Many of the viruses that cause colds (presumably like this one in 1935) will get sequenced in a new program.
Building on the global boom in viral surveillance during the pandemic, U.K. scientists on Tuesday unveiled an initiative to expand sequencing of the common seasonal respiratory bugs that have received comparatively little attention.
The Respiratory Virus & Microbiome Initiative, launched and funded by the Wellcome Sanger Institute, will track the evolution not just of SARS-CoV-2, the coronavirus that causes Covid-19, but also other coronaviruses, different flu families, RSV, and other pathogens that typically just cause the sniffles but collectively lead to waves of illness every year. Researchers hope the initiative will enable them to better monitor viruses in the U.K. as they change, alert them to any worrisome mutations, and get tipped to the emergence of new viruses.
“The ability to track and look for these events early is obviously something that’s really important,” said Ewan Harrison, the head of the initiative.
The program, a collaboration with the U.K. Health Security Agency and other scientists, hopes to generate tons of data for academics and public health officials to use in their work, and also aims to “supercharge” research that could ultimately lead to the development of vaccines and therapeutics, Harrison said. It’s also simply about better understanding these viruses. While flu has attracted lots of research over the years, some of the other bugs — like rhinovirus or adenovirus — are not as well-monitored. Scientists don’t even understand their transmission dynamics all that well, he said.
Viral sequencing exploded during the pandemic, with global efforts helping detect variants like Delta and Omicron (and all the Omicron sublineages) and guiding response strategies. A major moment in the pandemic was when, in early January 2020, scientists publicly released the genome of the virus, which allowed responders around the world to start developing diagnostic tests and served as a starter’s pistol for vaccine development. From there, scientists shared millions of sequences on public trackers.
More recently, the number of Covid infections being sequenced has collapsed as much of the world has moved past the emergency phase — a trend public health officials globally have lamented.
It’s not just the detection of major new variants that sequencing can enable. Sequencing viruses can help scientists track routes of transmission, whether in a hospital or from country to country. When combined with lab studies or epidemiological research, it can answer questions about the virus’s basic biology, whether the virus is becoming more transmissible, or whether the impact of an infection is changing — like how the Delta variant seemed to cause more severe disease. It’s also a tool that can help track how well vaccines are holding up against evolving viruses.
Expanding routine sequencing is the type of research that could come in handy with other viruses. In the United States, for example, experts are trying to figure out why an anticipated wave of a rare polio-like condition that can occur after an infection with a common enterovirus never materialized last fall, despite a surge of those enterovirus infections. Researchers are exploring the virus’ genome to see if it changed in some way.
The new initiative is designed to build an infrastructure that becomes part of routine viral surveillance, but also one that can be deployed during the next epidemic or pandemic, Harrison said. During the pandemic, researchers got their first experience with sequencing data helping inform responses to a public health crisis.
“It’s now something we now think is really important to build upon,” Harrison said.
As the team develops the techniques and tools they’ll use in their project, one goal is to keep it as low-cost as possible, with the idea that other research teams around the world could adopt such protocols. All of their methods and computational software will be made freely available.
“Sequencing know-how is incredibly widespread now, so I think the opportunity for this to happen globally is there,” said Judith Breuer, a professor of virology at University College London and one of the researchers involved in the new program.
What does being normal really mean? And who gets to decide what ‘normal’ is, and what normal isn’t?
Here is a list of 46 reasons why being normal is not that normal, and why you should let go of this ‘unhealthy aspiration’
46 Reasons Why You Should Give Up Trying to Be Normal
“Normal is:
1. Anything that makes us forget who we are and what we want; that way we can work in order to produce, reproduce, and earn money.
2. Setting out rules for waging war (the Geneva Convention).
3. Spending years studying at university only to find out at the end of it all that you’re unemployable.
4. Working from nine till five every day at something that gives you no pleasure just so that, after thirty years, you can retire.
5. Retiring and discovering that you no longer have enough energy to enjoy life and dying a few years out of sheer boredom.
6. Using Botox.
7. Believing that power is much more important than money and that money is much more important than happiness.
8. Making fun of anyone who seeks happiness rather than money and accusing them of “lacking ambition.”
9. Comparing objects like cars, houses, clothes, and defining life according to those comparisons, instead of trying to discover the real reason for being alive.
10. Never talking to strangers. Saying nasty things about the neighbors.
11. Believing that your parents are always right.
12. Getting married, having children, and staying together long after all love has died, saying that it’s for the good of the children (who are, apparently, deaf to the constant rows).
14. Waking up each morning to a hysterical alarm clock on the bedside table.
15. Believing absolutely everything that appears in print.
16. Wearing a scrap of colored cloth around your neck, even though it serves no useful purpose, but which answers to the name of “tie.”
17. Never asking a direct question, even though the other person can guess what it is you want to know.
18. Keeping a smile on your lips even when you’re on the verge of tears. Feeling sorry for those who show their feelings.
19. Believing that art is either worth a fortune or worth nothing at all.
20. Despising anything that was easy to achieve because if no sacrifice was involved, it obviously isn’t worth having.
21. Following fashion trends, however ridiculous or uncomfortable.
22. Believing that all famous people have tons of money saved up.
23. Investing a lot of time and money in external beauty and caring little about internal beauty.
24. Using every means possible to show that, although you’re just an ordinary human being, you’re far above other mortals.
25. Never looking anyone in the eye when you’re traveling on public transport, in case it’s interpreted as a sign that you’re trying to get off with them.
26. Standing facing the door in an elevator and pretending you’re the only person there, no matter how crowded it is.
27. Never laughing too loudly in a restaurant no matter how good the joke.
28. In the northern hemisphere, always dressing according to the season: bare arms in spring (however cold it is) and woolen jacket in winter (however hot it is).
29. In the southern hemisphere, covering the Christmas tree with fake snow even though winter has nothing to do with the birth of Christ.
30. Assuming, as you grow older, that you’re the guardian of the world’s wisdom, even if you haven’t necessarily lived enough to know what’s right and wrong.
31. Going to a charity tea party and thinking that you’ve done your bit toward putting an end to social inequity in the world.
32. Eating three times a day even if you’re not hungry.
34. Using your car as a weapon and impenetrable armor.
35. Swearing when in heavy traffic.
36. Believing everything your child does wrong is entirely down to the company he or she keeps.
37. Marrying the first person who offers you a decent position in society. Love can wait.
38. Always saying, “I tried” when you didn’t really try at all.
39. Postponing doing the really interesting things in life for later, when you don’t have the energy.
40. Avoiding depression with large daily doses of television.
41. Believing that you can be sure of everything you’ve achieved.
42. Assuming that women don’t like football and that men aren’t interested in home decorating and cooking.
43. Blaming the government for all the bad things that happen.
44. Thinking that being a good, decent, respectable person will mean that others will see you as weak, vulnerable, and easy to manipulate.
