Black Seed Oil Evaluated for Chronic Inflammation


Black seed contains an abundance of nutrients that can help improve your health by balancing blood pressure, controlling blood sugar, and targeting obesity. (kostrez/Shutterstock)

Black seed contains an abundance of nutrients that can help improve your health by balancing blood pressure, controlling blood sugar, and targeting obesity.

Short-term use of black seed oil may reduce chronic inflammation and is being tested in the treatment of COVID-19.

STORY AT-A-GLANCE

  • Black seed oil may be an alternative herbal treatment for combating COVID-19
  • The bioactive compounds have an antihistamine effect and anti-inflammatory properties that downregulate interferon regulatory factor 3 activation and promote autophagy
  • Researchers hypothesize that several of the terpenes in the oil are similar in structure to chloroquine and may act as a zinc ionophore; evidence also suggests one compound may block ACE2 receptors, which the virus uses to release viral RNA into the cell
  • Black seed oil has many traditional medicinal uses, including as an antidiabetic, antimicrobial, bronchodilator and antioxidant
  • The Front Line doctors list black seed oil as an alternative therapeutic agent in the treatment of COVID-19. However, the oil is high in linoleic acid and so should not be used preventively against COVID

Black seed oil has been used for its therapeutic benefits for thousands of years. Since the pandemic began, researchers have been evaluating the effect it may have on COVID-19.[1] The seeds come from the Nigella sativa (N. sativa) plant that grows in Southern Europe, Southwest Asia and the Middle East.[2] Traditional medicine healers have used the seeds in different forms.

Black seed is coal-black with a dull surface and shaped like tiny Brazil nuts. The bioactive components include thymoquinone, α-hederin, alkaloids and omega-6 fatty acids.

Black seed oil has also been used for dermatological applications. For example, a review of the literature in the Journal of Dermatology & Dermatologic Surgery[3] found black seed oil could promote wound healing in farm animals and reduce the impact of vitiligo in lizards.

In one clinical study[4] in humans, lotion infused with 10% of N. sativa oil reduced acne vulgaris after two months with 67% of the patients fully satisfied and 28% partially satisfied with the results.

In the current research,[5] scientists believe the oil may have promising benefits in the treatment and prevention of COVID-19. However, while short-term use for treatment may be advantageous, it is wise to avoid long-term use for prevention.

Black Seed Oil May Be a Promising Option for COVID-19

Historically, black seed oil has been used to help balance the inflammatory response in the body as well as reduce oxidative stress, inflammation and ischemia. Using recent computational findings, one research group found the active ingredients in N. sativa were “strongly suggestive of combating emerged COVID-19 pandemic.”[6]

The paper suggests that the active ingredients, especially thymoquinone, α-hederin, and nigellidine, may be an alternative herbal treatment in the combat against COVID-19. The paper reviews several pathways that the active ingredients in black seed oil may use to protect health.

For example, the researchers reviewed past studies that demonstrated the actions the active ingredients in black seed oil have on the immune system, which may help reduce the severity of COVID-19. The active compounds have a significant antihistamine effect in animal studies and thymoquinone downregulates interferon regulatory factor 3 activation, which plays a critical role in innate immune responses.[7]

Autophagy is a mechanism that clears out damaged cells in the body. Data has shown that COVID-19 suppresses autophagy and that pharmacological agents used to induce the process may therefore have an antiviral effect. One study[8] published in 2018 indicated thymoquinone promotes autophagy in the heart muscle.

The researchers suggest that further study should be undertaken to determine if thymoquinone has a similar effect with COVID-19. Severe COVID-19 is characterized by cytokine storms that may require intensive care.[9] Animal studies have demonstrated that the bioactive compound α-hederin has anti-inflammatory activity and can decrease histamine levels.

The researchers reported one study had found thymoquinone helped inhibit two enzymes that produce inflammatory leukotriene and prostaglandins. Researchers suggest that these actions may potentially make the active compounds in N. sativa useful in the treatment and prevention of SARS-CoV-2 viral infections.

Finally, in their review of comorbid conditions associated with COVID-19, the researchers found that N. sativa may have a positive effect against diabetes, high blood pressure, heart disease, autoimmune and auto inflammatory diseases and bacterial infections associated with COVID-19.

After a review of the evidence, the researchers suggest that further experiments with the active compounds found in black seed oil are required to determine if they have preventive potential or may provide a new treatment modality.[10]

Zinc Combinations Help Treat COVID-19

Research into medications that may influence COVID-19 have included antivirals. One such antiviral being studied is favipiravir. Data show the drug was approved and has been used for flu infections in Japan.[11] In late 2020, a study published in PNAS[12] revealed that when given in high doses to hamsters favipiravir had promising antiviral activity against SARS-CoV-2.

