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04/01/20

The scent of fresh-cut grass, your mom’s chicken soup or burning leaves may instantly transport you to a distant memory, one you can suddenly recall with razor-sharp clarity.

So-called odor-evoked memories often come along with powerful emotions and are known to activate the “neurolobiological substrates of emotional processing,” according to neuroscientist Rachel S. Herz, an adjunct assistant professor of psychiatry and human behavior at Brown University.1

Research published in Learning and Memory2 added to this, suggesting that odors may modulate the dynamics of memory consolidation, including memories linked to fear, and could potentially be used therapeutically to help people recall memories or treat memory-related mood disorders, such as post-traumatic stress disorder (PTSD).3

"If odor could be used to elicit the rich recollection of a memory — even of a traumatic experience — we could take advantage of that [therapeutically]," study author Steve Ramirez, assistant professor of psychology and brain sciences at Boston University, said in a news release.4

The Systems Consolidation Theory of Memory

The prevailing theory of memory formation — the systems consolidation theory — suggests that memories are initially processed in the brain’s hippocampus, giving the memory rich details. Over time, however, as memories become older or more remote, they become less dependent on the hippocampus and more dependent on processing by the front of the brain — the prefrontal cortex.

During this transition, which occurs particularly during sleep, memories may lose many of their rich contextual details. Further, memories that are retrieved shortly after an experience involve reactivation of cells in the hippocampus whereas retrieval of a memory later is thought to involve reactivation of cells in the prefrontal cortex.5

The systems consolidation theory explains why memories tend to become less detailed or clear as time goes by, as well as why people with a damaged hippocampus have trouble forming new memories while those with prefrontal cortex damage may have trouble remembering memories from the past.6

The theory, however, is just that — a theory — and it has some challenges as well. Researchers noted in Learning and Memory, “[P]eople often retrieve remote memories that are vivid and highly detailed. Likewise, several studies have shown that there is activity in both structures during both recent and remote memory recall … and that damage to the HPC [hippocampus] sometimes affects remote memory as well as recent memory.”7

Particularly in PTSD, people may recall intense memories years after the trauma occurred, which seemingly contradicts the systems consolidation theory, leading the researchers to conduct a study to clarify some of these contradictions.

Scent Alters the Way Memories Are Processed

In a study on mice, researchers from Boston University's Center for Systems Neuroscience startled mice with electric shocks while in a special container to induce fear memories. Half the mice were exposed to almond extract scent during the shocks while the other half received no scent exposure.

The next day, the same experiment took place, but without any electric shocks given. The odor group was exposed to the scent of almond extract while in the special container while the other group had no scent exposure. The idea was to prompt the mice to recall the fearful memory of being shocked — something all the animals did, as evidenced by significant activation of the hippocampus.

The memory recall session was repeated again 20 days later. In the no-odor group, the prefrontal cortex was activated, suggesting it was responsible for processing the fear memory, as researchers had expected. In the odor group, however, significant activity was still observed in the hippocampus. Ramirez noted:8

"[This finding suggests] that we can bias the hippocampus to come back online at a timepoint when we wouldn't expect it to be online anymore because the memory is too old. Odor can act as a cue to reinvigorate or reenergize that memory with detail."

It’s possible that odors may delay a memory being processed in the prefrontal cortex, or that an odor reactivates the hippocampus to restore details of a memory that’s already shifted to the prefrontal cortex.

While the specifics aren’t yet known, it’s possible that odors could be harnessed to help people with PTSD actively recall traumatic memories, so that they could then be suppressed or dampened using behavioral interventions.

"Now that we know that odor can shift memories to become more hippocampus dependent, we could potentially develop strategies that engage or disengage the hippocampus,” Ramirez said, adding, “We can potentially view memory as its own kind of drug — as an antidepressant or [anxiety reducer]. And [odor] could be an experimentally controllable factor that we could deliver to people. It may be a very powerful tool."9

Memories Induced by Scent Are More Emotional

Odor-evoked memory is dubbed the “Proust phenomenon” after a literary anecdote where Marcel Proust took a bite of a biscuit dipped in Linden tea and was transported to a moment in his childhood that he had long forgotten. Odor-evoked memories, Herz explained, are unique from memories evoked by other stimuli, such as verbal or visual stimuli.

Not only are they more rare and less frequently thought about, but they tend to come from early in life, typically within the first decade. What’s more, autobiographical memories triggered by odors tend to be much more emotional and have the perception of bringing people back to the original time and place that their memories occurred.

Part of the unique intensity of odor-evoked memories has to do with the way scent is processed by your brain. Smells get routed through your olfactory bulb, which the smell-analyzing region in your brain. It’s closely connected to your amygdala and hippocampus, brain regions that handle memory and emotion. According to Herz:10

“Odor-evoked memories are exceptionally viscerally involving because the neuroanatomy of olfaction has a privileged and unique connection to the neural substrates of emotion and associative learning.