45. Being equally convinced that aggression and rudeness are synonymous with having a “powerful personality.”
46. Being afraid of having an endoscopy (if you’re a man) and giving birth (if you’re a woman).” ~ Paulo Coelho
Do people often call you “weird”, “strange” or “crazy” just because you are being true to yourself and don’t follow the crowd? I would really love to know what are your thoughts on this topic and whether you have found a way to escape the “normality” of life or not. Share your insights by joining the conversation in the comment section below
Stop Trying to Be “Normal”
P.S. Who can figure out what is happening in that photo?
The air in Mexico City was once so toxic that people watched as dead birds fell out of the sky. In 1992, the United Nations declared the city the most polluted in the world, with its unregulated diesel engines, factory production, fossil-fuel powered energy plants, and widespread use of internal-combustion engines, all trapped in a high-altitude, mountain-lined valley.
In 2002, toxicologist and neuropathologist Lilian Calderón-Garcidueñas, who grew up east of the metropolis and attended medical school in the city, decided to look at the brains of 40 dogs that had lived either in the city’s polluted valley or in the cleaner air of Tlaxcala, a state on its eastern edge. The results were striking: The rural dogs’ brains appeared healthy. In the brains of the city dogs, however, she saw the beginnings of neurodegeneration in puppies as young as eight months old.
The findings prompted Calderón-Garcidueñas, who has joint appointments at the University of Montana and Universidad del Valle de México in Mexico City, to begin looking at human brains. And over the last 20 years, she has grown convinced that children raised in areas like Mexico City, with air quality that rarely falls into the healthy range, are at noticeably increased risk for Alzheimer’s and other neurodegenerative conditions.
Scientists have known for decades that air pollution has effects far beyond blurred skylines and burning lungs. The fine particles and gases in polluted air have been connected to asthma, heart disease, inflammation, and a variety of other health impacts. But demonstrating that this pollutant soup can have neurodegenerative effects has proved trickier. Only recently has new research begun to paint a picture of air pollution as dangerous not only for the heart and lungs but potentially for the brain, as well.
In a 2018 study published in the journal Environmental Research, Calderón-Garcidueñas and her colleagues examined more than 200 brains of Mexico City residents who were between 11 months to 40 years old when they died. All but one of the brains they studied showed at least the beginnings of changes that scientists have previously found in the brains of people with Alzheimer’s disease. In comparison, the researchers described nine control brains that had been gathered from people who’d lived (and died) breathing clean air, as “unremarkable.”
The Mexico City studies, while intriguing, were far from definitive and limited by methodological issues, some researchers said.
“Nobody in the neuropathology world would consider this other than an indication,” said Caleb Finch, a biomedical gerontologist at the University of Southern California in Los Angeles, referring to the Mexico City studies. “It’s not something from which one can draw major conclusions.”
But he noted that further research by scientists at USC and around the world have strengthened the link between air pollution and neurodegenerative disease. Finch noted that there is now a series of papers showing that brain atrophy and cognitive disorders are directly related to how much air pollution someone has been exposed to. “Population-based studies have come into complete agreement on three continents — North America, Western Europe, and Asia — that air pollution above a certain level predicts a higher risk of dementia, particularly Alzheimer’s, and cognitive decline. That’s now proven by at least 10 major studies,” he said.
There are also a small-but-growing number of studies that suggest a connection between high levels of air pollution and Parkinson’s disease. But Ray Dorsey, a neurologist and Parkinson’s disease researcher at the University of Rochester Medical Center, noted that “almost all environmental risk factors associated with Parkinson’s have a long latency.”
“You don’t inhale pesticides or air pollution and get Parkinson’s the next day, just like you don’t smoke tobacco and get cancer the next day,” he said. “We know the disease takes decades to unfold.”
Children wear masks in an attempt to protect themselves from high levels of air pollution in Mexico City, in 1992.
Pathways to the brain
The air we breathe is an ever-changing stew of tiny particles and noxious gasses, and it may be difficult to pin down the specific components of pollution that are involved in neurodegeneration. There is likely no single culprit. “Fifty years of work have identified 30 carcinogens in tobacco smoke — which one of them causes lung cancer? The whole package does,” said Finch, “and the chemistry of air pollution is even more complex.” The Environmental Protection Agency regulates six of the most concerning components: carbon monoxide, lead, nitrogen oxides, ozone, particulate matter, and sulfur oxides.
Researchers have placed special focus on the fine particulates known as PM2.5 — to indicate particles smaller than 2.5 microns, or 1/30th the width of a human hair — which have been shown to be especially dangerous. These particulates can be thrown up in the air by farms and factories, but the most common source of PM2.5 is the burning of fossil and bio fuels — in combustion engines, for example, or coal-fired power plants, or even from wildfires, which are becoming more frequent with climate change. Once suspended in air, the particles can be inhaled deeply into the lungs, which allows them to move into the bloodstream and beyond. These particles have been linked to inflammation, cancer, and severe cardiac and respiratory diseases, including asthma, heart attack, and stroke. The smaller the particles, the more malignant their effects.
Now work by Calderón-Garcidueñas and others has shown that these microscopic particles also enter the brain. Some probably travel through the bloodstream, but researchers believe a person’s nasal passages may provide an even more efficient route. In her research, Calderón-Garcidueñas focused specifically on the olfactory bulb when looking for early indications of neurodegenerative disease. “The nose is the front door of the brain,” Dorsey said. As someone breathes in polluted air, PM2.5 particles enter the nasal cavity and then travel directly into the brain’s olfactory bulb. That’s when neuronal cell death begins, he said.
Dorsey pointed to the fact that in both Alzheimer’s and Parkinson’s, loss of smell is an early warning sign, sometimes preceding other symptoms by 10 years or more. “Pathology of both diseases is found in the olfactory bulb and smell centers before it’s found in parts of the brain responsible for memory, and then movement,” he said.
Although the nose may be the most direct route, researchers are also uncovering a variety of other ways that air pollution can make its way to the brain. Michelle Block, an environmental neurotoxicologist at Indiana University School of Medicine in Indianapolis, has been drilling down on what she calls the lung-brain axis. By studying the inhalation of ozone, a gas that doesn’t cross the blood-brain barrier, she’s able to track other potential mechanisms for air pollution’s neurodegenerative effects.
