Day: 01/01/2023
Brain Supplements That Do and Don’t Work
Take a Pill, Protect Your Memory?
1/12
“Improves memory.” “Sharpens focus.” These are just some of the claims you may see on the supplements that 25% of adults over age 50 are taking to try to keep their brains healthy. Do these products work? It’s often unclear, as the FDA doesn’t require makers to prove the supplements are effective, as long they don’t make any claims about specific diseases. Here’s what experts do — and don’t — know about some of these popular items.
B Vitamins
2/12
B vitamins like B6, B12, and B9 (folic acid) all play a role in brain health. But unless you’re low on them or pregnant (folic acid is a must to prevent birth defects), a supplement is unlikely to help. If you’re at high risk for Alzheimer’s, ask your doctor. The research into the use of vitamin B supplements to boost cognitive ability is inconclusive. You should stick with food sources like leafy greens to stay sharp.
Caffeine
3/12
Caffeine pills and powders aren’t a good idea, because of the risks if you overdose. But you can enjoy coffee guilt-free, as long as it doesn’t worsen your sleep or make you jittery. Some might be good for your brain. It’s a stimulant that helps perk you up, plus it promotes energy by blocking brain receptors for a chemical called adenosine.
L-theanine
4/12
A natural amino acid, L-theanine seems to have potential for improving mental performance, especially when combined with caffeine. That said, most studies have been small, such as one in 2019 that included 30 people. Until there’s more research, a safe bet is to drink green tea: It naturally contains both L-theanine and caffeine, as well as antioxidants that may help your mental and physical well-being in other ways.
Omega-3s
5/12
The traditional Mediterranean diet, which includes omega 3-rich-fish, is linked to a lower risk of dementia. But can omega-3 supplements help? So far, large studies (including one sponsored by the National Institutes of Health) haven’t proved that. One possible exception: People with the APOE4 gene mutation, which is tied to Alzheimer’s, might benefit if they start taking the supplements early enough, a 2017 review shows.
Vitamin E
6/12
This antioxidant combats free radicals, including those that may damage brain cells. But large studies aimed at finding out whether vitamin E supplements can protect against dementia haven’t yielded great results, though at least one study found that they might slow the worsening of Alzheimer’s in people who already have it. For now, experts say most healthy people should stick with food sources like nuts, seeds, and vegetable oils.
Ginkgo Biloba
7/12
Although it’s a staple in traditional Chinese medicine, modern research has found that ginkgo supplements probably won’t protect your memory. Although some studies have suggested there might be benefits, the most well-designed trials — notably the Ginkgo Evaluation Memory study that included 3,000 older adults — showed that ginkgo doesn’t prevent or slow dementia.
Ginseng
8/12
Often used along with ginkgo, ginseng is another popular supplement that hails from Asia. As with ginkgo, some studies have suggested that ginseng might be a potent brain booster. But the evidence didn’t hold up when scientists homed in on the best-quality research: A review of several trials concluded there’s “no convincing evidence” that ginseng will protect your mental skills.
Curcumin
9/12
Found in turmeric (an ingredient in curry powder), curcumin has been hailed for its antioxidant powers. Does it help explain why Alzheimer’s rates are lower in India? A UCLA study found that people who took curcumin fared better on memory tests and had less buildup of abnormal proteins in their brains. But this study only included 40 people, and other research hasn’t found this result, so more studies are needed.
CDP-choline
10/12
In Europe, CDP-choline isn’t sold as a dietary supplement. Instead, it’s a prescription drug. According to researchers who reviewed 14 studies, there’s decent evidence that it can benefit memory in elderly people who already have memory problems. But whether it can prevent them in healthy people isn’t clear. Ask your doctor if you’re thinking of trying it.
What About Combos?
11/12
Many memory supplements aren’t sold as single ingredients. Though some ingredients might work well together, combined supplements are harder to study and could be risky. Supplements may cause side effects, and the risk rises with the number you take. Mixing them with prescription drugs can be risky, too. Review all the drugs and supplements you’re taking (or considering) with your doctor or pharmacist, so they can tell you what’s safe.
Food First
12/12
While certain supplements might help in some cases, most healthy people don’t need pills to stay sharp. Eating a diet that’s rich in vegetables, berries, whole grains, and fish (key parts of the so-called MIND diet) is a way to support brain health as you age. Staying physically active, getting enough sleep, taking care of any medical conditions you have, keeping up your social connections, and challenging your mind by being a life-long learner can make a big difference, too. And it’s good for the rest of your body!
How are viruses discovered and identified in the first place?
The earthshaking Etienne De Harven interview by Celia Farber
The question I’ve been asking since 1987—
If the experts are going to claim a particular virus causes a particular disease—how do they know that virus exists in the first place?
For example, the supposedly new coronavirus in China. For example, Ebola. For example, HIV. For example, the coronavirus supposedly causing SARS (2003). How do researchers know these viruses exist?
“Well, of course they know. They must.”
That is not a satisfactory answer—even though most people would offer it.
The question can become very interesting, when you stop and consider researchers working away in biowar labs fiddling with viruses. How do they know they’re tweaking viruses that actually exist?
On a more mundane frontier, when scientists tell us they’re rushing to develop a vaccine against a virus that is harming the population, how do they know that virus exists to begin with?
I came to this question when I was researching HIV in 1987. I began to think about it seriously in 1990. During all these years, I’ve reached out to independent researchers, and I’ve tried to stitch together their answers. I can’t say it’s been a smooth trip.
But I have found some answers; and I have certainly found some fake mainstream assertions, which glitter like baubles on plastic branches of 99-cent store Xmas trees.
Here are a few clues. You need to take a tissue sample from a live human being. You need to filter that sample correctly so you arrive at a much smaller sample you believe might contain a virus. You need to put a drop of that sample under an electron microscope and observe what looks like a virus.
How much virus? How many identical particles of virus? Opinions differ on this. It could be one definite virus, one particle. It could be many, many identical particles.
Sidebar: If you’re trying to prove this virus is actually causing DISEASE in a person, you have to go further. You have to show the very same virus is active and replicating at a very high rate in the person’s body, and his immune system isn’t defeating it. Beyond noticing the patient is sick, how do you test for all THAT? I’m still looking for a definitive technical answer—if there is one.
All right, let’s get back to the electron microscope. Let’s say you’ve observed many identical particles of what looks like a virus in the electron microscope photograph, called an EM. You can then say, “Found it.” But you need to be sure. You need to figure out that this virus isn’t just something that ordinarily lives in the human body like a couch potato and does nothing—a passive endogenous virus. No. You want to show this virus comes from the outside as an invader—an exogenous virus. And how do you perfectly make that differentiation every time? Another question that might have no precise formula as an answer.
Big question: CAN WE BE SURE ALL VIRUSES THAT ARE SAID TO EXIST AND SAID TO CAUSE EPIDEMICS ARE ACTUALLY FOUND AND OBSERVED AND IDENTIFIED ON ELECTRON MICROSCOPE PHOTOGRAPHS? CAN WE AT LEAST SAY THAT?
No.