The primary olfactory cortex includes the amygdala, which processes emotional experience and emotional memory, as well as the hippocampus, which is involved in associative learning. Thus, the mere act of smelling activates the amydala-hippocampal complex.”

Odor-Evoked Memories Influence Psychological, Physical Health

By boosting mood, lowering stress and reducing inflammation, it’s likely that the powerful emotions elicited by positive odor-evoked memories can influence psychological and physiological health.

“Any odor that for a given individual evokes a happy autobiographical memory has the potential to increase positive emotions, decrease negative moods, disrupt cravings, lower stress and decrease inflammatory immune responses, and thereby have a generally beneficial effect on psychological and physiological well-being,” Herz wrote,11 noting that individuals may also experience unique effects like improvements in self-confidence, motivation and vigor depending on the emotions a specific memory invokes.

For example, if an odor triggers a memory of winning a sporting event, it could energize your behavior and trigger beneficial physiological effects, making it a reliable therapeutic agent. Likewise, odors that evoke pleasant memories could be used as reminders of safe or happy places and events, making them useful for the treatment of psychiatric conditions and reducing stress and anxiety.12

The unique anatomy of the olfactory pathways hints at the importance of odors in emotions, learning, memory and more. While other sensory systems pass through the thalamus to reach the cortex, odors get relayed directly to the limbic system in the brain, which is associated with memory and emotional processes.

This is why odors have such a powerful influence on mood, information acquisition and even social interactions. As noted in Frontiers in Behavioral Neurosciences, memory is but one crucial behavior influenced by odors:13

“Indeed, olfaction is crucially involved in behaviors essential for survival of the individual and species, including identification of predators, recognition of individuals for procreation or social hierarchy, location of food, as well as attachment between mating pairs and infant-caretaker dyads.”

Aromatherapy: Another Way Scents Influence Mood and More

Aromatherapy — the use of plant-based aromas to influence mood and wellness — is not the same as odor-evoked memory. In the case of the psychological and physiological effects induced by odor-evoked memories, the odor has such effects because of the memories and emotions attached to it as a result of past personal experience.14

This isn’t to say that aromatherapy isn’t also beneficial for health and wellness, just that it works in a different, more generalized way. Many ancient cultures, including the Chinese, Indians, Egyptians, Greeks and Romans used essential oils in cosmetics, perfumes and drugs for purposes ranging from spiritual to therapeutic.15

In the modern day, aromatherapy is used in health care settings, health spas and homes, both by professional aromatherapists and amateurs, while accumulating research backs up its many potential uses and benefits.

For instance, the two primary terpenoid constituents of lavender essential oil, linalool and linalyl acetate, have anxiety-reducing effects, and lavender essential oil is known to induce a calming effect without side effects such as sedation.16

Lavender also has an effect on the nervous system, and when inhaled it’s believed to act via the limbic system, particularly the amygdala and hippocampus,17 although it may have effects even beyond mood and anxiety.

In a study on patients undergoing open heart surgery, a cotton swab containing lavender essential oil was placed in the patients’ oxygen mask for 10 minutes. The aromatherapy led to significant reductions in blood pressure and heart rate, with researchers concluding it could be “used as an independent nursing intervention in stabilizing mentioned vital signs.”18

Beyond lavender, a study on rats showed that inhaling Roman chamomile essential oil for two weeks reduced depressive-like behaviors,19 while essential oils placed nightly on towels around dementia patients’ pillows resulted in significantly longer total sleep time, increased sustained sleep and reduced early morning awakening.20

While it’s best to consult an experienced aromatherapist before delving into essential oils, generally speaking if you’re looking to feel energized and uplifted, consider essential oils such as peppermint, grapefruit, lemon, neroli and wild orange while more calming oils include lavender, chamomile, bergamot, ylang ylang and vetiver. For more information, consult our Ultimate Guide to Herbal Oils.

Loss of Sense of Smell Also Gives Clues About Health

Paying attention to any changes in your sense of smell, including a loss of it, is also important. In a study of 3,005 community-dwelling adults, those who had a dysfunctional sense of smell were more likely to die in the next five years than those with a good sense of smell.

In fact, olfactory function was deemed to be one of the strongest predictors of five-year mortality and researchers suggested it may “serve as a bellwether for slowed cellular regeneration or as a marker of cumulative toxic environmental exposures.”21

An inability to identify odors is also an early symptom of neurological disorders, including Alzheimer’s disease and Parkinson’s disease.22 So, make a conscious effort to keep track of your sense of smell, using it for memory recall, mood boosts and as a gauge for your health should it dissipate.

While odor-evoked memories can be powerful tools for health and behavior as well, they depend largely on happenstance, in that a scent must be introduced at the precise moment that a memorable event is occurring — then that scent must later be introduced to evoke the memory.