“One of the reasons we use ozone is because it has been linked to increased risk for Alzheimer’s disease, but also because it will never ever, ever reach the brain,” Block said, making the gas a particularly good tool to investigate communication between the brain and the lungs. “It’s environmentally relevant, but it’s also mechanistically important,” she said.
Block has found that ozone inhaled into the lung triggers an immune reaction, and her lab has seen changes in populations of immune cells that communicate with the brain. She’s also homing in on the role of microglia — tiny cells in the brain that help maintain neural networks, repair injury, and eliminate dangerous brain debris like microbes, dead cells, and aggregated protein. In a healthier brain, microglia will gather around clusters of protein fragments, called plaques, and condense them; researchers believe this may limit their pathology.
“Our work showed that air pollution affects these microglia and they don’t associate with the plaques like they should,” Block said. “They don’t do their job at all, and it promotes a more pro-inflammatory environment.”
Connecting the dots
Neurodegenerative diseases become more common as people age, but assessing how much pollution someone has been exposed to is challenging. Most studies of Alzheimer’s disease have looked at environmental exposures perhaps 5 to 10 years prior to onset, said Beate Ritz, professor of epidemiology and environmental health sciences at the University of California, Los Angeles Fielding School of Public Health. In Parkinson’s, she said, relevant exposures could occur anywhere from 5 to 20 years prior to disease onset. Yet by the time someone is 60, they may have lived in 10 different homes in three different cities, and historical air-quality data can be difficult, if not impossible, to find.
Another issue has been accurately identifying patients who have Parkinson’s disease, especially since most countries don’t maintain disease registries and those databases that do exist may not use verified diagnoses. Other registries, such as the oft-used Medicare database, don’t have address histories reaching back as far as researchers require to get high-quality results.
Still, Ritz and her colleagues have managed to find at least a few countries with the quantity and quality of data they need. Denmark and Taiwan, both of which have national health systems and substantive air-pollution records, have given Ritz a trove of data to mine. In Taiwan, the researchers found a positive association between Parkinson’s risk and traffic-related air pollution (nitrogen oxide and carbon monoxide). In Denmark, the results were remarkably similar. A different research group, in South Korea, found an association between high nitrogen oxide levels and increased risk of Parkinson’s. A third group, in Canada, found that in a study of residents of Ontario, Parkinson’s was associated with high levels of air pollution, especially PM2.5.
Air pollution may also cause or exacerbate other neurodegenerative diseases. One that some neurodegenerative disease researchers think may belong in this group is amyotrophic lateral sclerosis (ALS), or Lou Gehrig’s disease. The researchers note that there are tantalizing hints from both animal and epidemiological research, including a study in the Netherlands that linked long-term nitrogen oxide and PM2.5 exposures from traffic-related pollution to susceptibility to ALS. ALS, however, is a relatively rare disease and few countries maintain a disease registry for it, making data difficult to find, let alone parse.
Aerial view of low visibility due to air pollution in Mexico City in April 2021.
‘Over a lifetime, it adds up’
For many neurological diseases, aligning pathology with clinical findings has sometimes been a “best guess” undertaking. The Mexico City children whose brains Calderón-Garcidueñas examined may have shown the beginnings of Alzheimer’s pathology — hyperphosphorylated tau, for instance, which has been linked to neurodegenerative disease — but they didn’t have dementia. And in older brains, post-mortem studies have shown that some people with dementia do not exhibit pathology that is as extensive as would be expected with their symptoms, while others with substantial Alzheimer’s pathology die after showing few or no symptoms at all. “We know that there’s multiple other processes going on with aging so that almost everybody over age 60 has some clear kind of pathology, even though they’re not demented,” Finch said, adding, “I’m 83, so I can speak on this with authority.”
One major defense against aging is resiliency — in the brain, this comes in the form of what scientists call cognitive reserve. Cognitive reserve refers to the brain’s ability to function, even thrive, as neurodegenerative disease progresses. And researchers believe that the best ways to improve cognitive reserve are through education, healthy lifestyles (both diet and exercise), breathing clean air, and drinking clean water.
“We’re harming populations in a way that we’re making them less resilient over their lifetime,” Ritz said.
She added, “We don’t have children who have Alzheimer’s or Parkinson’s disease,” but said she finds the presence of identifiable disease pathology in the Mexico City study deeply concerning. If an infant or toddler already shows the beginnings of hyperphosphorylated tau and other disease-linked pathology, those children will have less reserve capacity at an older age. “We’re dealing with a long-term issue,” Ritz said. “Over a lifetime, it adds up.”
If air pollution is a significant contributor to neurodegenerative disease, any solution is likely to be difficult from an economic and societal perspective. But as Dorsey sees it, the answer is straightforward. “Air pollution can be taken care of overnight, and we did the experiment,” he said. “Look at the pre- and post-pictures of New Delhi during Covid. This is tractable.”
Did you know you have multiple acceptable screening methods available, yet most doctors simply recommend colonoscopy without reviewing the options, benefits and drawbacks of each for their patients? It’s important to realize that colonoscopy is not a risk-free procedure.
STORY AT-A-GLANCE
Colon cancer is the third most commonly diagnosed cancer in the U.S., and the second leading cause of cancer-related deaths for both sexes combined. Despite the fact that there are multiple screening methods, most doctors simply recommend colonoscopy, which is one of the riskier methods
Research shows that while colonoscopies can lower your risk of a colorectal cancer diagnosis, they do not significantly reduce your risk of dying from colorectal cancer
Recent research concluded that about 25% of all colonoscopies performed are unnecessary
A systematic review and meta-analysis published in 2017 concluded that regular aspirin use was as effective for preventing colorectal cancer incidence and death thereof as screening with flexible sigmoidoscopy or fecal occult blood test. And, when it came to preventing death from cancer in the proximal colon, aspirin was more effective than either of these screens
About 80% of endoscopes are cleaned using Cidex (glutaraldehyde), which fails to properly sterilize these tools, potentially allowing for the transfer of infectious material from one patient into another. If you must get a colonoscopy, make sure the hospital or clinic uses peracetic acid to disinfect their endoscopes. This will minimize your likelihood of contracting an infection from a previous patient
Colon cancer is the third most commonly diagnosed cancer in the United States, and the second leading cause of cancer-related deaths for both sexes combined.1
In 2022, an estimated 106,180 Americans were diagnosed with colon cancer and another 44,850 with rectal cancer. Of those, 52,580 died.2 The average lifetime risk of colorectal cancer is about 1 in 23 (4.3%) for men and 1 in 25 (4%) for women.3
Men and women over the age of 50 with average risk of colorectal cancer are typically recommended to get tested either by:4
•Stool-based tests:
◦Annual fecal immunochemical test (FIT)
◦Annual fecal occult blood test (FOBT)
◦Multi-targeted stool DNA test (mt-sDNA) once every three years
•Structural exams:
◦CT (virtual colonoscopy) once every five years
◦Flexible sigmoidoscopy (FSIG) once every five years
◦Colonoscopy once every 10 years after age 50 until age 755
Despite the fact that there are multiple screening methods, most doctors simply recommend colonoscopy, and researchers have found that in most instances, doctors completely fail to review all the options and the benefits and drawbacks of each with their patients. In essence, most doctors simply choose for their patients without going through the steps of informed consent, and most often they go straight to colonoscopy.