However, a computer-model molecular docking study published in Biological and Medicinal Chemistry[13] revealed that the bioactive compounds nigellidine and α-hederin found in black seed oil were able to inhibit SARS-CoV-2 with a greater potential than favipiravir, chloroquine and hydroxychloroquine.

Evidence from a second paper that reviewed the biological effects of the active compounds in black seed oil suggested that thymoquinone may block ACE2 receptors,[14] which is where the SARS-CoV-2 binds to the cell and releases the viral RNA into the cytoplasm.

Contrary to what the PNAS hamster study found, these researchers hypothesized that chloroquine, and potentially the derivative hydroxychloroquine, may also interfere with the virus’s ability to bind with the ACE2 receptors.

This is one pathway the researchers suggest that black seed oil may use in the treatment of COVID-19. Another pathway is as a zinc ionophore. The body uses zinc in several pathways to support the immune system, including:[15]

  • Proliferation and activation of natural killer cells, macrophages, neutrophils, and T and B cells
  • Mediating protection against reactive oxygen species produced during an inflammatory response
  • Stopping recombinant RNA dependent RNA polymerase activity needed to replicate SARS-CoV-2
  • Inhibiting replicase processing

Therefore, moving zinc into the cytoplasm is crucial to help prevent the replication of the SARS-CoV-2 virus and thus effectively stop infected cells from infecting other cells.

Oral supplementation of zinc alone is not sufficiently effective since zinc cannot move easily across the cell wall. It needs another compound to provide transportation. The second compound is called a zinc ionophore. The application of zinc with an ionophore has demonstrated improved outcomes in patients hospitalized with COVID.[16]

Research has identified several zinc ionophores, including chloroquine,[17] hydroxychloroquine,[18] quercetin and EGCG.[19] Scientists have suggested that several of the terpenes in black seed oil, such as nigellimine, are similar in structure to chloroquine. They hypothesize that this may mean they can function in a similar manner as a zinc ionophore.[20]

Thus, recent data have shown that the active ingredients found in black seed oil may have greater potential in the treatment of COVID-19 than antiviral drugs, may act as a zinc ionophore and may help block the ACE2 receptors the virus uses to infect cells.

Black Seed Oil Has Traditional Medicinal Uses

N. sativa is a popular and traditional medicinal and has a long history of use in several diseases and ailments.[21] Traditional medicine has used black seed oil as a diuretic, antidiarrheal, appetite stimulant, analgesic, lower blood pressure, liver tonic and skin disorder treatment.[22] However, research has also explored the pharmacological activity of black seed oil and found it has many properties, including:[23]

  • Antidiabetic
  • Anticancer
  • Immunomodulator
  • Analgesic
  • Antimicrobial
  • Anti-inflammatory
  • Spasmolytic
  • Bronchodilator
  • Hepato-protective
  • Renal protective
  • Gastro-protective
  • Antioxidant

The immune-modulating activities of black seed oil help to regulate the immune system and maybe another pathway in the treatment for COVID-19. In addition to the studies using black seed oil, researchers have also separated the bioactive ingredients and evaluated their potential benefit against SARS-CoV-2.

A data review[24] on thymoquinone was published in February 2021, in which the researchers reviewed the bioactivity of the compound found in past research. They wrote that thymoquinone increased the activity and number of natural killer cells, macrophages, lymphocytes and cytokines suppressors.

Additionally, they cite past research that showed the active ingredient had antiviral potential against other viruses, including human immunodeficiency virus, other coronaviruses, Epstein-Barr virus, cytomegalovirus and hepatitis C. In addition, they reviewed an Egyptian study in which thymoquinone demonstrated antiviral activity in a strain of SARS-CoV-2 isolated in patients and the inhibitory effect it has on the viral protease, which may reduce viral replication.

One study[25] from Saudi Arabia evaluated the effectiveness of black seed oil as a supplement in patients with mild COVID-19 who were between 18 and 65 years. The intervention group received 500 mg of soft gel capsules twice daily for 10 days in addition to their standard treatment.

Initial results were published on Clinical Trials.[26] The primary outcome measurement was the percentage of participants who showed clinical recovery within 14 days after treatment began. The team reported 62.1% of those receiving the black seed oil demonstrated recovery from mild COVID-19 while 36% of the control group recovered within 14 days.