It happens often enough that virtually everyone reading this has experienced it, but if you’re looking for a more direct way to harness the power of odors over your health, aromatherapy can be very useful.



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While melatonin works as a natural sleep regulator, it affects health in many other important ways as well.1 For example, melatonin:

Is a potent antioxidant2

Plays an important role in cancer prevention3

Is important for brain, cardiovascular and gastrointestinal health4

Boosts immune function in a variety of ways

May improve the treatment of certain bacterial diseases, including tuberculosis5

Helps quell inflammation

May prevent or improve autoimmune diseases, including Type 1 diabetes6

Is an important energy hormone7 — If your sleep efficiency is impaired, meaning you’re not sleeping as deeply as you should, for as long as is ideal, then your energy level is going to be adversely affected

As noted in the Journal of Critical Care:8

“Melatonin is a versatile molecule, synthesized not only in the pineal gland, but also in many other organs. Melatonin plays an important physiologic role in sleep and circadian rhythm regulation, immunoregulation, antioxidant and mitochondrial-protective functions, reproductive control, and regulation of mood. Melatonin has also been reported as effective in combating various bacterial and viral infections.”

Melatonin — A Potential Treatment for Sepsis?

The Journal of Critical Care paper,9 published in 2010, further highlights the potential role of melatonin in the treatment of sepsis (blood poisoning), a life-threatening condition triggered by a systemic infection that causes your body to overreact and launch an excessive and highly damaging immune response.

Unless promptly diagnosed and treated, it can rapidly progress to multiple-organ failure and death. The cytokine storm response appears to be a primary way by which the novel coronavirus COVID-19 (also referred to as SARS-CoV-2, due to its similarity to the SARS coronavirus) claims the lives of those who are immunocompromised and/or elderly. According to the Journal of Critical Care:10

“Melatonin is an effective anti-inflammatory agent in various animal models of inflammation and sepsis, and its anti-inflammatory action has been attributed to inhibition of nitric oxide synthase with consequent reduction of peroxynitrite formation, to the stimulation of various antioxidant enzymes thus contributing to enhance the antioxidant defense, and to protective effects on mitochondrial function and in preventing apoptosis.

In a number of animal models of septic shock, as well as in patients with septic disease, melatonin reportedly exerts beneficial effects to arrest cellular damage and multiorgan failure.”

In summary, melatonin appears to reverse septic shock symptoms by:11

  • Decreasing synthesis of proinflammatory cytokines
  • Preventing lipopolysaccharide (LPS)-induced oxidative damage, endotoxemia and metabolic alterations
  • Suppressing gene expression of the bad form of nitric oxide, inducible nitric oxide synthase (iNOS)
  • Preventing apoptosis (cell death)

According to the authors, the ways in which melatonin prevents septic shock are complex:

“Apart from action on the local sites of inflammation, melatonin also exerts its beneficial actions through a multifactorial pathway including its effects as immunomodulatory, antioxidant and antiapoptotic agent.”

Glyphosate, Melatonin and COVID-19

Stephanie Seneff, Ph.D., senior research scientist at MIT, also recently brought the potential role of melatonin to my attention, specifically in regard to the current coronavirus (COVID-19) outbreak. In an email to me, Seneff explains:

“I just figured something out about COVID-19 and glyphosate. Upper respiratory infections are a high risk for people who have a deficiency in mannose binding lectin (MBL). MBL has a long sequence in the protein that looks like collagen (GxyGxyGxy...): GINGFPGKD GRDGTKGEKG EPGQGLRGLQ GPPGKLGPPG NPGPSGSPGP KGQKGDPGKS.

I just discovered that there are two lung surfactant proteins (A and B) which also have this GxyGxy pattern in their stalks. Here's the relevant sequence in lung surfactant protein A: GSP GIPGTPGSHG LPGRDGRDGL KGDPGPPGPM GPPGEMPCPP GNDGLPGAPG IPGECGEKGE PGERGPPGLP. Here's what UniProt says about this protein:12

‘In presence of calcium ions, it binds to surfactant phospholipids and contributes to lower the surface tension at the air-liquid interface in the alveoli of the mammalian lung and is essential for normal respiration … Can recognize, bind, and opsonize pathogens to enhance their elimination by alveolar macrophages.’

I would wager that glyphosate disrupts the collagen-like stalk of the lung surfactants preventing them from binding to and clearing the COVID-19 virus … I was wondering why the elderly are suffering much more from sepsis and cytokine storm during COVID-19 infections. A significant difference in older patients compared to younger patients is their melatonin levels. Another good insight and treatment approach?”

Melatonin Ameliorates Cytokine Responses

In her email, Seneff goes on to cite a 2014 study13 in the Journal of Pineal Research which, like the Journal of Critical Care paper, points out that melatonin accumulates in mitochondria and has both antioxidant and anti-inflammatory activity that could be useful in the treatment of sepsis.