Is Colonoscopy Your Best Choice?
The idea behind cancer screening is that by catching it early enough, your risk of dying will be lessened. However, recent research published in The New England Journal of Medicine6 suggests the benefits of colonoscopies may be overestimated.
While colonoscopies were found to lower a person’s risk of a colorectal cancer diagnosis by 18% at 10 years when performed in healthy people between the ages of 55 and 64, the risk of actually dying from colorectal cancer was not significantly reduced, and the all-cause mortality was barely affected at all.
Let me rephrase this to make sure you understand this important point: Colonoscopies only increase the diagnosis of the cancer by 18%, but do absolutely nothing to decrease your risk of dying. As reported by the authors:7
“In intention-to-screen analyses, the risk of colorectal cancer at 10 years was 0.98% in the invited group and 1.20% in the usual-care group, a risk reduction of 18% (risk ratio, 0.82; 95% confidence interval [CI], 0.70 to 0.93).
The risk of death from colorectal cancer was 0.28% in the invited group and 0.31% in the usual-care group (risk ratio, 0.90; 95% CI, 0.64 to 1.16). The number needed to invite to undergo screening to prevent one case of colorectal cancer was 455 (95% CI, 270 to 1429).
The risk of death from any cause was 11.03% in the invited group and 11.04% in the usual-care group (risk ratio, 0.99; 95% CI, 0.96 to 1.04).”
1 in 4 Colonoscopies Is Unnecessary
Other recent research8 found as many as one-quarter of all colonoscopies are unnecessary. As reported by the Lown Institute:9
“… many people are screened for cancer even though they are unlikely to benefit. Nursing homes often screen very old people for cancer, even though they are likely to be harmed by surgery or treatment if cancer was found.
In one 2014 study,10 among older patients with very high mortality risk, 40% were screened for colorectal cancer. In another large survey,11 more than half of people over the recommended screening age reported being screened for colorectal cancer.
How often do we give patients colonoscopies who are too young, too old, or had another screening too recently …? In the first systematic review12 of screening colonoscopy overuse, researchers … provide an estimate.
They examined six studies which included about 250,000 screening colonoscopies. Overall, the rate of overuse among these studies ranged from 17% to 25.7%.
With 6.3 million screening colonoscopies performed in the US each year (before COVID), at least one million — and as many as 1.6 million — are unnecessary. This means many people are at unnecessary risk of harm from potential colonoscopy complications such as bleeding, perforated bowels, and even death.”
The elderly are the most vulnerable when it comes to the misuse of colonoscopies. They benefit the least from the screening and have the highest risk of adverse events, yet they’re also among the most heavily targeted groups for screening.
Side Effects and Drawbacks of Colonoscopies
It’s important to realize that colonoscopy is not a risk-free procedure. Examples of adverse events associated with colonoscopies include:
•Infection from poorly disinfected instruments — An estimated 80% of colonoscopy instruments are improperly sterilized, which can transfer infection from one patient to another. (See section below for more information.)
•Perforation of the colon and/or gastrointestinal bleeding13— A 2016 U.S. Preventive Services Task Force technical review14 estimated the risk of perforation is 4 per 10,000 and the risk of major hemorrhage 8 per 10,000. People at higher risk include those with diverticulitis, diseases of the colon, and adhesions from pelvic surgery.
•Dysbiosis and other gut imbalances,15 caused by the process of flushing out your intestinal tract before the procedure with harsh laxatives.
•Increased risk of stroke, heart attack and pulmonary embolism, weeks later16— These side effects are thought to be a side effect of the anesthesia, which can trigger blood clots. Many experts agree you should opt for the lightest level of sedation possible, or none at all, as full anesthesia increases risks.
•False results17— False positives lead to unnecessary treatments that are nearly always harmful, in addition to the anxiety a cancer diagnosis brings.
False negatives, on the other hand, create a false sense of security. One 2006 study18 warned that doctors who rush through the exam can miss even late-stage cancer, so avoid super-busy doctors who perform dozens of colonoscopies a day.
Infections Caused by Improperly Disinfected Scopes
The primary tools used to screen for colon cancer are sigmoidoscopes and colonoscopes. These devices are not disposable, so they must be sterilized between each use. This, it turns out, poses a very significant problem that most patients are not aware of.
According to Dr. David Lewis, a retired whistleblower microbiologist with the Environmental Protection Agency, about 80% of endoscopes are cleaned using Cidex (glutaraldehyde), which fails to properly sterilize these tools, potentially allowing for the transfer of infectious material from one patient into another.
Flexible endoscopes have several basic components. One is a long, flexible tube with a tiny camera at the end, which allows the doctor to view the inside of your colon. There are also two internal channels in this tube, a biopsy channel and an air/water channel.
When the physician sees evidence of a tumor, he or she can insert a little claw through the endoscope, into the patient, and grab a piece of tissue and pull it back out through the biopsy channel. The air/water channel allows the doctor to clean the lens of the camera, which frequently gets covered with blood and other patient material.
The air/water channel is much smaller in diameter than the biopsy channel, and this is where the greatest risk of contamination originates, because while the biopsy channel is large enough to be scrubbed clean with a long brush, the air/water channel is too small to accommodate a brush.
About 80% of the time, flexible endoscopes are simply submerged in a 2% glutaraldehyde solution (Cidex) for 10 to 15 minutes to disinfect them between patients, and this simply isn’t sufficient to clean out the air/water channel that’s been contaminated with tissue, blood and feces. As a result, this material can get flushed out into subsequent patients.
What’s worse, glutaraldehyde works like formaldehyde (it’s just a smaller molecule) so it basically preserves the tissue, allowing the trapped material to build up over time.
Make Sure Your Doctor Cleans the Scope With Peracetic Acid
The problem, in a nutshell, is that doctors are reusing devices that are impossible to properly clean. There is a safer cleaning alternative, however, and knowing this could very well save your life.
If you’re compelled to get a colonoscopy or flexible sigmoidoscopy, contact the office before the procedure and make sure they are properly decontaminating the scope using peracetic acid.