Consider Oil for Short-Term Use to Reduce Health Risk

The Front Line COVID-19 Critical Care Alliance (FLCCC)[27] lists black seed oil as an alternative for prevention and treatment of COVID-19. They stress there is no “magic bullet” for COVID-19, yet:[28]

“… a number of therapeutic agents have shown great promise for both the prevention and treatment of this disease including Ivermectin, Vitamin D, quercetin, melatonin, fluvoxamine, corticosteroids, curcumin (turmeric), Nigella sativa and antiandrogen therapy.”

The team recommends taking N. sativa with honey as they both have antimicrobial, antiviral, immunomodulatory and anti-inflammatory effects with proven safety profiles. They list N. sativa and honey in the prevention protocol for children and adolescents, and as an alternative for first-line treatment in the early treatment protocol at home.

While short-term use of black seed oil may be efficacious in the treatment of COVID-19, long-term use for prevention may have other unwanted effects. One study[29] of the chemical composition of black seed oil shows that the majority of fatty acids are from linoleic acid, an omega-6 polyunsaturated fat or (PUFA).

As I have discussed in an interview with Tucker Goodrich,[30] linoleic acid (LA) is likely the leading contributing cause of virtually all chronic diseases we have encountered in the last century.

When LA is consumed in excessive amounts, it acts as a metabolic poison. Chances are you’re getting an excess amount of this dangerous fat from foods that you may even consider healthy. For example, olive oil and chicken, which are fed LA-rich grains, increase your levels of omega-6 fatty acids.

Many are aware that the omega-3 to omega-6 ratio is important and should be close to equal. However, it is not as simple as raising omega-3 fatty acids. You need to minimize omega-6. fats A compelling report in the journal Gastroenterology[31] has offered a logically sound explanation as to why some patients with COVID-19 develop life-threatening organ failure.

The data indicate that the mortality rates appear to be heavily influenced by the amount of unsaturated fats you eat, such as LA. To date, there have been no clinical studies on the treatment they believe may help reduce the rate of organ failure and ICU admissions, namely the administration of calcium and egg albumen. It appears these compounds can bind the unsaturated fats and reduce injury to vital organs.

Take Care to Lower Your Omega-6 Intake

Fortunately, you can analyze your food for LA from the convenience of your home. All you need to do is accurately enter your food intake into Cronometer — a free online nutrition tracker — and it will provide you with your total LA intake. The key is to carefully weigh your food with a digital kitchen scale so you can enter the weight of your food to the nearest gram.

Cronometer.com is free to use as a desktop version. If you feel the need to use your cellphone (which is not recommended), then you will need to purchase a subscription. Personally, I have used the desktop version exclusively for the last five years as it has greater functionality and allows me to avoid electromagnetic fields from my phone.

Ideally, it is best to enter your food before you eat it. The reason for this is quite simple: It’s impossible to delete the food once you have already eaten it, but you can easily delete it from your menu if you find something that pushes you over the ideal limit.

Once you’ve entered the food for the day, go to the “Lipid” section on the lower left side. To find out how much LA is in your diet for that day, you merely need to see how many grams of omega-6 are present since roughly 90% of the omega-6 you eat is LA.

Thus, you can see that chronic use of black seed oil for prevention against COVID-19 will likely increase your risk of other chronic diseases that increase your risk of severe disease. If you are interested in using black seed oil, consider the extracts of the bioactive ingredients and not the whole oil.

If you are seeking an alternative for prevention and treatment, consider a combination of quercetin and zinc. Quercetin also has antiviral properties[32] and is a zinc ionophore.[33] While safe to take for about two weeks when you’re ill, it is important you are careful with zinc supplements as you may offset your zinc/copper balance and negatively impact your immune system.

Frequent Use of Antibiotics May Heighten Inflammatory Bowel Disease Risk in Adults Over 40


Summary: Adult exposure to antibiotics appears to be linked to an increased risk of developing an inflammatory bowel disorder, including Crohn’s disease and ulcerative colitis. The risk appears to be cumulative, greatest around two years after use, and for antibiotics that target gut infections.

Source: BMJ

Frequent use of antibiotics may heighten the risk of inflammatory bowel disease—Crohn’s disease and ulcerative colitis—among adults over 40, suggests research published online in the journal Gut.

The risk seems to be cumulative and greatest 1-2 years after use and for those antibiotics targeting gut infections, the findings indicate.

Mounting evidence suggests that environmental factors are likely implicated in the development of inflammatory bowel disease (IBD). Globally, close to 7 million people have the condition, with this number expected to rise over the next decade, say the researchers.