Melatonin is derived from serotonin, which in turn is derived from tryptophan, one of the three aromatic amino acids that are products of the shikimate pathway. Glyphosate famously disrupts the shikimate pathway in weeds, and this is believed to be the main mechanism by which it kills the weeds. Our gut bacteria also produce tryptophan via the shikimate pathway, so glyphosate can be expected to reduce the bioavailability of tryptophan as a precursor to melatonin.

The study mentioned above was a Phase 1 dose escalation study in healthy volunteers to evaluate the tolerability and health effects of melatonin at various dosages. They also assessed the effect of melatonin in an ex vivo whole blood model mimicking sepsis.

No adverse effects were reported for dosages ranging from 20 milligram (mg) to 100 mg, and the blood model testing revealed melatonin and its metabolite 6-hydroxymelatonin “had beneficial effects on sepsis-induced mitochondrial dysfunction, oxidative stress and cytokine responses …” The authors further explain:14

Oxidative stress in patients with sepsis has been consistently described over the last 20 years. Mitochondrial dysfunction initiated by oxidative stress drives inflammation and is generally accepted as playing a major role in sepsis-induced organ failure.

It has been recognized that exogenous antioxidants may be useful in sepsis, and more recently, the potential for antioxidants acting specifically in mitochondria has been highlighted.

We showed previously that antioxidants targeted to mitochondria, including melatonin, reduced organ damage in a rat model of sepsis. Exogenous melatonin has potent antioxidant activity, and it accumulates throughout cells, particularly in mitochondria. Metabolites of melatonin also have antioxidant activity, and products from the reactions with oxidant species are also antioxidants.

In vitro models of sepsis show that melatonin and its major hydroxylated metabolite, 6-hydroxymelatonin, are both effective at reducing the levels of key inflammatory cytokines, oxidative stress, and mitochondrial dysfunction. In rat models of sepsis, melatonin reduces oxidative damage and organ dysfunction and also decreases mortality.

The dose needed for antioxidant action is thought to be considerably higher than that given for modulation of the sleep–wake cycle, but the actual dose required in man is unclear, particularly because the major bioactive effects of oral melatonin in the context of inflammation are likely to be mediated primarily by metabolite levels.”

Antiseptic Effects of Melatonin

More recently, a 2019 animal study15 in the journal Frontiers in Immunology discusses how melatonin can protect against polymicrobial sepsis — i.e., sepsis caused by more than one microbial organism — a hallmark of which is severe loss of lymphocytes through apoptosis, resulting in a twofold higher lethality than unimicrobial sepsis (sepsis caused by a single microbe).16

In this case, melatonin appears to offer protection by having an antibacterial effect on white blood cells called neutrophils. A high neutrophil count is an indicator for infection. According to the authors of the 2019 study:

“Melatonin treatment inhibited peripheral tissue inflammation and tissue damage … consequently reducing the mortality of the mice. We found that macrophages and neutrophils expressed melatonin receptors.

Upon depletion of neutrophils, melatonin-induced protection against polymicrobial infection failed in the mice, but melatonin treatment in macrophage-depleted mice attenuated the mice mortality resulting from polymicrobial sepsis.

Moreover, melatonin treatment promoted the development of the neutrophil extracellular trap (NET), which contributed to anti-bacterial activity during polymicrobial infection, whereas the phagocytic activities of neutrophils were inhibited by melatonin.

The data from this study support previously unexplained antiseptic effects of melatonin during a polymicrobial infection and could be potentially useful for human patients with sepsis.”

Understanding COVID-19 Infection

The potential role of melatonin in COVID-19 infection was also addressed in an extensive and fully referenced March 14, 2020, article by medical researcher Doris Loh, published in the Italian online magazine Evolutamente.17

“Unofficial reports from doctors and healthcare workers from COVID-19 frontlines in Italy described most patients displayed symptoms of bilateral interstitial pneumonia that required intubation (invasive ventilation) to assist difficulty in breathing.

Even young patients without comorbidities have been observed with severe pneumonia that required intensive care in ICUs,” Loh reports. Why does SARS-CoV-2, the coronavirus responsible for COVID-19 infection, induce pneumonia in adult patients regardless of age?”

One answer may be because the viral load in those with COVID-19 infection is extremely high — 1,000 times higher than the viral load seen in SARS patients back in 2003.18

Preliminary research19 cited by Loh shows the COVID-19 virus is actively replicating in the throat during the first five days after the onset of symptoms. This higher viral load could be what allows the virus to overwhelm even the immune system of some younger and healthier individuals.