In which case, the researchers have been, at least some of the time, up the creek without a paddle. They’ve jumped the gun. They’ve bolted out of the starting gate too soon. They’ve laid their money down on a horse that may not even be in the race. They’ve written a check no one can cash. They’re talking about lockdowns and quarantines without having proved their favorite virus of the moment exists. Sure, people on the back end will make big money from these unwarranted presumptions, but money is not science. It might control science, but it ISN’T science.
All right. I’ve now set the stage for an excerpt from an interview, a profound interview with a late mainstream master who, in the face of fake science, suddenly was characterized as a rebel, Etienne De Harven. The interview was conducted several years ago by the brilliant reporter, Celia Farber. You can find the whole interview here. I strongly suggest you read it sixteen times. Yes, it gets technical. You’ll also notice names of elite scientists you haven’t run across. Learn the meaning of the words you’ve never seen before. Dig in. This isn’t television-type brush-off conversation. This isn’t a YouTube throwaway.
I have another reason for exposing readers to this interview—it’s what a conversation about serious scientific issues looks like…this is what trying to bridge the gap between researchers, honest reporters, and the public looks like. There should be hundreds and thousands of such print-interviews taking place, laid before readers. They can handle it. Dumbing down people is partly an illusion: they can wake up. They WILL wake up if they’re sufficiently interested.
Etienne De Harven’s background: president of the Electron Microscopy Society of America; researcher, Memorial Sloan-Kettering Cancer Center; Cornell professor of cell biology; professor of pathology, University of Toronto; recognized pioneer in the field of electron microscopy.
The interview focuses on HIV; whether it was ever found and isolated. The implications and questions spread out to any and all viruses.
DE HARVEN: Unacceptably frustrated by the total lack of success in all attempts to demonstrate virus particles in human cancer by EM, the “impresarios” of the cancer/virus “dream” (Gallo, Fauci, and others) totally engaged in the molecular approach.
Consequently, they invented molecular markers to compensate for the missing viral particles…This would have been acceptable if the specificity of these new molecular markers would have been clearly established. Unfortunately, this was not the case. The most misleading molecular marker was probably the first one, i.e. the enzyme [called] reverse transcriptase (RT). Following Temin and Baltimore 1970 papers in “Science”, the RT enzymatic activity has been, most abusively, used as a specific retroviral marker. Both Temin and Baltimore demonstrated RT activity in samples of supposedly “purified” retrovirus.
Embarrassingly, they both omitted to verify the “purity” of their samples by EM. Some of their samples were simply purchased from a commercial company… True, the label on the vials read “pure retrovirus”… However, it was known that these commercial “pure retrovirus” were heavily contaminated by cellular debris!
And since it is also known that all cells contain RT (see Varmus), cellular debris are most likely carrying similar RT enzymes.
Temin and Baltimore did not, therefore, prove that RT is a specific molecular marker for retroviruses. It would have been so simple to check, by EM, the degree of “purity” of the samples they used. This would have, most probably, shown important cell debris contamination, and would have obliged Temin and Baltimore to be much more cautious in the interpretation of their results. In 1975, the members of the Nobel Committee, most regrettably, failed to scrutinize this “purity” problem…
In 1983, at Pasteur Institute in Paris, reliance on the RT marker was a key element in the claimed “isolation” of a new retrovirus [HIV]. Still, Montagnier himself recognized “We did not purify”… He dangerously omitted to consider the misleading interference of cell debris, just as Temin and Baltimore did in 1970.
But a paper on the discovery of a new retrovirus looks much better if it contains at least… one EM picture! So, members of Montagnier’s team spent hours at the TEM [transmission electron microscope], looking at their mixed cell cultures, and they found the virus!
See Fig. 2 in their “historic” 1983 “Science” paper! It is, by the way, a good quality EM picture. It shows unquestionable retroviral particles, budding at the surface of a cell. But the legend of this Fig. 2 states that this cell is a cord blood lymphocyte. Indeed, cord blood lymphocytes were admixed to these complex cell cultures (why?)
Montagnier and his co-workers should have known that human embryonic tissues, and the placenta in particular, are very rich in endogenous retroviruses (HERVs), and that cord blood lymphocytes should therefore be expected to carry the same endogenous retroviruses (under the TEM, endogenous and exogenous viruses, looking identical, cannot be distinguished.)
The budding of these particles has perhaps been stimulated by some of the growth factors also present in these cell cultures. An essential control would have been to repeat the experiment using lymphocytes from the peripheral blood instead of from cord blood. This control is unfortunately missing.
In short, I would frankly state that the Pasteur 1983 paper (whose 30th anniversary has just been celebrated in a “grand messe” of official HIV retro-virology!) contributed very little in AIDS research because its conclusion (i.e. “the isolation of a new retrovirus”) is based on 1) the use of a non specific RT molecular marker, and 2) is falsely supported by EM pictures of, most probably, endogenous human retroviruses.
More details and appropriate references on this analysis can be found in my 2010 paper published in the Journal of American Physicians and Surgeons [— “Human Endogenous Retroviruses and AIDS Research: Confusion, Consensus, or Science?”] (jpands.org/vol15no3/deharven.pdf).
CELIA FARBER: When antibody and VL [viral load] tests became widespread as diagnostic tools for “HIV infection” over the ensuing decades, what happened with EM inside of HIV science and literature? It is my understanding that nobody has ever found HIV in human blood, on EM. Is this an accurate way to say it?
DE HARVEN: In my views, Western Blot [antibody] tests lost all credibility after the publication of Eleni Papadopulos’s et al. (1993) paper, and antibody tests (“Elisa”) [lost credibility] after Christine Johnson’s report (1996). The notion of a “Viral load” (VL), however, brought a new parameter in AIDS diagnosis (Ho,1996). It called attention to the actual number of HIV particles supposedly present in the blood plasma of AIDS patients, PCR technologies [tests] being presumed to offer a way to quantify that number.
If such a viremia (i.e. presence of virus particles in the blood) is indeed present in AIDS patients, it reminisces the retroviral viremia well known in leukemic mice. In such case, retroviral particles should be readily demonstrable, by TEM, of appropriately prepared patient plasma samples. Unfortunately, it has never been possible to demonstrate by TEM one single retroviral particle in the blood plasma of any AIDS patient, even if one selects patients presenting with a so-called “high viral load.”
I was apparently the first researcher to make that statement, during the opening session of President T. Mbeki’s major AIDS conference, in Pretoria, SA, in May 2000. My statement to that effect has never been refuted.
CELIA FARBER: How come?
DE HARVEN: That question must be answered because “something” is measured by PCR technologies in the blood of many AIDS patients. Actually, what is being measured is definitely not the number of retroviral particles (phantom-like, i.e. EM invisible!). In fact, what is being PCR identified, amplified, and supposedly quantified is the number of genomic nucleotide sequences that are extremely similar to sequences known to be part of the retroviral genome. Most regrettably, these sequences were misinterpreted as an indication as a certain number of … HIV particles! This did a lot to consolidate the quasi-religious dogma of HIV as the cause of AIDS, a dogma that has been sharply criticized, a few years ago, by David Rasnick who wrote, authoritatively, about “The AIDS Blunder”…
This interpretation would have been acceptable only if retroviral particles would have been readily demonstrated, by EM, in the blood plasma of these patients; but, since this is not the case, another explanation for the presence of these nucleotide sequences has to be founded.
