, graduate student, and postdoctoral researcher, Meyerson learned that each lab had its own style. Some lab directors gave students a very specific project with a limited scope of responsibilities. Others gave students more independence, which also came with greater risks for the lab director.

In his own lab, Meyerson gets to know students as individuals so that he can best match them with projects and partners.

Rameen Beroukhim, MD, PhD, is an associate professor at Harvard Medical School, an associate professor at Dana-Farber Cancer Institute, and an attending physician at Brigham and Womens Hospital. He joined the Meyerson lab after he heard Meyerson give a lecture about attempts to understand the cancer genome. Beroukhim ended up working as a postdoctoral fellow with Meyerson from 2005 to 2010 and eventually opened his own lab.

Back then we really didnt know so much about the cancer genome, but I thought, Well, mutations are the essential forces that drive cancer, so really understanding them would be a way of understanding cancer from the ground up, Beroukhim said. At the time, he was using single nucleotide polymorphism arrays, but those arrays had been developed to genotype people to figure out [inherited alterations]but he was applying them to cancers to understand which cancers had lost certain parts of their genomes and where those parts of the genome had been lost. That seemed like an elegant way to try to understand the genome that was different from how other people had attacked the situation.

Beroukhim says Meyerson is unusual as a mentor because of his social skills, both in and outside the lab. He makes a lot of effort not only to connect with his trainees, but also help them network with colleagues and promote their work. Off the top of his head, Beroukhim could name 5 of Meyersons former research fellows who are now faculty members at Dana-Farber, as well as others at Cornell University and Columbia University.

Matthew has a great way of sort of seeing the future and whats going to be interesting in the futurelooking at research that will be informative and where people will be interested, not just now, but in years to come, Beroukhim noted.

Meyerson says many people might be surprised by the social nature of the science field and how many ideas develop not as an independent eureka moment, but as part of a conversation. I think a lot of that scientific progress is thinking together and discovering together, and maybe thats a piece that people havent fully understood, that isnt always fully captured.

Regarding pursuing an education or a career, Meyerson tells his students the same thing he tells his children. I would say its important to find your own way. Find what you like doing, what suits you personally, he advised.

After 4 decades working as a researcher, Meyerson says hes gotten better at delegating and taking some time for his family. As a child growing up outside Philadelphia, he would collect rocks and minerals from Wissahickon Creek, and he has continued this habit throughout his travels. When his mother moved out of his childhood home, he took ownership of boxes of collected rocksand his wife created a collectors shelf for him.

To escape from the noise of Boston and the intensity of the lab, Meyerson and his wife recently bought a country home in Vermont where they cant see their neighbors. The quiet suits him, as does the chaos.

Just like with his research, Meyerson enjoys trying something new and exciting.

I like it a lot. Its funnyI tend to like everything, he said. I dont know if [thats] unusual or not, but I look for new things. I like the variety."

Read more:
Cracking the Cancer Code Requires Both Quiet and Chaos - OncLive

We have all heard of gut health and understand that it impacts our overall health in some way. But did you know that poor gut health has been linked to mood disorders and brain diseases like dementia?

Do you know what the gut or microbiome is? As a reminder, it's simply all the bacteria and microorganisms found in the gastrointestinal (GI) tract. And it has a huge impact on our health.

There are trillions of bacteria in the human gut, and they live in a symbiotic way to help us stay healthy. The average person will have about 30 trillion cells in their body. They will have around the same number of gut bacteria, give or take a few trillion. The point is that we are made up of bacteria, at least 43%. So, we are only half-human. We have our own human genome, and common wisdom is that our human genes determine and impact our health. In reality, the bacteria that reside within us also have a genome, and it is the interaction between the human genome and the bacterial genome that makes us human and healthy.

To illustrate just how impactful our gut bacteria can be on our health, Prof Rob Knight from the University of California San Diego took the bacteria from obese and lean people and transplanted them into the sanitised gut of lab rats and observed the outcome. What happened was that the rats with the gut bacteria from the obese human got fat. And the rats with the lean human bacteria remained lean. Another example is how Helicobacter pylori (H. pylori) bacteria break through the gut defences against stomach acid, resulting in stomach ulcers.