Inflammasomes and Cytokine Storms

Another mechanism that can help explain the high virulence of COVID-19 compared to SARS has to do with a furin cleavage site in the spike protein of the virus that wasn’t present in the SARS virus. As explained by Loh, “The presence of furins on almost all cell surfaces allow a dramatically increased ability to fuse to host cells, facilitating viral entry …” She adds:20

“Cleavage specificity can dictate the tropism and virulence of the virus. The fact that COVID-19 has cleavage sites for furin enzymes renders this virus to be highly pathogenic, with the capacity to replicate in MULTIPLE tissues and organs due to how furins are utilized and distributed in the human body.

Furin-like cleavage in human coronaviruses have been associated with the development of neurological diseases where the invasiveness and efficient establishment of lower pathogenicity can result in persistent infection of the central nervous system.

Thus it was not a surprise when in early March of 2020, doctors from Beijing Ditan Hospital affiliated to Capital Medical University, a designated institution for COVID-19 treatment, showed for the first time that COVID-19 can attack the human central nervous system, causing symptoms of encephalitis.

The presence of furin enzymes on all cell surfaces cleaves and activates the SARS-CoV-2 in a wide range of tissues and organs. Activated SARS-CoV-2 then unleashes NLRP3 inflammasomes, initiating a flurry of immune reactions that can result in deadly cytokine storms."

As the name implies, inflammasomes are part of your natural immune response that senses the presence of pathogens and other factors that could pose a threat. When a pathogen is detected, inflammasomes are activated and start releasing proinflammatory cytokines.

The inflammasome NLRP3, specifically, has been identified as a key culprit in acute respiratory distress syndrome (ARDS) and acute lung injury, both of which are potential outcomes of COVID-19 infection.21

The cytokine storm associated with COVID-19 infection appears to be due to the virus’ ability to stimulate your immune response via viroporins, virally-encoded ion channel proteins that in turn trigger the activation of NLRP3 inflammasomes. As explained by Loh, the more functional a virus’ viroporins are, the greater its viral replication rate and subsequent pathogenesis.

Is Elevated Melatonin Sparing Young Children from COVID-19?

As noted by Loh, the fatality rate of COVID-19 increases linearly with age, with patients over the age of 80 having the highest death rate.22,23,24 As of yet, the explanation for why children are less likely to contract the infection or show symptoms even when they are infected,25 is unknown.

Loh, however, raises the possibility that it might have something to do with melatonin production. She cites research showing melatonin production peaks in early childhood, steadily dropping once puberty hits. By the time you’re in your late 50s, melatonin production drops to negligible levels.

“What does melatonin have to do with SARS-CoV-2?” Loh asks. The answer is that melatonin helps inhibit NLRP3 inflammasomes.

“The fact that the pro-inflammatory cytokine storm effects are induced by the activation of NLRP3 inflammasomes, the ability of melatonin to INHIBIT NLRP3 inflammasome elevates this powerful molecule to a truly unique position in the fight against COVID-19,” Loh writes.26

“This also means that if a patient, regardless of age, has adequate melatonin, the infectiousness of COVID-19 will be greatly reduced, and the chances of developing ARDS/ALI significantly diminished.”

In her article, Loh references a number of scientific articles to support her claims. Aside from studies showing melatonin inhibits damage associated with sepsis, studies have also shown it can counteract severe inflammation and “markedly reduce pulmonary injury [and] lower infiltration of macrophages and neutrophils into lungs … by inhibiting the activation of NLRP3 inflammasomes,” thus protecting against acute lung injury.

Melatonin levels are also doubled in the third trimester of pregnancy compared to the first trimester,27,28 which may help explain why pregnant women infected with COVID-19 and their babies have gotten by fairly unscathed. A 2020 rodent study29 even demonstrated that melatonin can help protect against lung injury caused by mechanical ventilation intervention.

“The full therapeutic potential of melatonin in its ability to modulate the immune system, especially the critical function of suppressing cytokine storms to prevent progression of acute respiratory distress syndrome (ARDS) and respiratory failure in infected patients was clearly demonstrated in a study by Huang et al. (2019). 

Huang et al. infected rodents with the highly lethal and infectious H1N1 influenza A virus. Co-treatment of these infected rodents with melatonin and an antiviral drug significantly increased their survival rates compared to mice treated only with antivirals alone,” Loh writes.

The role of NLRP3 inflammasomes in COVID-19 infection also adds support for the use of ascorbic acid (vitamin C), as ascorbic acid has been shown to inhibit NLRP3 Inflammasomes in a dose-dependent fashion by scavenging reactive oxygen species in the mitochondria.30,31

“Thus, the combined use of melatonin and ascorbic acid may prove to be most effective in the treatment for COVID-19 patients, especially those with cardiovascular and hypertension comorbidities,” Loh suggests.32

You can learn more about the use of intravenous vitamin C against sepsis and coronavirus infection in “Essential Nutrition to Protect Yourself From Coronavirus.”