One factor associated with IBD risk in younger people is the use of antibiotics, but it’s not clear if this association might also apply in older people.

To explore this further, the researchers drew on national medical data from 2000 to 2018 for Danish citizens aged 10 upwards who hadn’t been diagnosed with IBD. They specifically wanted to know if the timing and dose of antibiotic might be important for the development of IBD, and whether this varied by IBD and antibiotic type.

More than 6.1 million people were included in the study, just over half of whom were female. In total, 5.5 million (91%) had been prescribed at least one course of antibiotics between 2000 and 2018. During this period, some 36,017 new cases of ulcerative colitis and 16,881 new cases of Crohn’s disease were diagnosed.

Overall, compared with no antibiotic use, use of these drugs was associated with a higher risk of developing IBD, regardless of age. But older age was associated with the highest risk.

Those aged 10-40 were 28% more likely to be diagnosed with IBD; 40-60 year-olds were 48% more likely to receive this diagnosis, while those over 60 were 47% more likely to do so.

The risks were slightly higher for Crohn’s disease than they were for ulcerative colitis: 40% among 10-40 year-olds; 62% among 40-60 year-olds; and 51% among the over 60s.

The risk seemed to be cumulative, with each subsequent course adding an additional 11%, 15%, and 14% heightened risk, according to age band.

The highest risk of all was observed among those prescribed 5 or more courses of antibiotics: 69% heightened risk for 10-40 year-olds; a doubling in risk for 40-60 year-olds; and a 95% heightened risk for those over 60.

Timing also seemed to be influential, with the highest risk for IBD occurring 1-2 years after antibiotic exposure, with each subsequent year thereafter associated with a lowering in risk.

Specifically, among 10-40 year-olds, IBD risk was 40% higher 1-2 years after taking antibiotics compared with 13% higher 4-5 years later. The equivalent figures for 40-60 year-olds were 66% vs. 21% and for those over 60, 63% vs. 22%.

As to antibiotic type, the highest risk of IBD was associated with nitroimidazoles and fluoroquinolones, which are usually used to treat gut infections. These are known as broad spectrum antibiotics because they indiscriminately target all microbes, not just those that cause disease.

Nitrofurantoin was the only antibiotic type not associated with IBD risk at any age.

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Mounting evidence suggests that environmental factors are likely implicated in the development of inflammatory bowel disease (IBD). Image is in the public domain

Narrow spectrum penicillins were also associated with IBD, although to a much lesser extent. This adds weight to the notion that changes in the gut microbiome may have a key role and that many antibiotics have the potential to alter the composition of microbes in the gut.

This is an observational study, and as such, can’t establish cause; nor was information available on what the drugs were for or how many of them patients actually took, note the researchers.

But there are some plausible biological explanations for the findings, they suggest, highlighting the natural diminution of both the resilience and range of microbes in the gut microbiome associated with aging, which antibiotic use is likely to compound.

“Furthermore, with repeated courses of antibiotics, these shifts can become more pronounced, ultimately limiting recovery of the intestinal microbiota,” they add.

Limiting prescriptions for antibiotics may not only help to curb antibiotic resistance but may also help lower the risk of IBD, they venture.

“The association between antibiotic exposure and the development of IBD underscores the importance of antibiotic stewardship as a public health measure, and suggests the gastrointestinal microbiome as an important factor in the development of IBD, particularly among older adults,” they conclude.

Fruit Flies Help Researchers Decode Genetic Link to Alzheimer’s Disease


Summary: Findings uncover a potential cause of neurodegeneration in the early stages of Alzheimer’s disease.

Source: Walter and Eliza Hall Institute

Researchers have used fruit flies to decipher an unexplained connection between Alzheimer’s disease and a genetic variation, revealing that it causes neurons to die.

The findings from the Walter and Eliza Hall Institute (WEHI)-led team uncover a possible cause of neurodegeneration in the early stages of Alzheimer’s disease and open the door for the future development of new treatments for cognitive diseases.

The study, “An increase in mitochondrial TOM activates apoptosis to drive retinal neurodegeneration,” with collaborators from Australian National University, is published in Scientific Reports.

Over 55 million people worldwide are believed to be living with Alzheimer’s disease or other forms of dementia. In Australia, there are up to 487,500 people living with dementia. There is no known cure for the disease, but early intervention can help prevent disease progression.

The new research enhances our knowledge of how cell death and quality control pathways are involved in neurodegeneration and reveals potential targets for early intervention in cognitive conditions.

