From the desk of Zedie.
From the desk of Zedie.
Prescription drugs cause over 100,000 deaths per year and cause another 1.5 million people to experience side effects so severe they must be hospitalized.
Adverse drug reactions are now the fourth leading cause of death in the US. (1)
Every medication carries some risks and memory loss is a very common side effect.
The Top 3 Types of Drugs That Cause Memory Loss
If you are taking any prescription medication, the odds are that it falls into one of these three categories of drugs known to cause memory loss and other cognitive problems:
The “Anti” Drugs
If you take a drug that starts with “anti,” such as antihistamines, antidepressants, antipsychotics, antibiotics, antispasmodics, or antihypertensives, it’s likely that it will affect your acetylcholine levels.
Acetylcholine is the primary neurotransmitter involved with memory and learning. Low acetycholine can lead to symptoms that resemble dementia including mental confusion, delirium, blurred vision, memory loss, and hallucinations. (2)
Prescription sleeping pills are notorious for causing memory loss.
The popular drug Ambien has been coined by some as “the amnesia drug.” Some users experience night terrors, sleep walking, sleep driving, and hallucinations.
Prescription sleeping pills have been found to put you in a state similar to being passed out drunk or in a coma while bypassing the restorative sleep your brain needs. (3) There are much better ways to get to sleep!
These cholesterol-lowering medications might just be the single worst group of drugs for your brain. (4) Memory loss is now required to be listed as a side effect on the label.
One quarter of your brain is made up of cholesterol. Cholesterol is necessary for memory, learning, and fast thinking. So it is not a total surprise that cholesterol-lowering drugs negatively effect the brain.
Learn why taking statins might not be in your best interest, and how to talk to your doctor about getting off of them in Exposed: Why Cholesterol Doesn’t Cause Heart Disease and If You Take Cholesterol Medication, You Must Know This!
20 Medications Known to Cause Memory Loss
Here is a list of medications known to have memory loss as a possible side effect:
- for Parkinson’s — scopolamine, atropine, glycopyrrolate
- for epilepsy — phenytoin or Dilantin
- painkillers — heroin, morphine, codeine
- sleeping pills — Ambien, Lunesta, Sonata
- benzodiazepines — Valium, Xanax, Ativan, Dalmane
- antibiotics (quinolones)
- high blood pressure drugs
- beta blockers (especially those used for glaucoma)
- antipsychotics — Haldol, Mellaril
- tricyclic antidepressants
- barbiturates — Amytal, Nembutal, Seconal, phenobarbital
- chemotherapy drugs
This list was assembled by Richard C. Mohs, Ph.D., former vice chairman of the Department of Psychiatry at the Mount Sinai School of Medicine. (5)
What You Can Do Next
Are you taking any of these medications? If so, we recommend you talk to your doctor if you believe it’s affecting your memory.
Get your doctor to work with you to find better options — different prescriptions and/or making healthy lifestyle choices — instead.
Meanwhile, use the lifestyle advice you find here on our website.
Even if you have to stay on your medication, you can lessen the load on your brain by taking proactive steps such as eating a brain-healthy diet, getting the physical exercise your brain needs, and taking the right brain supplements.
Give your brain the healthiest possible environment to stay mentally sharp in spite of your medications.
Movie makers have been sending humans into deep space for decades, and a typical way of explaining how they got there unscathed is by placing them in stasis. Event Horizon, Prometheus, and the Alien series of movies are good examples of this. Humans in capsules in a suspended biological state while they travel for months or even years. But while that may be science fiction, it could now end up turning into science fact.
NASA has backed a study by SpaceWorks Enterprises looking into the use of deep sleep in order to allow astronauts to travel long distances in space. The first of such missions is going to be sending humans to Mars, a journey that will take around 180 days using current space tech. Keeping a human alive for that amount of time isn’t hard, but it does require sending enough food and entertainment along with them so they don’t starve or go crazy. The vessel they travel in also needs enough energy to maintain a livable environment for the human.
If a human could be placed into a very deep sleep instead, they wouldn’t need entertainment, food and water could be strictly controlled by intravenous drips, and the energy required to keep them alive would be lowered significantly. Therefore, it’s obviously a highly desirable thing to do.
The focus of this study is on torpor: a kind of hibernation state that sees body temperature and metabolic rate decrease. Some animals already naturally go into a torpor state on a regular basis and humans can if suffering from hypothermia. But NASA wants to try and safely adapt it for humans and extend it to 180 days. If it can, it would bring us a step closer to sending a team of astronauts to Mars.
Doctors already know how to induce therapeutic hypothermia in a patient, so the techniques are not completely novel. The preferred method is an intranasal cooling system like the RhinoChill pictured above, which streams coolant and gas into the body lowering its temperature and achieving a torpor state in a few hours.