Avoid ACE Inhibitors During COVID-19 Outbreak

Nutrients and drugs that might be best avoided during this outbreak are those that inhibit angiotensin-converting enzyme (ACE). What’s the problem with ACE inhibitors? As explained by Loh, ACE inhibitors increase expression of ACE2, and COVID-19 infects host cells by binding to ACE2 receptors found on epithelial cells in your lungs, intestines, kidneys and blood vessels.33

ACE inhibitors, i.e., medications that relax and dilate your blood vessels, are commonly prescribed for high blood pressure, certain types of heart failure, stroke prevention and for the prevention and treatment of kidney disease. These drugs work by inhibiting the specific isoform of ACE, ACE1. As a consequence, ACE2 is upregulated. This is problematic with regard to COVID-19, because the virus gains entry to infect cells specifically via the ACE2 protein acting as a receptor.

Loh cites research34 published in The Lancet Respiratory Medicine suggesting that taking an ACE inhibitor, be it a medication or a nutritional supplement, may worsen your risk of COVID-19 infection and your risk of complications.

“Melatonin, nitric oxide and ascorbic acid (vitamin C) are all inextricably intertwined and deeply involved with ACE2,” Loh writes.35

“Melatonin, nitric oxide and ascorbic acid can reduce COVID-19 virulence by inhibiting NLRP3 inflammasomes to stop the perpetuation of cytokine storms. Their critical roles in biochemical reactions and biological pathways that involve ACE2 must be fully explored as part of our fight against COVID-19.”

At the end of her article, Loh offers suggestions for melatonin and vitamin C dosages, along with contraindications and timing of supplementation.

Stay Calm and Take Commonsense Precautions

Keep in mind that while all of this information may sound concerning, the lethality of COVID-19 is quite low for those under the age of 65. According to a March 18, 2020, report by the U.S. Centers for Disease Control and Prevention, preliminary mortality rates for COVID-19 in the U.S. are:36

  • Zero% for adolescents under the age of 19
  • Less than 1% among those aged 20 to 54
  • 1% to 3% among 55- to 64-year-olds
  • 11% for those aged 65 to 84
  • 10% to 27% among those over the age of 85

To minimize the spread of infection, remember to:37

  • Frequently wash your hands with soap and water for at least 20 seconds. For further details, see “The Impact of Effective Handwashing Against Infection
  • Avoid touching your eyes, nose and mouth
  • If you need to cough, cough into your flexed elbow or disposable tissue. Discard the tissue in a trash can and wash your hands
  • If feeling unwell, stay home and avoid public spaces

If you have symptoms of illness such as coughing or sneezing, be sure to wear a surgical mask to contain the spread whenever you’re around others. For additional details about the use of surgical or N95 respiratory masks, see “Will Wearing a Mask Protect You Against Coronavirus?



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In the fight against neurodegenerative diseases such as frontotemporal dementia, Alzheimer's and Chronic Traumatic Encephalopathy, the tau protein is a major culprit. Found abundantly in our brain cells, tau is normally a team player -- it maintains structure and stability within neurons, and it helps with transport of nutrients from one part of the cell to another.

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Updated CT scoring criteria that considers lobe involvement, as well as changes in CT findings (i.e., ground-glass opacity, crazy-paving pattern, and consolidation), could quantitatively and accurately evaluate the progression of coronavirus disease (COVID-19) pneumonia, according to a new article.

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In an effort to provide safer working environments for nuclear medicine professionals and their patients, clinics across five continents have shared their approaches to containing the spread of COVID-19. This compilation of strategies, experiences and precautions is intended to support nuclear medicine clinics as they make decisions regarding patient care.

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The bacteria that cause tuberculosis need iron to survive. Researchers have now solved the first detailed structure of the transport protein responsible for the iron supply. When the iron transport into the bacteria is inhibited, the pathogen can no longer grow. This opens novel ways to develop targeted tuberculosis drugs.

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The causes of 40% of all cases of certain medulloblastomas -- dangerous brain tumors affecting children -- are hereditary. A genetic defect that occurs in 15% of these children plays a key role by destabilizing the production of proteins. The researchers suspect that protein metabolism defects could be a previously underestimated cause of other types of cancer.

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By now, you’ve probably heard this warning about the new coronavirus pandemic: those who are older and have a chronic medical condition are at increased risk for severe disease and death. If you fall into this category, here’s important information about the coronavirus outbreak tailored to you.

If you look at the data, older adults and those with chronic health problems who get COVID-19 are more likely to require hospitalization and admission to an intensive care unit. And so far in the US, 80% of the deaths from the new coronavirus virus have occurred in people who were older.

But this raises a number of questions:

  • What do they mean by “older”?
  • Which chronic diseases are most important?
  • Why does older age and chronic disease increase your risk?
  • What are you (or your loved ones) supposed to do if you’re at increased risk?