Our gut bacteria have a pivotal role to play in our health. They manufacture vital chemical compounds, protect against diseases, regulate the immune system, and help with digestion. Over the last two decades, scientists have observed the link between gut health and various immune and metabolic functions, autoimmune disorders, and brain and mood disorders. For example, we know that a gut diverse in microbiota promotes health and prevents chronic diseases, whereas poor diversity is a characteristic of obesity, diabetes, asthma, and gut inflammation. Recently, science has begun to figure out that gut health is linked to diseases like multiple sclerosis, inflammatory bowel disease, colon cancer, dementia, Alzheimer's, anxiety, and depression. Research in these areas continues.

The gut has been called the second brain, and for good reason. The enteric nervous system is found in our gut and relies upon the same neurons and neurotransmitters as our central nervous system. A lot of cross-talk goes on between our brain and our gut using this nervous system, but our immune system and hormones also participate in this communication. Due to this communication, the "brain in our gut" plays a key role not only in physical diseases but also in our mental health.

If you have ever felt "butterflies in your stomach", you have experienced this brain-gut connection. It really brings new meaning to having ever had a "gut feeling" about something.

The brain and mental health is a massively complex field, so don't think that gut health is the only cause of diseases impacting these areas. However, as microbiome research progresses, we find that people experiencing anxiety and depression might be helped through dietary changes (using probiotic and non-probiotic foods and supplements) that support the growth and proliferation of the correct type of bacteria. Such steps help to sustain the microorganisms in the gut. These microorganisms help to regulate brain function via the gut-brain axis, impacting functions in the immune system and metabolism by providing essential inflammatory mediators, nutrients, and vitamins. Additionally, poor gut health can contribute to anxiety and other mood disorders because of the gut-brain link. Mental stress can also impact the health of gut bacteria, which also feeds back into the health of the brain-gut axis.

In another surprising finding, researchers have confirmed a link between depression and stomach ulcers. So we know there is a link between gut (H. pylori) bacteria and ulcers, as previously stated, and now also a link between stomach ulcers and depression. Such research absolutely supports the holistic approach to caring for patients with gastrointestinal diseases. Additionally, new research by UQ's Institute for Molecular Bioscience (IMB) and Queensland Brain Institute supports the idea of a feedback loop where gut health impacts brain and mood health and where those undergoing psychotherapy or psychiatric treatment have been observed to exhibit positively-impacted gut symptoms. This could indicate that the mood state can influence gut health as well as gut affecting mood.

Alzheimer's is the most common form of dementia, and the scientific community has long suspected that gut microbiota play a role in developing this disease. Researchers have now shown that the gut bacteria composition in Alzheimer's patients is altered and has reduced microbial diversity. There is also a real correlation between an imbalance in the gut microbiota and the development of amyloid plaque in the brain. Scientists now believe that gut bacteria can influence cerebral functioning, promote neurodegeneration, and modify the immune system's interaction with the nervous system. This is very promising for research into innovative neuroprotective strategies in brain disease treatment.

We all know that not getting enough sleep is detrimental to your health, with many and varied health problems resulting (cardiovascular disease, cancer, Parkinson's disease, autoimmune diseases, and psychological issues such as chronic stress, anxiety, and depression). But did you know that poor sleep can negatively affect your gut microbiome? Researchers have found that those who slept well had a better diversity of gut bacteria, and we know that the more diverse someone's gut bacteria is, the better their overall health. So this finding might indicate that gut microbiome-focused treatment protocols may help reduce the risk or severity of brain diseases and promote a good night's sleep.

One of the most significant things that kills off our internal gut flora is the modern miracle of antibiotics. Ironically, we take them due to illness, only to kill off our good bacteria, which then causes other health problems. Antibiotics can upset your microbiome for more than six months if the good bacteria isn't replaced after taking them. This can cause health effects that may go unnoticed and untreated for a long time until the cause is no longer evident. So, if you're taking antibiotics, make sure you talk to your doctor about it and understand why. They aren't bad; they serve a purpose, but taking antibiotics needs to be followed up with good probiotic replacement therapy if you want to avoid getting gut health-related issues later on.

Besides anti-biotics, eating the wrong foods can also cause gut problems. Food allergies and intolerances, genetics, poor lifestyle choices, chronic stress, and lack of sleep all impact the gut, the brain, and your overall health.

The best way to find out is to have a microbiome test performed by a gut health expert. However, the following symptoms may indicate that you have a gut health issue:

Naturally, if you notice any of these chronic symptoms, you should seek immediately medical attention to ensure you do not have a serious condition. Your gut health has a significant impact on your overall health. As a result, keeping your gut healthy is definitely a priority.