The big challenge is the time extension, with a week being the best achieved so far. There’s also going to be a major health monitoring hurdle to overcome. What if something goes wrong during the journey to Mars? NASA will need the ability to monitor in real-time and adjust the torpor state remotely or even wake up an astronaut if their health is at risk.
In the latest Clinical Problem-Solving article, a 42-year-old man with a history of coronary artery disease presented to the emergency department with left-upper-quadrant abdominal pain that radiated to his back and along the subcostal margin. He also reported substernal chest pressure similar to his usual angina.
Elevated lipase and amylase levels can be indicative of pancreatic inflammation, but elevations are also seen with other intraabdominal conditions, such as cholecystitis, bowel obstruction, or celiac disease. Certain drugs, such as opiates and cholinergic agents, can also spuriously raise lipase and amylase levels.
•What is the epidemiology and typical presentation of celiac disease?
Celiac disease is an autoimmune disorder that affects the small bowel and that is triggered by ingested gluten from barley, rye, and wheat. The disease has both intestinal and extraintestinal clinical manifestations. The intestinal symptoms occur in 40 to 50% of adults, a prevalence that is less than that in children, and include abdominal pain, diarrhea, and other nonspecific abdominal symptoms; a mild elevation in aminotransferase levels is reported in 15 to 20% of patients with celiac disease. Celiac disease is associated with an increase by a factor of three in the risk of pancreatitis.
•What are the extraintestinal manifestations of celiac disease?
Celiac disease is also manifested outside the gastrointestinal tract. Rashes (e.g., dermatitis herpetiformis), arthralgias, neurologic and psychiatric symptoms, fatigue, and infertility can be presenting manifestations. Patients can also present with sequelae of malabsorption, including weight loss, iron-deficiency anemia, and osteoporosis or osteomalacia due to calcium and vitamin D malabsorption. Celiac disease can be associated with other autoimmune conditions, such as type 1 diabetes, autoimmune thyroiditis, and hepatitis. Some retrospective studies, but not others, have shown an increased risk of incident ischemic heart disease, a finding that has been postulated to be associated with chronic inflammation.
Morning Report Questions
Q: What is the epidemiology and prevalence of celiac disease?
A: The prevalence of celiac disease in screening studies is 0.5 to 1%; the disease is seen in all populations for which gluten is part of the diet, although the prevalence varies depending on the population studied. The HLA class II genes HLA-DQ2 or, much less commonly, HLA-DQ8 are expressed in the majority of patients with celiac disease. Although men and women have a similar prevalence of celiac disease in population-based screening studies, the disease is diagnosed more frequently in women than in men.
Q: How may the diagnosis of celiac disease made?
A: The diagnosis of celiac disease is usually made on the basis of serologic screening, followed by a confirmatory small-bowel biopsy. The serologic test of choice is the IgA anti-tissue transglutaminase antibody assay, which is highly standardized, specific (94%), and sensitive (97%). Measurement of IgG anti-tissue transglutaminase antibodies or deamidated gliadin peptide IgG antibodies can be performed in persons who are IgA-deficient. IgA antiendomysial antibodies are highly specific, but testing is expensive and operator-dependent. Measurement of antigliadin antibodies is no longer recommended for diagnosis owing to low diagnostic accuracy. Positive serologic testing in adults should be followed by a small-bowel biopsy to assess the severity of the small-bowel involvement and to ensure that the serologic test results are not falsely positive. Findings on biopsy range from near-normal villous architecture with prominent intraepithelial lymphocytosis to complete villous atrophy.
A 7-year-project to develop a barcoding and tracking system for tissue stem cells has revealed previously unrecognized features of normal blood production: New data from Harvard Stem Cell Institute scientists at Boston Children’s Hospital suggests, surprisingly, that the billions of blood cells that we produce each day are made not by blood stem cells, but rather their less pluripotent descendants, called progenitor cells. The researchers hypothesize that blood comes from stable populations of different long-lived progenitor cells that are responsible for giving rise to specific blood cell types, while blood stem cells likely act as essential reserves.
The work, supported by a National Institutes of Health Director’s New Innovator Award and published in Nature, suggests that progenitor cells could potentially be just as valuable as blood stem cellsfor blood regeneration therapies.
This new research challenges what textbooks have long read: That blood stem cells maintain the day-to-day renewal of blood, a conclusion drawn from their importance in re-establishing blood cell populations after bone marrow transplants—a fact that still remains true. But because of a lack of tools to study how blood forms in a normal context, nobody had been able to track the origin of blood cells without doing a transplant.
Boston Children’s Hospital scientist Fernando Camargo, PhD, and his postdoctoral fellow Jianlong Sun, PhD, addressed this problem with a tool that generates a unique barcode in the DNA of all blood stem cells and their progenitor cells in a mouse. When a tagged cell divides, all of its descendant cells possess the same barcode. This biological inventory system makes it possible to determine the number of stem cells/progenitors being used to make blood and how long they live, as well as answer fundamental questions about where individual blood cells come from.