“Older” is more than a number

When it comes to coronavirus, the CDC’s magic number is now set at 65. That’s the age at which risk of severe disease, complications, and death from COVID-19 appears to rise. But while risk does rise with age, infants, children and adults under age 65 have become infected in significant numbers, and some have severe disease, so everyone needs to take precautions.

Which chronic diseases put people at higher risk from COVID-19?

What do health experts mean when they talk about chronic diseases that put some people at increased risk of severe disease with COVID-19? It varies, but generally includes people who have

  • heart disease
  • high blood pressure
  • diabetes
  • asthma or other chronic lung diseases
  • HIV
  • a suppressed immune system due to a disease or a treatment

Within these groups, there is much uncertainty. For example, if you had cancer years ago but are now in remission, are you at increased risk? What if your diabetes is mild and well controlled?

Why do older age and chronic disease increase risk for severe illness if a person gets COVID-19?

It’s not entirely clear, but here are some possibilities:

  • An immune system weakened by age or illness is unable to fight off the virus, which could lead to an overwhelming infection.
  • The immune system “misfires” or has an exaggerated response in some people, triggering so much inflammation and tissue damage that the immune reaction itself causes complications.
  • Organ damage due to existing or past illness might make additional damage caused by the virus more than a person can handle; one example is smoking-related lung disease complicated by respiratory infection from the new coronavirus.
  • The stress of a viral infection can increase demand on already damaged or aging organs (such as the heart).
  • Medications taken to treat chronic conditions could increase the severity of infection. One suggestion (unproven so far) is that a family of medicines called ACE inhibitors allows more viral organisms to enter cells. ACE inhibitors are commonly taken by people with diabetes and hypertension, perhaps explaining why these conditions are linked to more severe disease.

We need more research to understand whether one or more of these is most important, or whether there are other factors at play.

What are you or your loved ones supposed to do to lower your risk?

While there is no way to completely eliminate risk, it makes sense to:

  • Carefully follow the recommendations of health experts that apply to everyone, regardless of age or other risk factors, including:
    • Frequent handwashing (reminding others around you, also) and avoiding touching your face as much as possible
    • Social distancing (six feet of distance between you and anyone you don’t live with daily)
    • Avoid “emotional distancing” by using phones and apps to stay connected (some grandchildren or children can provide tech support by phone)
    • Wipe down “high-touch” areas of your home with approved household disinfectants
    • Stay home as much as possible
    • Avoid anyone who you know is sick
  • Be especially attentive to managing your medical conditions
    • Take your medications exactly as prescribed
    • If possible, keep a 90-day supply of your medications on hand
    • Monitor your condition frequently (for example, talk to your doctor about home blood pressure monitoring, home blood sugar checks, or tests of lung function you can do at home)
    • Don’t smoke!
  • Make sure your routine medical and nutritional needs are met by keeping adequate health supplies (such as a thermometer, acetaminophen, and a first-aid kit) and several weeks’ supply of nonperishable foods on hand.
  • Maintain connections to family, friends, and your doctors so you don’t feel isolated.
    • Talk early and often about your medical or other needs with friends and family by phone or online.
    • Socialize! Whether by phone or online, connect with friends and family to commiserate, discuss current events, or play games.
    • Arrange to have someone check in on you regularly by phone, online, or in person.
    • Keep a “who-to-call” list on your refrigerator with phone number of close family members, caretakers, doctors, pharmacy, and the local board of health.
    • Give a set of keys to your home to a neighbor that you or your family members can call in case of emergency.

The bottom line

Much of what is recommended for older adults with chronic medical conditions is the same as what would be recommended even without the pandemic.

Yet there are still lots of things you can do to keep busy, maintain morale, and keep from going stir crazy. Get outside and go for walks. Call friends and family you’ve been meaning to call before this outbreak. Write that novel or haiku or letter to the editor you’ve been thinking about.

These are unusual times. Hearing that you’re at increased risk of severe illness from a rapidly spreading and potentially serious virus is frightening to say the least. One way to manage the fear and uncertainty is to take action: be prepared, take the advice of experts, and keep a positive attitude. That’s about the best you can do.

Follow me on Twitter @RobShmerling

For more information, listen to our podcasts and see our Coronavirus Resource Center.

The post COVID-19: If you’re older and have chronic health problems, read this appeared first on Harvard Health Blog.



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As a primary care doctor who has incorporated medical cannabis into his practice, it is notable how many silver-haired patients are coming in to discuss the pros and cons of a trial of medical cannabis. These patients range from people in their 60s with kidney failure who can no longer take certain pain medications but still need to manage chronic pain, to patients in their 90s, who are looking for a good night’s sleep and are leery of the side effects of traditional sleep medications. Some of them — typically “children of the 60s” — are quite comfortable with the idea of using medical marijuana; others bring it up quietly, as if they are asking permission to break the law.