Authors: Miskawaan Health Group (MHG). For further information please visit us online at Miskawaan.com or contact us via: contact@miskawaanhealth.com or call (0)2086 8888.

Series Editor: Christopher F. Bruton, Executive Director, Dataconsult Ltd, chris@dataconsult.co.th. Dataconsults Thailand Regional Forum provides seminars and extensive documentation to update business on future trends in Thailand and in the Mekong Region.

See the rest here:
Alzheimer starts in the gut - Bangkok Post

KYLE HARPER RESPONDS to Monica Greens Review of Plagues Upon the Earth: Disease and the Course of Human History (October 18, 2021):

The history of infectious disease has to be history on a global canvas. Pathogens dont respect political borders, and health inequity is historically inextricable from patterns of wealth and power. Disease is integral to all the big questions of global history questions about long-run economic development, connectivity and encounters, colonialism, and imperialism. The recent review essay by Dr. Monica Green in LARB in response to my history of infectious disease explores the question of how well the book achieves its global intentions. I am grateful for a lengthy review essay from a colleague who shares my enthusiasm for new kinds of genetic evidence, and I appreciate the valuable discussion of how historians can draw from this exciting and rapidly growing source of data. But given the focus of Pasts Imperfect, I would like to continue the discussion of how we might pursue a global history of disease. The review is mostly a missed opportunity in this regard, because it prefers to assert that the book is stilted toward a Western and wealthy perspective. Unfortunately, this criticism rests on a curious and complete refusal to engage the books extensive treatment of non-Western experiences.

To take a representative example, it is claimed that the books effort to periodize the deep history of globalization is Western-focused, because it does not register the dispersal of peoples throughout the Pacific and the Americas as a phase of globalization. The dictionary definition of globalization is the integration of distant societies across space, and historians will forever debate how to configure the processes driving connectivity in the past. But it is unusual to characterize dispersal as a form of integration (and thus as a process of globalization in the conventional meaning). It would be fair enough to argue that we need a different definition of globalization, but it is surprising that the reviewer neglects to mention that two chapters do treat the dispersal of humans over the globe, at great length. A reader of the review would take away the impression that a major theme of the book is simply missing, rather than classified differently than the reviewer would apparently wish.

Unfortunately this omission is not the exception, but rather the rule. To take another example, the review criticizes the books opening vignette, which asks readers to think about some of the daily routines and technologies that many people use to sanitize their bodies and domestic environments. Far from being tone-deaf, the passage begins by asking readers to think about the quotidian experiences familiar to those who are privileged enough to live in a developed society. Moreover, the accusation that such a generic routine is necessarily Western is surely tendentious. After all, in non-Western societies, many people (though of course not all) have access to improved drinking water, toilets, and electricity. To assume that turning on the light switch, using a flush toilet, and washing your hands is the exclusive privilege of Europeans is false (and perhaps a little parochial). But worst of all, it would have only been generous, not to mention responsible, to note that this vignette is followed, immediately, by a stark declaration that the extent of control over infectious disease remains unequal around the globe, as a way of setting up the problem of geographic health disparities as a central theme of the book.

In any case, those instances are reflective of a pattern, which means we have missed an opportunity to ask critical questions about what makes for a good global history of disease. [1] In my view, writing a global history of disease requires an earnest effort to capture as much of the varied human experience as the sources will allow, without navely assuming that any one societys experience was normal. How can this be achieved in practice? In the history of disease, I suggest three strategies:

First, we should widen the infectious diseases that we write about beyond the usual suspects. Smallpox, plague, measles, typhus, tuberculosis, etc., are all canonical, and indeed must be central to the story. But we should recognize that this list leaves out important diseases, many of which are geographically constrained to the tropics and subtropics. In practice, for instance, I have tried to give ample coverage to schistosomiasis, lymphatic filariasis, falciparum malaria, yellow fever, yaws, and trypanosomiasis. All of these afflictions were absent or marginal in Europe, yet hugely important in human history. In general, any book that devotes as much space to these diseases as to the more cosmopolitan ones is probably not egregiously Europe-centered. Regrettably, this coverage is not even mentioned in the lengthy review, so a reader might come away with a mistaken expectation of what is in the book. It represents a missed chance for critical discussion about how expanding the range of diseases could more authentically represent the human experience from a global perspective. Moreover, we will need to take seriously these too-often-neglected tropical diseases to seek out the deep role of geography in human history.