“There’s never been such a robust experimental method that could allow people to look at lineage relationships between mature cell types in the body without doing transplantation,” Sun said. “One of the major directions we can now go is to revisit the entire blood cell hierarchy and see how the current knowledge holds true when we use this internal labeling system.”
“People have tried using viruses to tag blood cells in the past, but the cells needed to be taken out of the body, infected, and re-transplanted, which raised a number of issues,” said Camargo, who is a member of Children’s Stem Cell Program and an associate professor in Harvard University’s Department of Stem Cell and Regenerative Biology. “I wanted to figure out a way to label blood cells inside of the body, and the best idea I had was to use mobile genetic elements called transposons.”
A transposon is a piece of genetic code that can jump to a random point in DNA when exposed to an enzyme called transposase. Camargo’s approach works using transgenic mice that possess a single fish-derived transposon in all of their blood cells. When one of these mice is exposed to transposase, each of its blood cells’ transposons changes location. The location in the DNA where a transposon moves acts as an individual cell’s barcode, so that if the mouse’s blood is taken a few months later, any cells with the same transposon location can be linked back to its parent cell.
The transposon barcode system took Camargo and Sun seven years to develop, and was one of Camargo’s first projects when he opened his own lab at the Whitehead Institute for Biomedical Research directly out of grad school. Sun joined the project after three years of setbacks, and accomplished an experimental tour de force to reach the conclusions in the Nature paper, which includes data on how many stem cells or progenitor cells contribute to the formation of immune cells in mouse blood.
With the original question of how blood arises in a non-transplant context answered, the researchers are now planning to explore many more applications for their barcode tool.
“We are also tremendously excited to use this tool to barcode and track descendants of different stem cells or progenitor cells for a range of conditions, from aging, to the normal immune response,” Sun said. “We first used this technology for blood analysis, however, this system can also help address basic questions about cell populations in solid tissue. You can imagine being able to look at tumor progression or identify the precise origins of cancer cells that have broken off from a tumor and are now circulating in the blood.”
“I think that not only for the blood field, this can change the way people look at stem cell and progenitor relationships,” Camargo added. “The feedback that we have received from other experts in the field has been fantastic. This can truly be a groundbreaking technology.”
Wondering how much your sleep-in Saturdays or that one all-nighter will set you back? New research might help us gauge how to adjust our sleep schedules by shedding light on how many ZZZs we reallyneed.
The study, published in the journal Sleep, used the data of 1,885 men and 1,875 women collected from the Finnish “Health 2000″ survey. The sleep data included information about participants’ nightly quantity and quality of sleep, whether they had any sleep disorders, and how tired they were during the day. Additionally, the researchers used the Social Insurance Institution to gather information about how often those participants took sick days from work.
Results showed that those who took the fewest sick days slept, on average, 7.6 hours (for women) and 7.8 hours (for men) per night. In fact, those who got more or less than the “perfect” average of hours per night had an increased risk for sickness absence: up to eight more sick days per year. But, men reporting the optimal amount of sleep only took 5.93 days of sick leave each year on average; optimal female sleepers took 7.64 days. The researchers also found a few more interesting patterns: The male participants reported using sleeping pills more often and experiencing shorter durations of sleep than their female counterparts, while the women reported experiencing a greater effect of the seasons on their sleep duration.
This study supports previous research, which suggests the magic sleep number is somewhere between five and nine hours per night. It’s not just sleep quantity that matters; poor sleep quality has been shown to cause confusional arousal, or “sleep drunkenness.” Regardless, we know that sleep needs change with age and by individual, so it’s unclear how applicable this recent study’s results are to the population at large. And, although this research shows correlation between non-optimal sleep duration and increased number of sick days, that doesn’t mean one is caused by the other. Besides, nobody has ever taken a sick day when they weren’t actually sick, right? Right…
The most eye-catching statistic in the news last week was that the global animal populations have declined by 52% in the last 40 years, writes Anthony Reuben.
The figure comes from the Living Planet Report from the Zoological Society of London (ZSL) and WWF.
So there were half as many mammals, birds, reptiles, amphibians and fish (they only measure vertebrates) in 2010 as there were in 1970, according to the report.
This is one of those figures that makes you wonder how on earth they found out and indeed has sparked questions about both the statistical robustness of the figure and indeed whether having a single figure is relevant.
This is particularly the case because two years ago the same report said that the numbers had fallen by about 30%.
So what has changed since then? It’s all in the weighting.
Saying things about a big group by finding out about a smaller group and extrapolating is never a perfect approach.
In the past, this report has looked at all the data available from species around the world and assumed that the trend seen in those species reflected the trend for all vertebrates worldwide.