Gap in dementia research

A strong genetic link exists between increased levels of the mitochondrial TOMM40 gene and Alzheimer’s disease, but the mechanisms underlying this phenomenon are largely unknown.

This connection has been hard to untangle because this gene neighbors the “Alzheimer’s gene” (ApoE), the strongest predictor of late onset Alzheimer’s disease. But recent work has shown a genetic variation that causes overproduction of TOMM40 can cause brain shrinkage, independent of the Alzheimer’s gene.

Lead researcher Dr. Agalya Periasamy said the findings piqued the team’s curiosity, prompting them to investigate how too much TOMM40 causes the neurodegeneration underlying Alzheimer’s disease.

“If we can unpack this, we might be able to find a new way to intervene with the process to prevent neurons from dying,” Dr. Periasamy said.

“Currently, we don’t have good treatments for Alzheimer’s and we urgently need new options. Our research offers a possible alternative avenue for development of much-needed therapeutic interventions for this devastating disease.”

Fruit fly model

The WEHI and Australian National University team used a common model of neurodegenerative disease, the fruit fly, to explore potential connections between elevated TOMM40 levels and Alzheimer’s. The eyes of fruit flies contain cells called photoreceptors that are specialized neurons, making them ideal for research on neurodegeneration.

To investigate how an over-abundance of TOMM40 was linked to neurodegeneration, the team genetically engineered fruit flies to produce too much Tom40 protein, the protein produced by the TOMM40 gene, and observed the effect.

They found that enriching the protein caused marked cell death in the retina, with the amount of degeneration corresponding to the level of the protein.

After looking for the cause of the dying eye tissue, Dr. Periasamy found evidence of a specific kind of cell death called apoptosis, typically involved in regular cell turnover and maintenance.

This shows neurons
A fly larva eye under the microscope—the specialized neurons inside it have been made to overexpress Tom40 protein which fluoresces red.

“We looked at the eyes of fly larvae under the microscope and found an increase in a protein that marks the activation of apoptosis, called ‘caspase-3’ in humans. This confirmed to us that apoptosis was the missing link we were looking for,” she said.

TOM protein complex and cell death

Tom40 is part of a larger protein complex called “TOM” that assembles on the mitochondria, where its main function is to import essential proteins.

The team investigated the impact of excessive Tom40 and found that TOM complex formation was sent into overdrive. This throws out the balance in the mitochondria and activates apoptosis.

“While the data show that the trigger for cell death is an overabundance of the TOM assembly, we found no evidence that protein import was involved in neurodegeneration,” said principal investigator Dr. Jacqui Gulbis. “Our findings identify a new entry point into cell quality control pathways that could be targeted to interrupt TOMM40-induced neurodegeneration.n

“While this research is still in its early stages, it will be exciting to explore and tap into the relationship between TOMM40-linked apoptosis and Alzheimer’s disease to set the groundwork for the development of new therapies for cognitive conditions.”


Abstract

An increase in mitochondrial TOM activates apoptosis to drive retinal neurodegeneration

Intronic polymorphic TOMM40 variants increasing TOMM40 mRNA expression are strongly correlated to late onset Alzheimer’s Disease. The gene product, hTomm40, encoded in the APOE gene cluster, is a core component of TOM, the translocase that imports nascent proteins across the mitochondrial outer membrane.

We used Drosophila melanogaster eyes as an in vivo model to investigate the relationship between elevated Tom40 (the Drosophila homologue of hTomm40) expression and neurodegeneration.

Here we provide evidence that an overabundance of Tom40 in mitochondria invokes caspase-dependent cell death in a dose-dependent manner, leading to degeneration of the primarily neuronal eye tissue.

Degeneration is contingent on the availability of co-assembling TOM components, indicating that an increase in assembled TOM is the factor that triggers apoptosis and degeneration in a neural setting. Eye death is not contingent on inner membrane translocase components, suggesting it is unlikely to be a direct consequence of impaired import.

Another effect of heightened Tom40 expression is upregulation and co-association of a mitochondrial oxidative stress biomarker, DmHsp22, implicated in extension of lifespan, providing new insight into the balance between cell survival and death.

Activation of regulated death pathways, culminating in eye degeneration, suggests a possible causal route from TOMM40 polymorphisms to neurodegenerative disease.

The Rebirth of Psychedelic Medicine


Summary: Often considered dangerous, mind-altering drugs, researchers are turning to the study of psychedelic therapies as a potential to treat an array of psychiatric conditions including depression and PTSD.

Source: Stanford

It was 1985 and John Lawn had seen enough.