About 20% of flexible endoscopes in the U.S. are cleaned with peracetic acid between patients rather than Cidex. Peracetic acid (which is similar to vinegar) is used in organic chemistry labs to dissolve proteins, and it does a far better job than glutaraldehyde.
So, if for whatever reason you are compelled to get a colonoscopy or flexible sigmoidoscopy, then it is IMPERATIVE that you contact the office before the procedure to make sure they are properly decontaminating the scope using peracetic acid.
The reason most clinics use Cidex is because it’s cheaper. Even pennies per procedure add up when you’re doing them by the thousands each year, and hospitals are under pressure to save money wherever they can. However, when your health and life are at stake, saving pennies becomes inconsequential, and you’d be wise to forgo any hospital that still uses Cidex to clean their equipment.
How will you know how any given facility cleans their scopes? You have to ask. If you’re having a colonoscopy or any other procedure using a flexible endoscope done, be sure to ask:
How is the endoscope cleaned between patients?
Specifically, which cleaning agent is used?
How many of your colonoscopy patients have had to be hospitalized due to infections?
If the hospital or clinic uses peracetic acid, your likelihood of contracting an infection from a previous patient is slim. If the answer is glutaraldehyde, or the brand name Cidex, cancel your appointment and go elsewhere. As for the third and last question, the answer you want is zero.
The Surprising Benefits of Aspirin
Interestingly, research has shown colonoscopies may be unnecessary if you’re taking daily aspirin. While this may sound too good to be true, researchers found that aspirin can, in fact, eliminate certain cancerous tumors, such as liver tumors.19
A systematic review and meta-analysis published in 201720,21 also concluded that aspirin was as effective for preventing colorectal cancer incidence and death thereof as screening with flexible sigmoidoscopy or FOBT, and aspirin was actually more effective for preventing death from cancer in the proximal colon. As reported by the authors of that analysis:22
“The effect of aspirin on colorectal cancer mortality was similar to FOBT and flexible sigmoidoscopy. Aspirin was more effective than FOBT and flexible sigmoidoscopy in preventing death from or cancer in the proximal colon. Aspirin was equally effective as screening in reducing colorectal cancer incidence, while flexible sigmoidoscopy was superior to FOBT.
Conclusions: Low-dose aspirin seems to be equally effective as flexible sigmoidoscopy or guaiac FOBT screening to reduce colorectal cancer incidence and mortality, and more effective for cancers in the proximal colon. A randomized comparative effectiveness trial of aspirin vs. screening is warranted.”
There is even a study23 of over 600,000 men and women in which aspirin use at least 16 times per month was associated with a 40% reduced risk of colon cancer mortality over the six-year study period.
A 2016 study24 in JAMA Oncology also found aspirin use staved off colorectal cancer. This study included nearly 136,000 people who were followed for 32 years. Taking either a 325 mg tablet or an 81 mg tablet at least twice a week reduced overall cancer incidence by 3%, the risk for gastrointestinal cancer by 15% and colorectal cancer by 19%.
What might explain these findings? Well, there are several potential mechanisms by which aspirin can be helpful against cancer, including the following:
Aspirin is a prostaglandin inhibitor, so it can help address hormone imbalances that contribute to colorectal cancer development
It lowers your iron, which is another potential cancer contributor
It has anti-inflammatory effects
It has anti-lipolytic effects, so it inhibits insulin resistance and Type 2 diabetes, both of which are risk factors for cancer
If you decide to implement this recommendation it is likely that taking one regular aspirin a day, preferably with your largest meal to avoid any gastrointestinal damage, would be the best strategy. If you are taking blood thinners, are very sick, or are on multiple medications, using willow bark would likely be a safer option.
Should You Get Routine Colonoscopies After 50?
I’m 68 and I’ve never had a colonoscopy and have no plans of ever getting one. While I believe they can be valuable in some circumstances, I feel confident that with my rigid avoidance of omega-6 LA and lifestyle it’s highly unlikely I would ever develop any cancer, let alone colon cancer. For those at high risk, however, colonoscopies may be useful.
Another alternative is to get tested by flexible sigmoidoscopy every five years. It’s similar to a colonoscopy, but uses a shorter and smaller scope, so it cannot see as far up into your colon. It’s associated with far fewer complications, but you still need to check with the hospital or clinic to make sure they’re using peracetic acid to clean the device.
Overall, visual inspection is the most reliable way to check for colon cancer, and this is what the colonoscopy allows your doctor to do. If polyps are found in their early stages, your doctor can simply snip them off right then and there. So, a colonoscopy is not only a diagnostic tool, it can also serve as a surgical intervention. They take a picture of the polyp, clip it, capture it, and send it to biopsy. So, it could save your life, and it’s definitely something to consider.
However, you do not want to risk complications or infections by having the procedure done with a contaminated piece of equipment! So, please remember to make sure they’re using the proper cleaning solution. It could save your life.
Originally published December 28, 2022 on Mercola.com
In an observational study of real-world patients with nonvalvular atrial fibrillation, those treated with rivaroxaban had a significant risk reduction for severe stroke and all-cause mortality after stroke compared with patients who were prescribed warfarin, according to research published in Stroke.
In a retrospective cohort study of patients who began treatment with rivaroxaban (Xarelto, Janssen/Bayer) or warfarin within 30 days of nonvalvular AF diagnosis, researchers found that rivaroxaban reduced the risk for stroke by 19% (HR = 0.81; 95% CI, 0.73-0.91) compared with warfarin.
Moreover, analysis by stroke severity found that rivaroxaban provided a 48% risk reduction for severe stroke (NIH stroke scale score, 16 to 42; HR = 0.52; 95% CI, 0.33-0.82) and 19% for minor stroke (NIH stroke scale score, 1 to < 5; HR = 0.81; 95% CI, 0.68-0.96) compared with warfarin, but revealed no difference for moderate stroke (NIH stroke scale score, 5 to < 16; HR = 0.93; 95% CI, 0.78-1.1).
“This study showed risk reduction with rivaroxaban treatment in stroke overall and across all but the moderate stroke category,” Mark Alberts, MD, FAHA, chief of neurology at Hartford Hospital and physician-in-chief at Ayer Neuroscience Institute, Hartford, Connecticut, and colleagues wrote. “A possible explanation for the nonsignificant risk reduction for moderate stroke is insufficient power, given that the occurrence of stroke is so rare in this study population of patients with nonvalvular AF taking anticoagulants.”
In other findings, patients with nonvalvular AF who were treated with rivaroxaban experienced a risk reduction for all-cause mortality of 24% poststroke (HR = 0.76; 95% CI, 0.61-0.95) and 59% within 30 days (HR = 0.41; 95% CI, 0.28-0.6) compared with patients treated with warfarin.