I presented at the RA conference in Oakland, CA, in 2009, and further developed in my 2010 JAPS paper such a much needed explanation for the presence of these retroviral-like nucleotide sequences. My explanation is based on the well known, variable amounts of circulating DNA in the blood of severely ill patients, and on the fact that we all carry [irrelevant] retroviral-like sequences in our DNA, as endogenous, defective retroviruses, i.e. HERVs (HERVs, for “Human endogenous retroviruses”) (See “Virus in all of us”, R. Lower at al., 1996 PNAS paper).
No surprise, therefore, that these nucleotide sequences are recognized by PCR [tests] in the blood of many AIDS patients, who are indeed severely ill. As already demonstrated in 2008 in Robin Weiss laboratory, HERVs can interfere as confounding factors in the search for novel retrovirus in chronic human diseases…
CELIA FARBER: …Paint a picture for us. The story of the [HIV] virus, the “new deadly virus,” what happens first: What steps did they [—] Montagnier, on one hand, Gallo on the other [—] take to “find” the new entity? Then once they ‘found’ it, what shape was it in? It was not an entity, a thing, with a body, right? It was not coherent. Can we say that? So it lived where? It was seen only through the technologies developed to find it, Elisa, WB [both are antibody tests]? Later PCR/VL [tests]? But what happened back THEN when they tried to see it on EM? Why didn’t everybody look for it on EM? Too expensive?
DE HARVEN: No, EM is not cheap but not that expensive! And its cost has certainly nothing to do with the fact that it has barely been used for the past 30 years in AIDS research! It has not been used because “They” knew it was not going to show anything of retroviral significance in samples coming directly from AIDS patients. And since AIDS had become big business, the stocks of involved giant pharmaceutical companies could not be jeopardized! It had to be saved at all cost, even at the cost of trusting non specific molecular markers… Fear is good business, and viruses generate fear most efficiently… So, the HIV flag has to be maximally agitated. In worldwide medias, with thousands of computer-generated, colorful caricatures of an idealistic retrovirus… By contrast, the medias have been dominated by the most rigorous censorship when it comes to inform the public about views of rethinking dissidents. This total censorship put a safety lock on any information that could jeopardize the colossal, entirely HIV derived profits of the major pharmaceutical companies.
But I am glad we have Internet!
Daring to say that HIV does not exist amounts to some sort of a capitalistic crime…
Yes, the HIV dogma is probably the darkest page in the history of modern medicine.
CELIA FARBER: Etienne, if you could sum up: Does HIV exist? If so, where and how and as what?
If you could examine 1,000 HIV positive people’s blood under EM, what would you expect to find? If you don’t find HIV on EM in human blood, can any argument be made that the virus is “hiding” and so forth, or that the drugs suppressed the virus to undetectable levels? This is what the defenders of the orthodoxy seem to be saying about the results seen in the Nushawn Williams case.
DE HARVEN: This is the main question! Questioning the very existence of HIV is not something that should be debated only between specialized retro-virologists. It is an essential question that concerns all of us.
CELIA FARBER: Why?
DE HARVEN: Simply because 100% of AIDS research funding is based on the dogmatically postulated existence of HIV. If HIV does not exist, it would follow that AIDS research is the most appalling case of total misappropriation of public research funds! And it would also follow that the monumental amounts of money, so far exclusively devoted to HIV research, would be much better used in other directions. Could you imagine what world we would live in, today, if the total amount of money wasted over the past 30 years on HIV research had been, instead, used for feeding starving Africans, for clean water supply equipment, for public hygiene infrastructures, and for public health education? This would happen only if HIV research is totally stopped! And for this, the scientific and public health organizations have to face the fact that, indeed, HIV does not exist!
…we all have to, courageously, face the fact that the very existence of an exogenous HIV has never been scientifically verified.
—end of interview excerpt—
Again, you can read the whole interview here.
De Harven unmasks HIV research. How many other unproven viruses have likewise been prematurely massaged into existence and prominence? How many times have researchers pulled “special markers” like rabbits out of hats—spuriously claiming these markers establish the existence of otherwise never-observed viruses?
And therefore, when these researchers state they have published the genetic sequences of these viruses—what are they really sequencing? Harmless and passive endogenous viruses that wouldn’t hurt a fly and prefer to lie around in the body for the whole course of a lifetime watching television?
And when someone steps forward, and claims a new and never-before-seen virus is actually a manmade weapon, and he knows this from studying its genetic sequence—is he right, or is he looking at the sequence of an irrelevant microbe that has been rudely coaxed from its long languishing snooze in the warmth of the human body?
Coronavirus: Run, Here Come the Experimental Drugs
As I’ve shown in recent articles (archive here), the virus hunters have fallen far short of proving a coronavirus is causing this “outbreak.” But here come the antiviral drugs.
They’re ordinarily used for other diseases (malaria, HIV) or, in one case, no disease yet (unapproved, unlicensed). But it’s time for “heroic measures.” A better term would be “reckless experimentation.”
Public health officials are expressing a mixture of hope and…vampire-ish worry that the epidemic may not last long enough to properly test the efficacy of the drugs.
LA Times, 2/13/2020, “Doctors fight coronavirus outbreak with drugs that target HIV, malaria and Ebola”:
—Characterizing the remarks of a Harvard professor of medicine, the Times author writes: “The lack of certainty surrounding treatment for coronaviruses is partly due to the boom-and-bust nature of outbreaks — they can spread like wildfire and then disappear… Although that is good for the public’s health, it also means scientists sometimes don’t have the time or the means to thoroughly test a treatment in humans.” Tsk, tsk, what a shame.
Here’s another telling quote from the Times article: “The ramp-up in [drug] research and investments into outbreaks can wreak havoc on private drug companies, especially if the virus disappears at some point, as SARS did, said Dr. Jesse Goodman, a professor of medicine at Georgetown University in Washington, D.C. The federal government helps offset these costs through initiatives…” What do you know about that? The SARS virus “disappeared.” And pity the poor drug companies. Their research was interrupted.
Among the drugs suddenly being used on people diagnosed with the coronavirus: Kaletra (anti-HIV); chloroquine (anti-malaria); remdesivir (unapproved, anti-Ebola).