In Boston nightclubs and Dallas bars, MDMA—better known by its street name, ecstasy—had become an enormously popular recreational drug. It had also terrified the Reagan administration, which was in the midst of its historic War on Drugs.

Lawn, the administrator of the Drug Enforcement Administration at the time, acted quickly. Despite the outcry of medical professionals pointing to the range of MDMA’s clinical uses, Lawn classified the drug as Schedule 1, one of many to be banned in a backlash against psychedelics like LSD and psilocybin. The message was clear: these drugs were dangerous, immoral, and medically useless.

Nearly four decades later, researchers at Stanford’s Wu Tsai Neurosciences Institute are at the forefront of a seismic shift that’s putting a spotlight on a once taboo field. Scientists are starting to take seriously what Lawn’s DEA long ago dismissed: that the mind-expanding properties of these demonized “party drugs” might be clinically valuable after all.

It’s an exciting time for a reborn field. Early clinical trials suggest MDMA may help patients with PTSD confront their traumatic memories. In other early studies, ketamine has reduced suicidal thoughts and other symptoms in patients with clinical depression.

Psilocybin too may be able to help people with intractable depression, decreasing symptoms in some patients for a year or more, though the data here are still limited. And many other studies and trials are ongoing in the field.

This recent pivot toward psychedelic drugs has been described by some as a “psychedelic revolution” in psychiatry, if not a “miracle cure” for mental health disorders in general. But many of the basic mechanisms of these drugs remain poorly understood, in a field of medicine that has barely begun to recover from decades of government-enforced stigmatization.

“There are a lot of questions that need answering,” said Robert Malenka, the Pritzker Professor of Psychiatry and Behavioral Sciences at Stanford and a Wu Tsai Neurosciences Institute deputy director, who studies the mechanisms that drive MDMA’s therapeutic properties. “We’re still concerned about the evidence that these drugs will be therapeutically useful—and if they are, how to best use them therapeutically.”

Partly because of these big unknowns, psychedelic medicine has struggled to shake off the same fears first expressed by Lawn’s DEA. For some potentially addictive compounds like MDMA, abuse potential remains a charged question, and broader ethical concerns surrounding the vulnerable state that many psychedelics produce remain at play for other substances.

To pull this 1960s-era field into the present, psychedelic researchers are going back to basics. They’re working to untangle the mechanisms behind these drugs’ properties—from their therapeutic effects to their abuse potential. By understanding how these drugs work, researchers hope to design better and safer treatments that come with all the benefits of psychedelics, and few of the downsides.

The wild world of psychedelics

Warped colors and fantastical images are familiar hallmarks of “classical” psychedelics, including hallucinogens like LSD and psilocybin. But the new “psychedelic revolution” actually involves several different families of drugs—some of which, like MDMA and ketamine, are not technically psychedelics at all.

MDMA is an example of an entactogen, a batch of compounds that alter social perceptions and amplify empathy. Take one of these drugs, and you’ll start feeling more connected to those around you, whether it be your fellow partygoers, your therapist, or even your significant other, as some therapists have found helpful in bridging fractured relationships.

Meanwhile, ketamine is an example of a dissociative anesthetic, which acts by distancing users from reality. Such drugs can place patients in a dream-like state of sensory deprivation where even your sense of self fades away.

For researchers, the goal is to understand—from a mechanistic standpoint—why only certain drugs work for some disorders and not for others, isolate those effective drug mechanisms, and focus research efforts around those mechanisms to develop far more targeted, disorder-specific treatments.

Scientists are now beginning to tease out the brain mechanisms behind the distinctive mind-altering properties of these different drug families, a critical step in turning them into mainstream treatments.

Classic psychedelics seem to work by binding to the serotonin 2a receptor, one of the 15 specialized receptor molecules the serotonin system uses to coordinate brain activity. Entactogens and dissociative anesthetics don’t directly act on this receptor, which is why they “feel” different from hallucinogens.

Research into these compounds is even murkier: while early studies into MDMA have implicated serotonin in the drug’s effects, it’s only one chemical in a mixed bag of neurotransmitters and hormones. Meanwhile, ketamine has been tenuously linked to a specific receptor in the brain’s glutamate system.

“We need more research using the same rigorous methods applied to many other promising compounds for mental illnesses. By studying both efficacy and mechanisms, we can be more precise in developing better treatments with fewer side effects,” said Carolyn Rodriguez, a professor of psychiatry and behavioral sciences who co-authored a July 2022 position statement by the American Psychiatric Association on the mental health uses of psychedelics and empathogens.