For this retrospective cohort study, researchers included de-identified patients from the Optum Clinformatics Database who received rivaroxaban or warfarin within 30 days of initial diagnosis for nonvalvular AF. Before diagnosis, patients had 6 months of continuous health plan enrollment and a CHA2DS2-VASc score of at least 2.
“This study’s findings may help health care providers choose more effective treatments for managing their patients with nonvalvular AF, which may improve stroke prevention, optimize functional outcomes secondary to risk reduction of severe stroke and reduce mortality from stroke,” the researchers wrote. – byScott Buzby
Patients with venous thromboembolism treated with anticoagulants for more than 3 months had a lower risk for major adverse cardiovascular events, according to a study published in CHEST.
Further, VTE treatment with direct oral anticoagulants (DOACs) showed a greater decreased risk for major adverse cardiovascular events (MACE) and cardiovascular death than vitamin K antagonists (VKAs), according to researchers.
Patients with venous thromboembolism treated with anticoagulants for more than 3 months had a lower risk for major adverse cardiovascular events.
“We found that the risk of MACE that occurred following VTE was significantly reduced in patients treated for a long duration,” Steve Raoul Noumegni, MD, PhD, of the internal medicine, vascular medicine and pneumology department at Brest Teaching Hospital in France, and colleagues wrote. “We also found a significant relationship between the type of anticoagulant treatment and the risk of MACE, with a reduced risk in patients treated with DOACs compared with those treated with VKAs.”
In a prospective observational cohort study, Noumegni and colleagues analyzed 3,790 adults (mean age, 60.48 years; 47.2% men) treated with an anticoagulant for symptomatic VTE to determine whether this treatment impacts the risk for MACE, given that data show patients with VTE are at higher risk for cardiovascular events.
From the total study population, 2,788 patients received a VKA, 441 received a DOAC and 561 received low-molecular-weight heparin.
Researchers then divided the total cohort into three groups according to how long they were on their therapy: 1,228 patients (32.4%) received treatment for 0 to 3 months, 1,271 (33.5%) for 3 to 12 months and 1,291 (34.1%) for more than 12 months.
MACE, which included nonfatal acute coronary syndrome, nonfatal stroke and all-cause death, served as the study’s primary endpoint. MACE-2, which included cardiovascular death, nonfatal acute coronary syndrome and nonfatal stroke, was a secondary outcome.
In order to observe the association and risk between anticoagulant therapy and MACE/MACE-2, researchers used Cox proportional and Fine-Gray models.
Median follow-up was 68 months. In that time, 1,520 patients (40.1%) experienced MACE, equating to an annual incidence of 6.3 per 100 patient-years (95% CI, 6-6.62).
Of the defined causes, researchers found that all-cause death was the most common occurrence in 84.3% of patients with MACE, and nonfatal stroke followed after in 10.8%. Overall, the mortality rate was 5.59 per 100 patient-years (95% CI, 5.31-5.89).
Researchers found a significant decreased risk for MACE among patients receiving anticoagulation for 3 to 12 months (adjusted HR = 0.64; 95% CI, 0.54-0.76) or more than 12 months (aHR = 0.47, 95% CI, 0.39-0.56) compared with those treated for less than 3 months after adjusting for confounders in multivariable analysis.
Of 3,201 patients, 539 patients (16.8%) experienced MACE-2, for an annual incidence of 2.24 per 100 patient-years (95% CI, 2.04-2.44). Cardiovascular death was the most common occurrence of MACE-2 at 55.7%, with 324 of the 1,398 patients who died (23.2%) during the study dying of cardiovascular death.
Assessing the risk for MACE-2, researchers found comparable findings to their previous analysis, with patients treated for 3 to 12 months (adjusted sub-HR = 0.61; 95% CI, 0.47-0.79) and more than 12 months (adjusted sub-HR = 0.52; 95% CI, 0.39-0.68) demonstrating a lower risk than patients treated for 3 months or less.
When comparing types of anticoagulation, researchers observed that DOACs significantly reduced the risk for MACE (aHR = 0.53; 95% CI, 0.39-0.71) and MACE-2 (adjusted sub-HR = 0.48; 95% CI, 0.29-0.77) compared with VKAs in both univariable and multivariable analysis.
Notably, low-molecular-weight heparin treatment significantly raised the risk for MACE by 46% (aHR = 1.46: 95% CI, 1.23-1.75) compared with VKAs in adjusted models.
“These findings may influence the choice of type and duration of anticoagulant treatment for VTE; however, they need confirmation by randomized controlled clinical trials,” Noumegni and colleagues wrote.
This study by Noumegni and colleagues adds to the literature indicating that DOACs may provide a “feasible and simple” strategy for the extended secondary prevention of VTE while also preventing MACE, according to an accompanying editorial byCecilia Becattini, MD, and Maria Cristina Vedovati, MD,of the internal vascular and emergency medicine stroke unit at the University of Perugia.
“In conclusion, extended prevention of recurrent VTE with DOACs may offer the possibility to reduce both recurrent VTE and arterial cardiovascular events,” Becattini and Vedovati wrote. “If confirmed in further studies, these data may change the paradigm for secondary prevention of VTE.”
Wearable technology, including wrist-worn smartwatches that monitor heart rate variability, may help identify and predict flares of inflammatory bowel disease, according to data presented at the Crohn’s and Colitis Congress.
“It is challenging to identify and predict IBD flares, and we lack easy and convenient means to monitor patients,” Robert P. Hirten, MD, assistant professor of medicine at the Icahn School of Medicine at Mount Sinai,told Healio. “Currently we rely on the use of blood or stool tests, imaging tests such as CT scans or MRIs, colonoscopies [and] symptom reporting by patients. It is our hope to one day be able to use wearable devices, which are commonly used, convenient and passive, to be able to monitor for changes in the body that could alert us to a current or impending disease flare.”
Wrist-horn smart watches and wearable technology that monitors heart rate variability may help identify and predict flares of IBD.
To determine whether wearable technology assessing physiological metrics — including heart rate variability, a marker of autonomic nervous system function — may be able to predict IBD flares and other inflammatory events, Hirten and colleagues launched The IBD Forecast study.
Within this prospective study, the researchers enrolled patients with IBD (n = 125) aged 18 years or older in the United States, who were willing to use a commercially available wearable device, download a custom eHive app and answer daily questions.
Hirten and colleagues analyzed heart rate variability metrics using a mixed-effect cosigner model that integrated BMI, age and sex. They also used daily patient reported outcome (PRO)-2 surveys to assess clinical flares (flare; PRO-2 Crohn’s disease >7, PRO-2 ulcerative colitis >2), while inflammatory flare was evaluated through patient-reported C-reactive protein, defined as at least 5 mg/L.