rxlist.com provides a list of adverse effects of Kaletra:
* diarrhea
* headache
* weakness
* nausea
* vomiting
* stomach upset
* drowsiness
* dizziness
* a bad taste in the mouth
* trouble sleeping
* skin rash
* changes in the shape or location of body fat (especially in your arms, legs, face, neck, breasts, and waist)
“Tell your doctor if you have serious side effects of Kaletra including”:
* unexplained weight loss
* persistent muscle aches or weakness
* joint pain
* numbness or tingling of the hands/feet/arms/legs
* severe tiredness
* vision changes
* severe or persistent headaches
* signs of infection (such as fever, chills, trouble breathing, cough, non-healing skin sores)
* signs of an overactive thyroid (such as irritability, nervousness, heat intolerance, fast/pounding/irregular heartbeat, bulging eyes, unusual growth in the neck/thyroid known as a goiter)
* signs of a nerve problem known as Guillain-Barre Syndrome (such as difficulty breathing/swallowing/moving your eyes, drooping face, paralysis, slurred speech)
* increased thirst
* increased urination
* confusion
* persistent nausea or vomiting
* stomach or abdominal pain
* yellowing eyes or skin
* dark urine
Chloroquine adverse effects (from Drugs.com)—“Check with your doctor immediately if any of the following side effects occur while taking chloroquine”:
* anxiety
* attempts at killing oneself
* back, leg, or stomach pains
* black, tarry stools
* bleeding gums
* blistering, peeling, or loosening of the skin
* blood in the urine or stools
* blurred or decreased vision
* change in near or distance vision
* chest discomfort or pain
* chills
* cold sweats
* confusion
* continuing ringing or buzzing or other unexplained noise in the ears
* cough
* dark urine
* diarrhea
* difficulty in focusing the eyes
* difficulty with speaking
* difficulty with swallowing
* disturbed color perception
* dizziness
* dizziness, faintness, or lightheadedness when getting up suddenly from a lying or sitting position
* double vision
* drooling
* fast, slow, irregular, or pounding heartbeat
* feeling that others are watching you or controlling your behavior
* feeling that others can hear your thoughts
* feeling, seeing, or hearing things that are not there
* fever
* general tiredness and weakness
* halos around lights
* headache
* hearing loss
* inability to move the eyes
* increased blinking or spasms of the eyelid
* joint or muscle pain
* large, hive-like swelling on the face, eyelids, lips, tongue, throat, hands, legs, feet, or sex organs
* light-colored stools
* loss of balance control
* lower back or side pain
* muscle trembling, jerking, or stiffness
* muscular pain, tenderness, wasting, or weakness
* night blindness
* nausea
* overbright appearance of lights
* painful or difficult urination
* pale skin
* pinpoint red spots on the skin
* puffiness or swelling of the eyelids or around the eyes, face, lips, or tongue
* red skin lesions, often with a purple center
* red, irritated eyes
* restlessness
* shuffling walk
* skin rash, hives, or itching
* sore throat
* sores, ulcers, or white spots on the lips or in the mouth
* sticking out of the tongue
* stiffness of the limbs
* sweating
* swollen or painful glands
* tightness in the chest
* trouble breathing
* tunnel vision
* twitching, twisting, or uncontrolled repetitive movements of the tongue, lips, face, arms, or legs
* uncontrolled movements, especially of the face, neck, and back
* unusual bleeding or bruising
* unusual tiredness or weakness
* upper right abdominal or stomach pain
* vomiting
* yellow eyes and skin
Adverse effects of remdesivir—the drug has not been approved for public use. I find at least one human clinical trial has been done on people “infected by the Ebola virus,” and another clinical trial is underway now. So far, I see no published list of adverse effects—probably because the drug is still in the test phase. Using this drug on “coronavirus patients” would certainly be experimental.
This is what I’m sitting here picturing: A person in Wuhan, who is having respiratory problems, owing to the unprecedented mixture of toxic pollutants in the air of the city, enters a clinic. He is given a chest CT Scan. He’s told he has a lung infection—pneumonia. Because a CT Scan is now absurdly sufficient for a diagnosis of “epidemic coronavirus,” he is given that label. NO test for the purported coronavirus is done. The person is shunted into a treatment room, and a doctor tells him his condition is quite serious, and he will be treated with a drug: chloroquine.
Go back and read the list of adverse effects again.
Suppose this patient tells his doctor he has a relative who lives out in the country, where the air is much better, and he wants to stay with her.
The doctor will, of course, tell the patient this is not possible. The city is locked down. If the patient left Wuhan, he could “spread the virus to others.”
He will be given the drug. What about informed consent? Will the doctor read the patient the complete list of adverse effects? Are you kidding? Wouldn’t that be “counter-productive?”
Mustn’t interrupt the “research” of pharmaceutical companies.
We can only hope and pray the “epidemic” is SAID TO LAST long enough so these benevolent corporations can complete their testing. What else is a pool of human guinea pigs for?
And worry not, the pill kings have their bases covered. When “test subjects” become sicker or die, the kings can simply say, “The coronavirus was responsible.”
It all works out for the best, doesn’t it?
We haven’t even gotten to the coronavirus vaccine yet. The professionals are working hard on cooking one up. When they do, there will be no danger of an interruption in their work, if “the virus disappears.” The vaccine will be injected into healthy people. If and when some of these people keel over, all sorts of reasons can be trotted out: underlying genetic condition; the coronavirus hidden in their cells suddenly activated; undisclosed immune-system deficiency; an unrelated disease; allergic cross-reaction; and, of course, “a rare and unavoidable adverse effect among all the life-saving injections given, at no charge, to the global population…”
I’m looking through mainstream articles. I’m trying to find one that publishes the complete lists of adverse effects of the experimental drugs now being deployed on “coronavirus” patients. Odd. I can’t find one. I wonder what that means. Maybe I should ask a doctor. He would possibly be able to set me straight. Perhaps I should query a public communications pro at a pharmaceutical company. Certainly, he could contact major press outlets and urge them to print the adverse-effect lists, in the interest of full disclosure.
Right?
Right?
Nature’s Most Powerful Pain Relievers
Nature has safe nontoxic answers to the crisis of over-reliance and addiction to pain medications with their known harmful effects
Pain is increasingly a part of everyday life for many people. The use of pain medications, including over the counter and prescription non-steroidal anti-inflammatory drugs (NSAIDs) — ibuprofen, aspirin, naproxen and diclofenac — and opioids — legal ones such as morphine, codeine, oxycodone, fentanyl and methadone or illegal narcotics such as heroin — is escalating to epic proportions.
More than 96% of all those over the age of 65 have used an NSAID for pain control within the last two weeks.[i] NSAIDs are known to have serious side effects such as gastrointestinal bleeding and ulcers as well as kidney failure and higher cardiovascular risks for strokes and heart attacks.[ii] In England, NSAIDs were associated with 30% of all hospital admissions for preventable adverse drug reactions.[iii]
In 2018, the World Health Organization reported 58 million people worldwide used opioids and overdoses resulted in 350,000 deaths.[iv] According to the U.S. Centers for Disease Control and Prevention, nearly 450,000 people died from overdoses involving an opioid, including prescription and illicit opioids, to manage their pain from 1999 to 2019 in the U.S. alone.[v]
Nature provides many powerful nondrug pain relievers that are effective alternatives to commonly used pain medicines without the detrimental side effects. The four natural options that follow are most helpful as adjunct treatment to reduce the dose and frequency of NSAID and opioid drug use.