Rodriguez, who directs the Stanford Translational Therapeutics Lab, is leading studies on the mechanisms underlying ketamine’s effects, a crucial component of her work on ketamine as a potential therapy for OCD.

Previously, Rodriguez has demonstrated ketamine’s ability to reduce the compulsive behaviors characteristic of OCD. Her study on ketamine’s mechanism of action aims to better understand how ketamine helps OCD patients—one stepping stone toward a targeted OCD treatment.

Another key question is how these drugs change the brain itself to produce their unique mental states. Karl Deisseroth, the D. H. Chen Professor of bioengineering and of psychiatry and behavioral sciences at Stanford and a Howard Hughes Medical Institute investigator, has studied how ketamine alters brain dynamics to produce the characteristic “dissociative” state that appears to help some patients with depression and other disorders.

In a 2020 study, the Deisseroth lab linked these dissociative states to a specific rhythm of activity in particular circuits in the mouse brain. When the team artificially reproduced this rhythm in normal mice, they found they could directly trigger dissociation, even without ketamine.

Don’t trip? Or maybe do

Psychedelic therapy isn’t as simple as just taking a drug such as LSD, ketamine, or MDMA and waiting for your depression to go away. It unfolds over several preparatory sessions, each dedicated to pinning down how and when to enter the psychedelic experience.

When the drug arrives, it’s accompanied by ambient music and a pair of eye shades. The patient pops the pill, sits back, and lets the drug get to work on their brain. Lastly comes the therapist-aided process of integration, where the patient takes what they’ve experienced and tries to fit it back into their life.

“It’s a big, holistic process,” said Boris Heifets, an anesthesiologist and neuroscientist at the Wu Tsai Neurosciences Institute who has previously worked alongside Malenka to study the mechanisms of MDMA. “These drugs are more like ‘catalysts’ than they are treatments.”

The downside of this holistic approach, according to Malenka, is that psychedelic therapy is hard to regulate. In part, this is because psychedelic therapy often requires far more oversight than traditional therapy. For instance, because psychedelic drugs put patients in an altered, vulnerable state, each individual is normally accompanied by at least one and often two therapists for the sake of safety. This makes psychedelic therapy not only expensive, but tricky to scale up.

“The FDA has never had to evaluate a treatment that involves both a drug treatment and a psychotherapeutic intervention,” Malenka said. “Everybody’s very interested in seeing how federal agencies and states regulate the distribution of these substances as therapeutics.”

The ideal psychedelic treatment would drastically streamline this therapeutic process, reducing psychedelic therapy to nothing more than a simple, safe-to-use pill. It’s a tremendously difficult—and thus far elusive—goal.

At the heart of the matter is the “trip,” or the acutely brain-altering experience that characterizes these psychedelic drugs. Many researchers think that the process of consciously undergoing this experience is deeply intertwined with the therapeutic properties of drugs like LSD and MDMA.

“There’s this suspicion that the therapeutic part might come from the process of mixing things up and jumbling your rigid way of thinking,” Heifets said. “You can call it a realignment of your values, or a perspective change.”

One example might be found in MDMA. Patients with PTSD typically experience intense anguish in response to trauma-related triggers, yet MDMA’s brain-altering properties reduce these fear barriers while also producing a shift in perspective: one that allows patients to confront their trauma while remaining grounded in the present.

At the same time, MDMA’s ability to aid social interaction can greatly increase the emotional rapport between patient and therapist, further supporting the patient in working through their disorder.

But the question remains: do the clinical benefits of psychedelics always require patients to undergo these profound, and sometimes grueling, drug-induced experiences? It would certainly be much simpler for researchers—and speed the pace of progress for patients—if the benefits of psychedelics could be achieved without the trip.

Heifets, an anesthesiologist, has used general anesthesia to better investigate this question. By placing patients under anesthesia, he aims to test whether it’s possible to get the benefits of psychedelic drugs without actively experiencing the “trip”—suggesting that these drugs are operating on some deeper, more mechanistic level.

“What we’re studying is what would happen if we eliminated all external sensory input—if we made sure that patients were unaware of the drug’s effect on their brain by making them unconscious,” Heifets said. “Would we still get that therapeutic effect?”

Currently, researchers are working to develop this approach in ketamine trials, with the potential for future applications in other compounds. From what researchers have seen so far, however, there has not been compelling evidence that these drugs can work without the holistic process of preparation, “trip” and integration.

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Still, a solution without the “trip” remains the white whale (something obsessively pursued but difficult to achieve) of psychedelic medicine.