Is that fair? This year’s report followed data from about 3,038 of the estimated 62,839 vertebrate species, which is a pretty big sample.
But the sample is not random. There is much more research done into populations of birds and mammals than into reptiles, amphibians or fish.
The researchers have weighted the data to reflect what species actually exist and not just the ones that governments, academics or enthusiasts want to investigate.
This seems like a basically sensible approach, but there are still questions. For example, species that are in decline and a matter of concern may be more likely to be tracked than those that are not.
Also, species from less developed countries are more important to these figures than those in rich countries, because rich countries have often already lost areas such as forests and jungles where there is the greatest biodiversity.
So wildlife from the poorest countries get the greatest weighting in this research, but they are the ones for which by far the smallest amount of data is available.
Only 181 of the 3,038 species investigated came from low-income countries.
The researchers say that this is the first year they have had enough data to apply this weighting and that they will seek more figures for areas and species that are less represented to make future reports better than this one.
But while there are those who argue about whether the precise figure is accurate, there seem to be few who doubt the general trend.
The Nobel Prize for physiology or medicine has been awarded to three scientists who discovered the brain’s “GPS system”.
UK-based researcher Prof John O’Keefe as well as May-Britt Moser and Edvard Moser share the award.
They discovered how the brain knows where we are and is able to navigate from one place to another.
Their findings may help explain why Alzheimer’s disease patients cannot recognise their surroundings.
“The discoveries have solved a problem that has occupied philosophers and scientists for centuries,” the Nobel Assembly said.
Prof O’Keefe, from University College London, discovered the first part of the brain’s internal positioning system in 1971.
On hearing about winning the prize, he said: “I’m totally delighted and thrilled, I’m still in a state of shock, it’s the highest accolade you can get.”
His work showed that a set of nerve cells became activated whenever a rat was in one location in a room.
He absolutely deserves the Nobel Prize, he created a cognitive revolution”
Dr Colin LeverFormer student of John O’Keefe
A different set of cells were active when the rat was in a different area.
Prof O’Keefe argued these “place cells” – located in the hippocampus – formed a map within the brain.
He will be having a “quiet celebration” this evening and says the prize money “should be used for the common good”.
In 2005, husband and wife team, May-Britt and Edvard, discovered a different part of the brain which acts more like a nautical chart.
These “grid cells” are akin to lines of longitude and latitude, helping the brain to judge distance and navigate.
They work at the Norwegian University of Science and Technology in Trondheim.
Prof May-Britt Moser said: “This is crazy, this is such a great honour for all of us and all the people who have worked with us and supported us.”
The Nobel committee said the combination of grid and place cells “constitutes a comprehensive positioning system, an inner GPS, in the brain”.
They added: “[This system is] affected in several brain disorders, including dementia and Alzheimer’s disease.
“A better understanding of neural mechanisms underlying spatial memory is therefore important and the discoveries of place and grid cells have been a major leap forward to advance this endeavour.”
He absolutely deserves the Nobel Prize, he created a cognitive revolution”
Dr Colin LeverFormer student of John O’Keefe
Dr Colin Lever, from the University of Durham, worked in Prof O’Keefe’s laboratory for ten years and has already dreamt on two occasions that his former mentor had won the award.
He told the BBC: “He absolutely deserves the Nobel Prize, he created a cognitive revolution, his research was really forward thinking in suggesting animals create representations of the external world inside their brains.”
“Place cells help us map our way around the world, but in humans at least they form part of the spatiotemporal scaffold in our brains that supports our autobiographical memory.
“The world was not ready for his original report of place cells in 1971, people didn’t believe that ‘place’ was what best characterised these cells, so there was no great fanfare at that time.
“But his work on hippocampal spatial mapping created the background for discovering grid cells and with grid cells, the world was prepared and we all thought wow this is big news.”
Previous winners of the Nobel Prize for physiology or medicine
2013 – James Rothman, Randy Schekman, and Thomas Sudhof for their discovery of how cells precisely transport material.
2012 – Two pioneers of stem cell research – John Gurdon and Shinya Yamanaka – were awarded the Nobel after changing adult cells into stem cells.
2011 – Bruce Beutler, Jules Hoffmann and Ralph Steinman shared the prize after revolutionising the understanding of how the body fights infection.
2010 – Robert Edwards for devising the fertility treatment IVF which led to the first “test tube baby” in July 1978.
2009 – Elizabeth Blackburn, Carol Greider and Jack Szostak for finding the telomeres at the ends of chromosomes.
Also commenting on the announcement, Prof John Stein form the University of Oxford, said: “This is great news and well deserved.
“I remember how great was the scoffing in the early 1970s when John first described ‘place cells’.
“Now, like so many ideas that were at first highly controversial, people say ‘Well that’s obvious!'”