1. Curcumin
Curcumin, the major component in turmeric, has anti-inflammatory properties that make it an ideal pain reliever.[vi]
In fact, 367 primary knee osteoarthritis patients with a pain score of five or higher received either ibuprofen at a dose of 1,200 milligrams (mg) per day or Curcuma domestica (turmeric) extract (1,500 mg per day) for four weeks showing the tumeric group had comparable pain relief benefits to the ibuprofen group but with fewer gastrointestinal adverse events.[vii]
Similarly, in a meta-analysis of eight trials, researchers showed extracts from the Zingiberaceae family, including turmeric and ginger, were as effective in reducing chronic pain as NSAIDs but without the renal risks.[viii]
The effective action of curcumin on neuropathic pain was shown in a mouse model using curcumin doses of 5, 15 or 45 mg per kg, twice per day for three weeks, and as doses increased so did their power to effectively alleviate pain caused by mechanical and thermal stimuli in mice.[ix]
In a formalin-induced orofacial pain model in rats, the analgesic response of curcumin was observed at doses of 25, 50, 100, 200, 400 and 600 mg per kg administered 15 minutes prior to formalin injection; in the group receiving a low dose of diclofenac (0.2 mg per kg) with curcumin at 25 mg per kg, curcumin increased the power of the lower dose of the NSAID diclofenac.[x]
In an acetic acid pain-induced model of rats, curcumin at 20 and 40 mg per kg produced the same pain reducing effect as the opioid morphine at 1 mg per kg.[xi]
2. Cannabidiol (CBD) Oil
In a review of medical cannabis as a therapy for symptom management in palliative care, there is sufficient evidence to determine the effectiveness and safety of cannabinoids for chronic pain.[xii] Osteoarthritis pain is one of the most common types of pain and scientific evidence shows that cannabinoids are effective pain relievers to fight inflammatory, nociceptive and neuropathic pain modalities found in joint pain.[xiii]
In 11 trials of 1,219 patients with neuropathic pain, those who took cannabinoids versus conventional treatments of pharmaceuticals and/or physical therapy had small reductions in pain scores, improvements in quality of life and increased sleep with no major adverse effects. However, larger studies are needed to clarify the most effective dosage, duration and quality of cannabinoids for pain relief.[xiv]
The 16-week trial results of treatment with the cannabinoid dronabinol show it is a safe and effective long-term treatment option that reduced neuropathic pain intensity in a study of 240 multiple sclerosis patients.[xv]
Cannabinoids also proved to be low-cost and well-tolerated therapies to reduce pain and fatigue symptoms and increase the quality of life of 17 women with fibromyalgia.[xvi] In three case studies of patients with epidermolysis bullosa, a genetic blistering disorder characterized by intense pain, cannabinoids improved pain scores, reduced itchy skin and decreased intake of opioids, the most common treatment for this type of pain.[xvii]
Increasing evidence shows that cannabinoids act synergistically with opioids and as opioid sparing agents, allowing lower doses and fewer side effects when compared to chronic opioid therapy for severe pain.[xviii]
3. Aromatherapy
Aromatherapy, using essential oils such as lavender, rose, bergamot and frankincense, is an effective and safe natural alternative for alleviating pain. Administration of opioids and NSAIDs has been the mainstay for postoperative pain control but patients often have serious adverse effects from these drugs, while essential oils have few if any serious side effects.
For example, in an aromatherapy trial, 82% of the patients in the placebo group required NSAIDs for postoperative pain while only 46% did in the lavender group and the lavender group required significantly less morphine, 2.38 mg versus 4.26 mg, postoperatively than the placebo group.[xix]
In a clinical trial of 64 children of 3 to 6 years of age having surgery, the group that was given inhalation aromatherapy with rose oil showed significantly lower pain scores than the placebo group given almond oil, demonstrating the efficacy of aromatherapy for postoperative pain in children without any significant side effects.[xx]
Similarly, in a study of 50 patients with second- and third-degree burns, those given inhalation aromatherapy with rose oil had decreased pain intensity and severity caused from dressing the burns compared to those in the control group.[xxi]
In a study of 58 hospice cancer patients, those who were treated to an aroma hand massage with lavender, bergamot and frankincense oils for five minutes a day for a week had less pain compared to the placebo group given almond oil massages.[xxii]
To study the effects of aromatherapy on 12 healthy volunteers, those taking frankincense at 125 mg or two capsules of the Boswellia serrata supplement significantly increased their pain threshold and pain tolerance force and time compared to the placebo group.[xxiii]
Examining the use of aromatherapy for pain management in a meta-analysis of 12 studies, researchers found evidence of reduced pain overall and the most consistent and effective results in treating postoperative, obstetrical and gynecological pain.[xxiv]
4. Palmitoylethanolamide
Palmitoylethanolamide (PEA), a nutraceutical supplement that is also available in PEA-rich foods such as soy lecithin, soybeans, egg yolks, peanuts and alfalfa, has been used successfully for pain management.[xxv] In a meta-analysis of 10 studies from 786 patients, those who received the PEA supplement experienced significantly lower acute or chronic pain compared to placebo groups.[xxvi]
The use of PEA as an add-on treatment to the opioid drug tapentadol in a study of 55 patients with chronic lower back pain resulted in significantly reduced pain intensity, less disability and lower opioid dosage over time.[xxvii]
In a study of 54 patients with irritable bowel syndrome and 12 healthy controls, patients taking 200 mg of PEA over a 12-week period showed markedly improved abdominal pain severity compared to the control group.[xxviii]
Comparing the effectiveness of PEA against the NSAID ibuprofen in a trial of 24 patients with temporomandibular joint osteoarthritis, those taking PEA for pain relief had significantly less pain and more mouth movement after two weeks compared to the ibuprofen group.[xxix]
For both sciatic and carpal tunnel syndrome pain, PEA demonstrated efficacy and safety as an anti-inflammatory and analgesic treatment in over 30 clinical trials and more than 6,000 patients making it an excellent alternative to opioids in treating nerve-related pain without harmful side effects.[xxx]
Pain Relief From Nature
Nature has provided us with many options that are safe and effective in managing pain. While pharmaceuticals may have a place in severe pain relief in small doses and short treatment windows, it is important to know what alternative treatments are available to reduce drug overuse, addiction and harmful side effects.
CONSUMER ALERT: The Deadly Reason Tylenol Should Be Removed from the Market
Tylenol, a trademarked form of the chemical known as acetaminophen or paracetamol, is one of the most commonly used painkillers in the United States today, yet is also one of the most dangerous. For instance, nearly 500 die and 30,000 are hospitalized each year in the US as a result of its well established, yet seldomly discussed toxic effects.
Marketed by Johnson & Johnson primarily for pain and fever relief (including to highly vulnerable populations such as infants and children), few consumers are aware of the true extent of the risks it carries, as well as what safer, natural alternatives may exist, as documented by a growing body of biomedical and clinical literature.
For instance, a 2017 article published in Journal of Hepatology titled, “Public Health: Acetaminophen (APAP) Hepatotoxicity–Isn’t It Time for APAP to Go Away?,” summarizes the alarming nature of Tylenol’s toxicity problem as follows:
“Acetaminophen (APAP) is the most commonly used drug for the treatment of pain and fever around the world. At the same time, APAP is capable of causing dose-related hepatocellular necrosis, responsible for nearly 500 deaths annually in the U.S. alone, as well as 100,000 calls to US Poison Control Centers, 50,000 emergency room visits and 10,000 hospitalizations per year. As an over-the-counter and prescription product (with opioids), APAP toxicity dwarfs all other prescription drugs as a cause for acute liver failure in the United States and Europe, but is not regulated in any significant way.”
The article points out that acetaminophen (APAP) is a “dose related toxin,” and that so-called APAP toxicity is the cause of 46% of all acute liver failure in the United States, and between 40-70% of all cases in Great Britain and Europe. Taken together, this exceeds the number of deaths related to acute liver failure (ALF) resulting from all prescription drugs combined, as you can see by the following graph.