According to a recent study in the Journal of the American Medical Association, cannabis use among older adults (defined as 65 and older) in the US has been steadily increasing. In this study, the prevalence of past-year use increased from 2.4% to 4.2% from 2015 to 2018. This study is consistent with other research, as well as with reports from physicians who recommend cannabis in their daily practices.

What might be behind this trend?

A confluence of factors seems to be responsible, including the decrease in stigma associated with cannabis use and the increased interest in the use of medical marijuana by older patients. Stigma is a complicated issue, but most would agree that the stigma associated with cannabis use is lessening, especially for medical cannabis. In a recent poll, 94% of Americans voiced support for legal access to medical marijuana, and most states have approved some form of legal access.

One marker for the decrease in stigma is the recent statement by the 38 million-member AARP, in which they declared their support for the medical use of marijuana for older adults in states that have legalized it, in close consultation with their medical providers, where they can discuss the most up-to-date clinical evidence, weighing the balance of benefits and harms.

What conditions are older adults using cannabis for?

Studies show that older adults commonly use medical cannabis for the same conditions younger patients do: pain, insomnia, neuropathy, and anxiety.

What are the risks for older people using medical cannabis?

This is new territory, as either there haven’t been large numbers of older adults who report using medical cannabis, or if they have been using it they have kept it quiet, due to its illegality and due to the stigma. Medical cannabis is typically well tolerated among older adults; however, as with all medications, there is no such thing as a free lunch, meaning that there are always side effects and downsides to consider.

Cardiac health and cannabis use

Cannabis is known to increase heart rate and can increase blood pressure, though there doesn’t seem to be much if any quality evidence directly linking cannabis use with coronary events, according to a recent review by the Journal of the American College of Cardiology. Still, the authors of this review do recommend screening people with coronary disease for cannabis use. The scenario that I would be most concerned about is an older patient, with underlying coronary disease, taking a very high dosage of cannabis (perhaps by mistake via edibles) and then having an anxiety attack, which could trigger a coronary syndrome or an arrhythmia.

Medication interactions

Older people tend to have comorbid health conditions and may be taking multiple medications. Cannabis has about 600 chemicals in it, and in theory, the two main active ingredients in cannabis, THC and CBD, could either increase or decrease the blood levels of other drugs you are taking, by affecting the enzymes in your liver that help metabolize your medications. CBD, in particular, is at risk for increasing the other drugs in your system by “competitively inhibiting” (or, in plain English, using at the same time) the molecules that you need to break down and clear these medications from your body.

People should be particularly cautious using cannabis with anti-seizure medications and with blood thinners, as these medications tend to have serious side effects and not as much room for error, and it is important that you always communicate with your medical providers about your cannabis use. Disclosing marijuana use is particularly important if you plan to have surgery, as the drugs used for anesthesia and post-surgical pain management may need to be adjusted.

Changes in thinking, both pro and con

The psychoactivity, or the high that cannabis causes, is another potential concern for older adults, especially those at risk for confusion and dementia. These days, with the ability to buy cannabis in medical dispensaries, there is more control over the types or strains of cannabis that one can buy and consume, and it is easier to avoid the high by controlling the dose and by keeping the THC content low. Strains that are low in THC (the chemical that causes the high) and higher in CBD, which is non-intoxicating, may be preferable to avoid the psychoactive experience of marijuana. Still, if an older person has experienced delirium, or any psychiatric conditions, they and their doctors should proceed with caution.

Interestingly, there is some research that cognitive functioning can actually improve when patients use medical cannabis, due to, among other things, improved sleep and pain control. It seems plausible that older patients might be using lower doses of pain and sleep medications, which can affect thinking, and they are combatting the negative effects of chronic pain and insomnia, which also have an effect on cognitive functioning. However, as with most things cannabis-related, this too needs further study to confirm and clarify.

What’s the bottom line?

Cannabis use among the elderly is growing as there is more public acceptance and reduced stigma. Medical cannabis is increasingly viewed as an effective option for managing insomnia and chronic pain. It’s key to have an informed discussion with your doctor to weigh the safety risks, especially if you have cardiac issues, are taking multiple medications, or have cognitive changes due to aging. Educate yourself (and your doctor) as much as possible about cannabis before starting to use it. Most of the adverse effects associated with cannabis usage are dose-related, so it is important to know the strength of the marijuana you are taking and to “start low and go slow”: start with the lowest effective dose and take your time working your way up to a dose that alleviates your symptoms with a minimum of side effects.

The post Older adults and medical marijuana: Reduced stigma and increased use appeared first on Harvard Health Blog.



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MIT engineers are working on developing soft, flexible neural implants that can gently conform to the brain's contours and monitor activity over longer periods, without aggravating surrounding tissue. Such flexible electronics could be softer alternatives to existing metal-based electrodes designed to monitor brain activity, and may also be useful in brain implants that stimulate neural regions to ease symptoms of epilepsy, Parkinson's disease, and severe depression.

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