According to preliminary analysis, the mesor of the circadian pattern of heart rate variability metrics was higher among patients undergoing clinical flare (mean = 44.43; 95% CI, 41.25-47.75) vs. those in clinical remission (mean = 43.03; 95% CI, 39.94-46.22). Additionally, the mesor of the circadian pattern was lower in patients with an inflammatory flare (mean = 38.16; 95% CI, 30.86-45.72) vs. patients with normal inflammatory markers (mean = 49.51; 95% CI, 43.12-56.26).
“We find that there are significant changes in autonomic nervous system function, reflected in heart rate variability measurements, when individuals with IBD develop symptoms or develop inflammation,” Hirten said. “This demonstrates the possibility of using wearable devices to identify, and possibly, predict flares.”
Although the IBD Forecast Study is still ongoing, Hirten noted that he hopes machine-learning algorithms can be developed with data from wearable devices to reliably track changes in autonomic function that precede an IBD flare.
“These early results demonstrate that wearable devices may hold promise in the ability to identify and predict IBD flares, though much more work is still needed,” Hirten told Healio. “I hope these results demonstrate that in the future we can use new technologies, like wearable devices, to monitor our patient’s health and improve their care.”
The FDA issued a complete response letter on the accelerated approval of donanemab for treatment of early symptomatic Alzheimer’s disease, citing the limited number of patients with longer drug exposure data.
Manufacturer Eli Lilly said in a press release that the FDA specifically requested that the company provide data from at least 100 patients who received a minimum of 12 months of continued treatment with donanemab.
The FDA issued a complete response letter for the accelerated approval of donanemab for the treatment of early symptomatic Alzheimer’s disease.Source: Adobe Stock
The accelerated approval application was based on phase 2 trial data, which demonstrated reduction of amyloid plaques in the brain, the company said. A phase 3 trial remains ongoing, with data expected in the second quarter of 2023.
Donanemab’s specificity to target deposited amyloid plaque informed the clinical trial design of the current phase 3 trial, which allowed patients to complete their course of treatment when they reached a predefined level of amyloid plaque clearance, according to Eli Lilly.
Although the phase 2 trial included more than 100 patients treated with donanemab, because of the speed of plaque reduction, many patients were able to stop treatment after 6 months, which resulted in less than 100 patients receiving 12 months of donanemab, according to Eli Lilly.
“We look forward to our upcoming confirmatory phase 3 results and subsequent FDA submission, which we’ve always seen as the most impactful next steps for patients,” Anne White, Lilly Neuroscience executive vice president and president, said in the release. “We anticipate this study will confirm the benefit and safety profile we observed in the phase 2 study and believe that patients and physicians will be well-served by having the full phase 3 data available alongside our phase 2 data when they need to make treatment decisions.”
The Alzheimer’s Drug Discovery Foundation (ADDF) issued a statement in response to the FDA’s request.
“This drug did what it was intended to do — remove amyloid plaques in the brain — and because of the trial’s innovative design, treatment was halted for patients once the biomarker PET scans confirmed the plaques were gone,” Howard Fillit, MD, co-founder and chief science officer at the foundation, said in an ADDF press release. “In some cases, this occurred in less than 12 months, which is why fewer patients stayed on the drug for a full year.”
The Alzheimer’s Association also responded, issuing a statement that it “appreciates” the FDA’s methodical process in reviewing treatments for AD.
“The FDA’s determination that additional data is required to reach a decision on accelerated approval of donanemab demonstrates the rigorous approach the agency takes in reviewing individual treatments,” the association said in a press release.
Patients with the rs2305480 variant of the GSDMB gene who had a pet dog as a baby did not have an increased risk for persistent wheeze or asthma, according to a study published in TheJournal of Allergy and Clinical Immunology.
This finding occurred despite the fact that the GSDMB missense variant (G allele) of rs2305480, which is located in the 17q12-21 locus, has been associated with asthma and asthma exacerbations. Infants with the variant and pet cats, however, did not experience the same effect, Mauro Tutino, PhD, research associate in the division of infection, immunity and respiratory medicine of the School of Biological Sciences at University of Manchester, and colleagues wrote.
Patients with the rs2305480 variant of the GSDMB gene who had a pet dog as a baby did not have an increased risk for persistent wheeze or asthma.
To evaluate gene-environment interactions between the 17q12-21 locus and pet ownership in infancy, the researchers examined data from the Study Team for Early Life Asthma Research (STELAR) consortium, which comprised five unselected birth cohorts of 15,941 children in the United Kingdom. These participants had never or infrequent wheeze (52.4%), early-onset preschool remitting wheeze (18.6%), early-onset middle-childhood remitting wheeze (9.8%), persistent wheeze (10.4%) and late-onset wheeze (8.8%).
Overall, 2,587 of the children had data on genotype, with 52% harboring the G allele of rs2305480, and pet ownership during their first year of life (cat owners, n = 438; dog owners, n = 344; both, n = 109). Further, 2,475 participants had latent class analysis (LCA) data, and 2,354 had data on asthma ever at age 16 years (AE16).
The researchers also examined data from the Avon Longitudinal Study of Parents and Children (ALSPAC) cohort separately, which included 6,149 children with both genotype (52% harboring G allele of rs2305480) and pet ownership information, 5,850 of whom had LCA data and 2,991 had data on AE16 phenotype.
In an additive model, researchers confirmed the G allele of rs2305480 was associated with increased risk for persistent wheeze (OR = 1.37; 95% CI, 1.25-1.51).
IBased on a meta-analysis of summary statistics for pet ownership during the first year of life, the researchers determined that there was no association between ownership of cats or dogs with asthma or any wheezing classes.
When stratifying results by pet ownership, results of fixed-effects models showed that infants who did not own a pet and had the G allele of rs2305480 had an increased risk for the AE16 phenotype (OR = 1.24; 95% CI, 1.12-1.38) and the LCA classes for late-onset (OR = 1.25; 95% CI, 1.06-1.48) and persistent (OR = 1.61; 95% CI, 1.4-1.86) wheeze.
Also among those with the G allele of rs2305480, cat owners had an increased risk for the AE16 phenotype (OR = 1.2; 95% CI, 1.02-1.43) and persistent wheeze (OR = 1.28; 95% CI, 1.02-1.6), whereas dog owners showed reduced risk for persistent wheeze (OR = 0.95; 95% CI, I0.73-1.24).