According to the review, acetaminophen is a multi-billion dollar product, yet despite having the reputation of being extremely safe, and having little regulatory oversight of the FDA because it is an over-the-counter drug, it is “deadly.”
Recognition of this fact began a half century ago, as the drug became associated with suicide attempts, many of which were successful. A Lancet editorial from 1975 opined: “Surely the time has come to replace paracetamol [a synonym for acetaminophen] with an effective analogue which cannot cause liver damage.”1
In 2016, a class action lawsuit with over 100 plaintiffs involving claims that Tylenol caused liver damage and death was settled by McNeil (an over-the-counter arm of Johnson and Johnson). As a result of the lawsuit, it was revealed that the FDA and McNeil/Johnson & Johnson delayed implementing suggestions to improve safety of acetaminophen despite its well known harms.2
Should Tylenol Be Classified As A Neurotoxic Chemical with Psychiatric Effects?
While Tylenol’s liver-damaging effects are those most commonly recognized harmful effects by the medical community, few still seem to be aware of the accumulating research showing that Tylenol use has serious neurological and psychiatric impacts, including contributing to autism spectrum disorder, risk-taking behavior, attention deficit disorder and the blunting of emotional responses, including reducing human empathy (e.g. flat affect).
We have documented all these possible consequences in depth in previous articles, which you can investigate further in the links below:
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- Attention Deficit Disorder with Hyperactivity and Tylenol
- Risk-Taking Behavior and Tylenol
- Empathy Reduction and Tylenol: Study 1
- Empathy Reduction and Tylenol: Study 2
What should be highlighted is that in the risk-taking and empathy reduction studies, a single 1,000 mg dose produced these adverse neurobiological and psychiatric effects. This is extremely concerning and likely indicates how extremely toxic this chemical class is; especially since Tylenol’s pain- and emotion-blunting effects may actually reduce the taker’s awareness of its harmful effects.
What Evidence-Based Natural Alternatives Exist to Prevent Tylenol Toxicity, or Might Replace it Completely?
There are a number of substances that have been studied to prevent or mitigate the adverse effects of Tylenol toxicity. In fact, the research community has investigated over 125 natural substances which may accomplish this, examples of which you can view on our Tylenol Toxicity database here.
On Greenmedinfo.com we have also gathered a number of studies on natural substances that have been researched by the scientific community as possible alternatives to painkillers such as Tylenol. The following three natural substances have been studied in comparison with Tylenol, and have been found to compare favorably.
- Ingesting a Turmeric-Boswellia formulation (1,000 mg daily for 7 days)
- Consuming Sesame Seeds (40 grams a day for two months)
- Topical application of Black Seed Oil (1 milliliter of black seed oil applied on the knee joint 3 times a day every 8 hours for 3 weeks.)
There are a far wider range of studies available on natural, evidence based alternatives to drugs like ibuprofen, another highly toxic (specifically, heart-damaging) drug, six of which an be read here: 6 Natural Ibuprofen Alternatives Backed by Clinical Research.
Aspirin, which has also recently fallen from grace as no longer recommended for the primary prevention of heart attack, has been studied alongside a pine bark extract which appears superior in a number of ways. You can learn more about this possible aspirin alterantive by reading: The Powerful Aspirin Alternative Your Doctor Never Told You About
Beyond Popping Pills, Chemical or Otherwise
No matter what health complaints you may have, my primary advocacy is focused on the root-cause resolution of health problems. In 9 out of 10 cases, dietary modification and lifestyle changes like more exercise and a positive mind set, will go much farther in improving one’s well-being, happiness, and overall health metrics than popping a hand full of vitamins, or betting on magic bullets, regardless of whether they are “nutraceutical” or pharmaceutical.
If you have pain, your body is sending you a clear message that things needs to change. The symptom is not an enemy, unless you treat it that way, and ultimately we all are on our own individual health journeys and need to discover the true causes – some physical, some emotional, and some spiritual – of what ails us.
Temperature-Regulating Neurons Identified, Hint at Treatment Strategies for Heat Stroke, Obesity
The results of a study in rodents carried out by scientists at Nagoya University suggest that a group of neurons, called EP3 neurons, in the preoptic area (POA) of the brain play a key role in regulating body temperature in mammals. The discovery could pave the way for the development of technology that artificially adjusts body temperature, as a way of helping to treat conditions such as heat stroke, or hypothermia, and potentially obesity.
“On top of that, this technology could lead to new strategies for survival of people in hotter global environments, which are becoming a serious worldwide problem,” said research lead Kazuhiro Nakamura, PhD. The scientists reported on their study in Science Advances, in a paper titled, “Prostaglandin EP3 receptor–expressing preoptic neurons bidirectionally control body temperature via tonic GABAergic signaling.”
Thermoregulation is a physiological function that is fundamental to homeostasis in mammals, the authors noted. “Body core temperature is maintained within a control range by autonomous regulation of the balance between heat production within the body and heat loss to the environment.” In humans and many other mammals, body temperature is regulated at around 37°C (98.6°F), which optimizes all regulatory functions. But when body temperature noticeably deviates from the normal range, these functions can be impaired, potentially leading to heat stroke, hypothermia, and, in the worst case, death. These conditions might possibly be treated if body temperature could be artificially adjusted to remain within the normal range.
The brain’s temperature regulation center resides in the preoptic area, a part of the hypothalamus that controls the body’s vital functions. For example, when the preoptic area receives signals from a mediator called prostaglandin E (PGE2) that is produced in response to infections, this area releases a command to raise body temperature to fight against viruses, bacteria, and other disease-causing organisms. “The POA receives and integrates thermosensory (cool- and warm-sensory) neural signals from skin thermoreceptors and a pyrogenic humoral signal mediated by prostaglandin E2 (PGE2), which is produced in response to infections,” the team noted.
However, it is still unclear exactly which neurons in the preoptic area release commands to increase or decrease body temperature. To identify such neurons, Nakamura, together with Yoshiko Nakamura, PhD, and colleagues at Nagoya University, in collaboration with Hiroyuki Hioki, PhD, at Juntendo University, designed a study in rodents. They focused on how EP3 neurons in the preoptic area that express the EP3 subtype of PGE2 receptor may be involved in regulating body temperature. “… we investigated the physiological role of POAEP3R neurons in the central circuit mechanisms of thermoregulation and fever,” the team explained.
Nakamura and colleagues started by looking at how the activity of EP3 neurons in the preoptic area varied in response to changes in ambient temperature. “We first examined activation of POAEP3R neurons in response to ambient thermal challenges and then histochemically and physiologically determined the neurotransmitter phenotype of POAEP3R neurons,” they noted. A comfortable environmental temperature for rats is around 28°C. For two hours, the researchers exposed the rats to cold (4°C), room (24°C), and hot (36°C) temperatures. Results showed that exposure to 36°C activated EP3 neurons, while exposure to 4°C and 24°C did not. “These observations indicate that the POAEP3R neuronal group includes a substantial subpopulation of warming-activated neurons but not cooling-activated neurons,” the investigators suggested.