Second, we can decenter narratives of the classic diseases like plague and smallpox, to avoid the misleading impression that somehow the Western experience was paradigmatic. In the case of plague, for instance, both the genetic evidence (as Dr. Green has shown elsewhere) and non-Western written evidence can be tools to revise the traditional narratives. In the case of the Black Death, for instance, we can (and I try to) let the rich Arabic sources have as much space as the European sources. We must also ask hard questions about the impact and timing of plague in China, South Asia, and Africa, too. The history of smallpox is probably more challenging, for now at least, but I have tried to reframe the conventional story of the Columbian Exchange, in which Europeans brought smallpox to the New World with deadly effect in the 16th century, by putting it in a wider, planetary perspective. Smallpox was a bigger problem, everywhere, starting in the 16th century, from Mexico City to Ming China. Sometimes with striking synchronicities, it raged across the planet, from the American Southeast to late Stuart England to early Qing China. In my view, we dont fully understand why this was so, but a global perspective prompts us to question the blinkered model of the virgin-soil epidemics in the New World.

Third, we should try to understand the progress of the last two centuries from a global perspective and not simply a Western triumphalist one, such as is sometimes dominant in the economics literature. Even a global perspective will still need to devote due attention to Europes pioneering role in many facets of public health and biomedicine. But, critically, we should recognize that as modern growth and globalization fueled great health crises (like cholera, the Third Plague Pandemic, and the 1918 influenza), the power dynamics of European imperialism and incipient capitalism meant that health and processes of modernization were deeply entangled, to the disadvantage of many non-Western societies. Rather than seeing modernity as a period of unbroken and continuous triumph, we should try to recognize the complex and sometimes causal relationships between progress and inequity. At the same time, we should also try to offer an honest assessment of the globalization of good health the upward convergence of health outcomes in the 20th century, as developing societies in the age of decolonization rapidly embraced the opportunities to bring infectious diseases under control. One would never guess it from the review, but non-Western experiences of modern development get the majority of the space in the last two chapters of the book.

When you deliberately excise all of the non-Western material, what is left unsurprisingly looks like Western civ. But such selective reading doesnt really advance the cause of global history. Meanwhile, there are genuinely severe challenges in trying to tell the story of infectious disease on a global canvas. Our energy would be better focused on a good-faith discussion of the big methodological and substantive challenges we all face. For instance, the historical demography literature so valuable in trying to understand how people died in the past is wildly skewed toward Europe. So is the paleogenomic evidence, at present. How do we get around these biases in the source material, using what we know from this evidence to make inferences about pre-modern societies, without navely assuming that what we have is actually universally representative? More conceptually, the entanglements of geography, power, and disease are probably among the most complicated questions we can ask about the history of economic development. Economists have been (much) better at helping us understand the causal factors behind improvements in health, but historians have done a better job at treating non-Western experiences and the problem of imperialism. How can we achieve a disciplinary rapprochement? I do not claim to have overcome these problems, only to have confronted them earnestly from a global perspective.

Monica Green Responds to Kyle Harper:

I thank Professor Harper for his detailed reading of my review and his recognition of its call for dialogue on the pressing question of how global health is to be defined and its history pursued in a way that is meaningful for all humanity.

Kyle Harper is professor of classics and letters at the University of Oklahoma.

Monica H. Green is an expert in the history of medicine in premodern Europe and global infectious diseases.

[1] Also notably unhelpful is the insinuation that the simpler terms time travel and tree thinking, used as shorthand for the unwieldly technical terms paleogenomics and phylogenetics, are my cute nicknames. Time travel comes from Svante Pbo and Johannes Krause, two founders of the field, and tree thinking is commonly used as well as the name of one of the standard monographs on how to employ phylogenetic reasoning. In my view, pedantry will not help us as we all work hard to bridge numerous disciplines with their sometimes demanding technical language. Furthermore, I am at a loss to understand how tracking is a third distinct method of using genetics. What is described as tracking in the review is simply phylogenetics (tree thinking) or perhaps its spatial application, phylogeography. I am unfamiliar with specialists in the field who have previously considered this a way of using genetic data entirely apart from phylogenetics.

View post:
Letter to the Editor: Kyle Harper Responds to Monica H. Green - lareviewofbooks