The researchers also found evidence of a significant multiplicative interaction odds ratio (ORint) between dog ownership and the rs2305480 genotype in relation to persistent wheeze, whereby dog ownership significantly attenuated the risk of the rs2305480 asthma-risk allele (random-effect ORint = 0.59; P = 8.3 × 10–4). Cat owners experienced a similar trend that did not reach statistical significance, whereas dual cats and dogs experienced the same attenuation of risk for persistent wheeze as those who owned dogs.
Using data from one of the cohorts to examine biological mechanisms for these findings, researchers also found that dust endotoxin levels were significantly higher in the houses of pet owners, with higher endotoxin levels associated with reduced risk for persistent wheeze (OR = 0.89; P = .04).
“The attenuating effect of dog ownership on persistent wheeze for those with the asthma-risk allele observed in the current study is likely due to an environmental exposure for which dogs are a proxy (ie, microbiota, endotoxin levels),” the researchers wrote, adding that future studies should use precise phenotyping to confirm the generalizability of these results among non-European populations.
This study is significant because there have been controversies about the so-called protective effect against asthma of having a cat or a dog in infancy since 1999. This paper shows that among patients with a particular genetic background, dog exposure seems to be protective.
In my own experience, I have encountered patients who were allergic to cat or dog regardless of whether they were exposed to dogs during infancy.
However, these findings will have no practical effect, because a dog lives for 10 to 20 years, and the child will be exposed to dog allergens during this entire period. This paper only assessed exposure during the first year of life. As soon as the child is sensitized to dog, if he or she is exposed to a dog or cat, there will be an increased risk for asthma.
Next, the researchers should assess the effect of dog exposure from infancy through age 12 years in this subgroup.
Frédéric de Blay, MD
Head of Chest Diseases Department, University Hospital of StrasbourgPresident, French Federation of Allergology
Worldwide, Alzheimer’s disease affects twice as many women as men, partly because women, on average, live longer, but this cannot fully explainthe difference.
At menopause, estrogen levels drop, and this reduction in hormones may increase the risk of developing Alzheimer’s.
Studies into the effect of hormone-replacement therapy (HRT) on Alzheimer’s risk have produced conflicting results, with some showing an increase and others a decrease.
A new study has suggested that HRT may decrease the risk of Alzheimer’s in women who have a gene that increases their risk of the condition.
The World Health OrganizationTrusted Source predicts that by 2050 some 139 million people worldwide will be living with dementia. According to the CDCTrusted Source, the most common form of dementia— Alzheimer’s disease (AD)—accounts for up to 80% of dementia cases, so by 2050, it is likely that, globally, more than 100 million people will have AD.
AD is largely a disease of old age, so these increases are mostly due to the aging population. And living longer is one reason why women are almost twice as likely as men to develop AD.
“It remains unclear in 2023 why more women develop Alzheimer’s dementia than men. It is true, that on average, women live longer than men. It is also true, that on average, male brains tend to have higher total brain volumes and are bigger than female brains.”
— Dr. Clifford Segil, D.O., neurologist at Providence Saint John’s Health Center in Santa Monica, California, speaking to Medical News Today
As age alone cannot explain the higher prevalence in women, experts are investigating other possible causes. One hypothesis is that the drop in hormones, particularly estrogen, at menopause, may increase dementia risk.”
Some previous research Trusted Sourcefound that HRT reduced the risk of all neurodegenerative diseases, including Alzheimer’s disease, particularly when used long-term.
Now, researchers from the Universities of East Anglia and Edinburgh, in the United Kingdom, have found that HRT may be particularly beneficial in women with a genetic risk factor for AD.
Around menopause, many women opt for HRT to alleviate symptoms such as hot flashes, night sweats, anxiety, and reduced sex drive.
Dr. Jennifer Bramen, senior research scientist at the Pacific Neuroscience Institute in Santa Monica, California, suggested one way HRT might work in decreasing Alzheimer’s risk.
“There are numerous mechanisms by which HRT might protect against AD, especially during early menopause. For example, estrogen attenuates the negative effects of cortisol. Cortisol spikes are a normal part of menopause, and high levels of cortisol are generally believed to increase cognitive impairment and neurodegeneration,” she explained to MNT.
The researchers were particularly interested in whether HRT had more impact on women with the APOE4Trusted Source gene. Having a single copy of APOE4 approximately triples a person’s risk of developing AD; having two copies can increase that risk by 8-12 times.
The gene is carried by around 25%Trusted Source of people, with 2-3% of people having 2 copies of the gene. To compare the effect of HRT on AD risk in those with and without the gene, the researchers divided the participants into those with APOE4 and those without.
Anyone who was being, or had been, treated with oral or transdermal estrogen, or estrogen plus progestogen, was recorded as having HRT.
For women without the APOE4 gene, HRT made no difference to cognitive function or brain volume.
In women with the APOE4 gene, HRT was associated with better memory and larger brain volume, with the greatest effect seen in those who started HRT earlier.
In people with AD, the hippocampusTrusted Source — a part of the brain that has a major role in learning and memory — shrinks by up to 25%Trusted Source. For the APOE4 carriers in this study, early HRT was associated with a greater hippocampal volume, which may indicate that HRT had a protective effect.
“The study throws out the idea that early treatment with HRT during a critical window may be neuroprotective, and claims like this arise often in research papers but are extremely hard to prove in clinical practice. One proposed mechanism would be HRT slows down brain shriveling or atrophy in women with APOE4 per the results of this paper.” — Dr. Clifford Segil, speaking to MNT
So, for women with a genetic predisposition to develop AD, starting HRT as soon as menopausal, or even perimenopausal, symptoms are noticed may be beneficial.
Prof. Michael Hornberger, professor of applied dementia research at the University of East Anglia’s Norwich Medical School, one of the study authors, commented:
“It’s too early to say for sure that HRT reduces dementia risk in women, but our results highlight the potential importance of HRT and personalized medicine in reducing Alzheimer’s risk.”
He added that the next stage of research needed was an intervention trial to confirm the impact of early HRT on cognition and brain health. This should be followed by an analysis of which types of HRT are most beneficial.
Dr. Emer MacSweeney, CEO and consultant neuroradiologist at Re:Cognition Health welcomed the study, and emphasized the need for further research.
“Circa 25% of the population carry an APOE4 gene and women develop Alzheimer’s disease more frequently than men. Any correlation of this type, that could lead to an intervention to decrease the risk of developing Alzheimer’s, is desperately needed, to reduce lifetime risk of Alzheimer’s,” she said.
“Further prospective research, in a larger study, will hopefully support and confirm the benefit of HRT, and identify exactly which HRT is most beneficial,” she added.
ARYAN'S BLOG 