The group then observed nerve fibers of EP3 neurons in the preoptic area to identify where the signals from EP3 neurons are transmitted. Their observations revealed that nerve fibers are distributed to various brain regions, particularly to the dorsomedial hypothalamus (DMH), which activates the sympathetic nervous system. Their analysis also showed that the substance that EP3 neurons use for signal transmission to DMH is gamma-aminobutyric acid (GABA), a major inhibitor of neuronal excitation. “Although many POAEP3R neuronal cell bodies express a glutamatergic messenger RNA marker, their axons in the DMH predominantly release γ-aminobutyric acid (GABA), and their GABAergic terminals are increased by chronic heat exposure,” they stated. The combined results, the team further wrote, “… demonstrate that POAEP3R neuron–derived axons predominantly form GABAergic synapses onto DMH neurons.”
To further investigate the role of EP3 neurons in temperature regulation, researchers artificially manipulated their activity using a chemogenetic approach. They found that activating the neurons led to a decrease in body temperature, whereas suppressing their activity led to their increase. “Chemogenetic stimulation of POAEP3R neurons at room temperature reduces body temperature by enhancing heat dissipation, whereas inhibition of them elicits hyperthermia involving brown fat thermogenesis, mimicking fever,” they noted.
The combined study results demonstrated that EP3 neurons in the preoptic area play a key role in regulating body temperature by releasing GABA to send inhibitory signals to DMH neurons to control sympathetic responses. “The present study demonstrates that POAEP3R neurons, a target of PGE2 for its pyrogenic action, play a pivotal role in the preoptic efferent control of central sympathetic outflow for basal thermoregulation,” the team wrote. “Our study shows strong evidence that POAEP3R neurons provide tonic GABAergic inhibitory signaling to sympathoexcitatory efferent pathways as a fundamental determinant of body temperature for thermal homeostasis and fever.”
Lead author Nakamura further suggested, “Probably, EP3 neurons in the preoptic area can precisely regulate the signal strength to fine-tune body temperature. For example, in a hot environment, signals are augmented to suppress sympathetic outputs, resulting in increased blood flow in the skin to facilitate the radiation of the body’s heat to prevent heat stroke. However, in a cold environment, signals are reduced to activate sympathetic outputs, which promote heat production in brown adipose tissue and other organs to prevent hypothermia. Furthermore, at the time of infection, PGE2 acts on EP3 neurons to suppress their activity, resulting in activation of sympathetic outputs to develop fever.”
This study’s findings could pave the way for the development of a technology that artificially adjusts body temperature, which might then be applied to a wide range of medical fields. Interestingly, this technology may also be helpful in the treatment of obesity, by keeping body temperature slightly higher than normal to promote fat burning.
“On top of that, this technology could lead to new strategies for survival of people in hotter global environments, which are becoming a serious worldwide problem,” said Nakamura.
Eating refined grains may raise premature CAD risk
Iranian adults who reported eating more refined grains were at elevated risk for developing premature CAD, whereas those who consumed more whole grains were at reduced risk, researchers reported.
Epidemiological studies show grain intake is associated with CAD risk depending on grain type; however, few studies have examined their relationship with premature CAD in the Middle East region, Mohammad Amin Khajavi Gaskarei, MD, of the Isfahan Cardiovascular Research Center and Cardiovascular Research Institute at Isfahan University of Medical Sciences in Isfahan, Iran, and colleagues wrote in an abstract presented at the joint American College of Cardiology Middle East 2022/Emirates Cardiac Society Congress in Dubai, United Arab Emirates.
“There are many factors involved in why people may be consuming more refined grains as opposed to whole grains and these cases differ between people, but some of the most important factors to consider include the economy and income, job, education, culture, age and other similar factors,” Khajavi Gaskarei said in a press release. “A diet that includes consuming a high amount of unhealthy and refined grains can be considered similar to consuming a diet containing a lot of unhealthy sugars and oils.”
Khajavi Gaskarei and colleagues analyzed data from 2,099 adults with premature CAD who underwent coronary angiography; women were aged 70 years and younger and men were aged 60 years and younger. The case group (n = 1,369) included patients with CAD with obstruction of 75% or more in at least a single coronary artery or at least 50% in the left main artery. The control group (n = 1,168) included patients with normal coronary arteries.
Participants completed food frequency questionnaires to assess dietary intake. Researchers used logistic regression analysis to assess the association between whole-grain and refined-grain intake and risk for premature CAD.
In a crude model, the researchers did not observe an association between refined-grain intake and CAD risk (OR = 1.13; 95% CI, 0.92-1.39). However, after adjustment for all potential confounders, higher intake of refined grain was associated with increased risk for premature CAD (OR = 1.61; 95% CI, 0.41-2.27).
Whole-grain intake was inversely related with premature CAD occurrence in both the crude and fully adjusted models, with ORs of 0.69 (95% CI, 0.56-0.84) and 0.54 (95% CI, 0.4-0.72), respectively.
“As more studies demonstrate an increase in refined grains consumption globally, as well as the impact on overall health, it is important that we find ways to encourage and educate people on the benefits of whole grain consumption,” Khajavi Gaskarei said in the release. “Tactics to consider include teaching improved dietary choices in schools and other public places in simple language the general population can understand, as well as on television programs and by continuing to do high level research that is presented at medical conferences and published in medical journals. Clinicians must also be having these conversations with each other and their patients.”
As Healio previously reported, the American Heart Association published an updated dietary guidance in November 2021 that outlines 10 recommendations for improving diet quality and cardiometabolic health in the U.S. Among those, the guidance encourages consumption of fruits, vegetables, whole grains, lean and high-fiber protein and liquid nontropical plant oils and discourages consumption of ultra-processed foods, red meat, added sugars and high amounts of salt.
Smartphone speech analysis detects worsening heart failure prior to an event
A novel speech analysis system was able to detect impending heart failure events in ambulatory patients with congestive HF more than 3 weeks ahead of time, a speaker reported.
The system (HearO, Cordio Medical) was not only able to predict HF events with greater sensitivity compared with daily weight and oxygen saturation monitoring, but also demonstrated fewer average false positives per patient per year, according to the results of the HearO community study presented at the Heart Failure Society of America Annual Scientific Meeting.
“The energy generator of speech are the lungs. We look at this analysis technology as being primarily reflective of changes in lung fluid content or pulmonary congestion, but it’s worth noting that hydration may affect speech parameters at various levels, including the soft tissues in the vocal tract as well as the vocal folds,” William T. Abraham, MD, professor of internal medicine and board-certified advanced heart failure and transplant cardiology physician at The Ohio State University Wexner Medical Center, said during a presentation. “The Cordio HearO community study is a multicenter, noninterventional, single-arm, open clinical study being performed outside of the U.S., primarily in Israel, and the goal here was simply to explore the diagnostic performance in ambulatory heart failure patients.”
William T. Abraham
Abraham stated that the front end of the system is a smartphone app, able to function on an Android or iOS device, which asks the patient each day to speak five preset sentences into the phone. From there, it is uploaded into a HIPAA-secure cloud-based system where the speech analysis and comparison with the stable baseline data occurs.
In a prior feasibility study of the system published in JACC: Heart Failure, researchers assessed whether speech measures identified using the speaker verification, speech processing and smartphone app algorithm would predict clinical states of pulmonary congestion indicative of HF events in patients with acute decompensated HF.
At hospital admission and discharge, patients were asked to record five sentences, repeated three to four times each in their native language.
As Healio previously reported, 94% of cases were identified as distinctly different from baseline and in 87.5% of cases, distinct differences from baseline were detected in all five speech measures.
For the present analysis, 253 ambulatory patients with congestive HF were enrolled for the HearO community study (mean age, 69 years; 19% women; 37% with left ventricular ejection fraction < 40%).
Each patient was asked to complete five voice recordings per day for 2 years. Among them, the primary language was 72% Hebrew, 19% Russian, 7.5% Arabic and 1.6% English.
Abraham said the speech processing system creates a patient-specific speech model while they are in a clinically stable state and compares that model going forward against daily speech samples to detect changes thought to be related to changes in lung fluid content.
The primary outcome was HF events, defined as HF hospitalization and treatment with IV diuretics.
Abraham reported that the HearO system could predict approximately 80% of HF events on average 22.5 days before the events occurred.
Researchers observed a false-negative rate of approximately 18%.
Over a total number of 186,152 analysis days, the system’s false-positive rate was on average 2.8 alerts per year, translating to one false positive every 4.3 months per patient per year.
The HearO system demonstrated greater sensitivity for the detection of impending HF events when compared with current standards for detection such as daily weight (80% vs. 35%) and oxygen saturation measurements (80% vs. 25%) and had fewer false positives per patients per year.
Moreover, researchers observed a high rate ( 70%) of compliance to daily voice recording among trial participants.
“Speech analysis technology may be a useful tool in remote monitoring of heart failure patients, providing early warning of worsening heart failure, including impending decompensation resulting in hospitalization,” Abraham said during the presentation. “Ongoing and future studies will continue to define the role of speech measures in the management of heart failure, and I think this approach has the potential to reduce [acute decompensated] HF hospitalizations and improve patient quality of life and economic outcomes. But of course, we’ll need to show that in a subsequent prospective and randomized controlled trial.”
Abraham added that HearO is currently being evaluated in a new U.S. trial that will test the system’s sensitivity across various dialects, accents and languages representative of the general U.S. population.
Perspective
Debra Moser, PhD, RN, FAHA, FAAN
That was probably one of the most fascinating trials because it gets at the main problem of trying to figure out, early on, when people are congested because they’re either not good at perceiving their own symptoms or they’re not adherent to daily weighing, which is not that sensitive anyway. The other options are implantable hemodynamic monitoring devices that are invasive. It would be fabulous to have this app with patients talking to it a few times a day to be able to detect congestion. It looks like it can detect it 3 weeks ahead of an acute exacerbation. It could really keep people out of the hospital.
It’s an observational study and needs a randomized control trial, but I think it’s a promising device that could change the way we detect congestion early on.
Debra Moser, PhD, RN, FAHA, FAAN
Assistant Dean of the PhD Program
Linda C. Gill Professor in Nursing
University of Kentucky
Disclosures: Moser reports no relevant financial disclosures.
Perspective
The voice analysis approach may be a novel way to do remote monitoring. The current methods we have are so crude in terms of daily weights, etc, that perhaps technology will lead the way. Decompensation is a huge problem that we have in this country, but if you could find those patients early, intervene and abort that admission, it would be a huge advance. This is an early study of a technology, but it’s very exciting and I’m looking forward to seeing additional studies from that group.
Mark Drazner, MD, MSc
Clinical Chief of Cardiology
The University of Texas Southwestern Medical Center
President, Heart Failure Society of America
Coffee subtypes associated with reduced CVD, arrhythmias, mortality
Regular coffee intake of multiple subtypes was associated with preventing CVD, mortality and incident arrhythmias, according to a study.
“Regular coffee intake has a beneficial effect on incident arrhythmias, cardiovascular disease and mortality,” Peter Kistler, MBBS, PhD, head of clinical electrophysiology research at the Baker Heart and Diabetes Institute and head of electrophysiology at the Alfred Hospital in Melbourne, Australia, told Healio. “Coffee consumption is associated with cardiovascular benefits and should not empirically [be] discontinued in those with underlying heart rhythm disorders or cardiovascular disease. Daily coffee intake should not be discouraged by physicians, but rather considered part of a healthy diet.”
Source: Adobe Stock
As Healio previously reported, in the main results of a large prospective cohort study, there was a significant reduction in the incidence of arrythmia, CVD, stroke, all-cause mortality and CVD mortality in regular coffee drinkers compared with nondrinkers.
Coffee subtype consumption
Peter Kistler
For the present analysis, the researchers examined the relationships between different coffee subtypes and CVD outcomes. The subtypes included in the study were caffeinated (instant, ground) and decaffeinated. The 449,563 participants (median age, 58 years; 55% women) were grouped into categories based on daily coffee intake (0, < 1, 1, 2-3, 4-5 and > 5 cups per day) and followed for 12.5 years.
The primary outcome was the relationship between coffee subtype consumption and the incidence of arrhythmias, CVD and mortality. Secondary outcomes were the relationships between coffee subtype consumption and subcategories of arrythmia (atrial fibrillation/flutter, supraventricular tachycardia, ventricular tachycardia/ventricular fibrillation) and CVD (CHD, congestive cardiac failure, stroke).
The researchers observed that any ground coffee intake up to five cups per day was associated with reduced risk for arrhythmia, CVD and all-cause mortality. Arrhythmia risk was lowest with four to five cups per day (HR = 0.83; 95% CI, 0.76-0.91; P < .0001), all-cause mortality risk was lowest with two to three cups of ground coffee per day (HR = 0.73; 95% CI, 0.69-0.78; P < .0001) and CVD mortality was lowest with four to five cups per day (HR = 0.65; CI, 0.51-0.83; P < .0001).
There was a U-shaped relationship between instant coffee intake and CVD endpoints, with two to three cups per day associated with the lowest risk for arrythmias (HR = 0.88; 95% CI, 0.85-0.92; P < .0001), CVD (HR = 0.91; 95% CI, 0.88-0.94; P < .0001), CHD (HR = 0.91; 95% CI, 0.88-0.94; P < .0001), stroke (HR = 0.83; 95% CI 0.76-0.9; P < .0001) and all-cause mortality (HR = 0.89; 95% CI, 0.86-0.93; P < .0001), according to the researchers.
Researchers observed that decaffeinated coffee intake of two to three cups per day reduced risk for CVD (HR = 0.94; 95% CI, 0.9-0.99, P = .0093), CHD (HR = 0.94; 95% CI, 0.89-0.99; P = .0127), congestive cardiac failure (HR = 0.86; 95% CI, 0.79-0.94; P = .0004) and all-cause mortality (HR = 0.86; 95% CI, 0.8-0.91; P < .0001). The risk for CVD mortality was lowest with one to three cups per day (HR = 0.74; 95% CI, 0.61-0.89; P = .0012), according to the researchers.
Differences with arrhythmias
However, decaffeinated coffee intake only had a neutral effect on the risk for arrythmias.
“By blocking adenosine receptors, caffeinated coffee may mitigate the effects of endogenous adenosine and protect against arrhythmias,” Kistler and colleagues wrote.
“This may explain the differing effects of caffeinated vs. decaffeinated coffee on the incidence of arrhythmias.”
Further clinical research on coffee intake is necessary, according to the researchers.
“There needs to be a randomized controlled trial to determine whether people who do not drink coffee should be encouraged to do so,” Kistler told Healio.
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