“We’re talking about designing drugs that have the same therapeutic efficacy, without the possible side effects, without the potential for bad stuff to happen,” Malenka said. “If that’s possible, that would be wonderful.”

Want to understand addiction? Look to evolution

It might not be possible to get the therapeutic benefit without the “trip,” but it might be possible to get the “trip” without one of the key risks—namely, addiction.

Addiction is a particularly vexing problem in non-classical psychedelic drugs like MDMA and ketamine, which trigger the release of dopamine, the neurotransmitter linked to addictive behavior. But is this same addiction mechanism responsible for the drugs’ therapeutic benefit?

For Malenka, the key to understanding these drugs’ addictive potential lies in understanding the ancient circuits they alter. The pleasure of socializing with other human beings is a core drive for our species, burned into our neural circuitry by their evolutionary value to human survival.

“What in the brain tells us that a social interaction is fun and rewarding?” Malenka said. “Why is it that, for most people, it’s more fun to go out to dinner with friends than eat by yourself?”

The Malenka lab’s research explores how these mechanisms get hijacked by drugs of abuse, including potentially beneficial ones like MDMA. Researchers had already established that MDMA’s addictive potential came from its ability to stimulate the release of dopamine, a neurotransmitter involved in reward and motivation that plays a role in most forms of addiction.

This shows a psychedelic brain
Early clinical trials suggest MDMA may help patients with PTSD confront their traumatic memories.

But in a series of studies, Malenka and Heifets—then a researcher in Malenka’s group—wanted to find out if MDMA’s therapeutic, empathy-boosting abilities might involve a different brain pathway, making it possible to separate out its positive effects from its abuse liability.

One leading possibility was the brain’s serotonin system, which can play a role in stabilizing feelings of well-being and happiness—the basis for MDMA’s therapeutic use. To test this question, the Malenka lab separately blocked MDMA’s ability to release either serotonin or dopamine in mice.

Normally, MDMA dramatically boosts rodents’ social drives, much like in humans. But inhibiting serotonin prevented this effect—strong evidence for a link between this neurotransmitter and the drug’s prosocial effects. In contrast, inhibiting dopamine had virtually no influence on animals’ sociability.

“This was compelling evidence that it might be possible to design a version of MDMA that elevates sociability through the serotonin system while greatly reducing or eliminating the regular drug’s addictive downsides,” Malenka said.

This mechanistic separation between therapeutics and abuse might not be possible in all drugs, however. While scientists are still working on these varied psychedelic compounds, the risk looms that abuse potential might come as an inseparable side effect of treatment.

“It’s hard to make categorical statements about abuse liability,” Heifets said. “Every drug is different, so at least when it comes to addiction, you have to talk about each like its own animal.”

The future of psychedelic treatment

With the field of psychedelics booming, researchers are operating in a high-stakes environment. On the one hand, it’s never been a better time to study these compounds: the Food and Drug Administration (FDA) has indicated their intent to approve both MDMA and psilocybin as mental health treatments in the next two years, according to a federal letter made public only weeks ago. Yet others fear that the excitement surrounding these compounds has gone too far, and that these potential treatments might be more hype than substance.

The obstacles are clear. According to Malenka, the risk that widespread medical legalization of these substances might lead to rampant misuse, could threaten the future of psychedelic medicine altogether.

“As soon as something bad happens, the pendulum will swing the other way,” he said. “We don’t want to return to the early 70s, where some individuals and communities used these substances inappropriately and bad things happened.”

It remains to be seen how regulators will scale up and facilitate this pipeline from lab breakthrough to mainstream treatment. But many researchers are excited to get their hands on a new set of tools to help treat mental disorders that have long resisted conventional forms of treatment. If these drugs deliver on their promised benefit, a new era for psychiatric medicine might be at hand—and all it took was for us to finally open our minds to the possibilities.

Brain Aging in People With Schizophrenia


Summary: Advanced brain aging may explain why, on average, people with schizophrenia have a significantly reduced life span.

Source: Cordis

People suffering from schizophrenia can expect to die 15 years sooner than they ordinarily would. A new study has now found that this could be partly caused by advanced brain aging.

The research findings were published in the journal Molecular Psychiatry.

Schizophrenia is associated with an increased risk of premature death, partially as a result of suicide or poor physical health. Studies to date have suggested that the high prevalence of disease, long-term cognitive decline and excess deaths in people with schizophrenia could in part be caused when their brain’s biological age overtakes the chronological age.

According to a few small-scale studies, this discrepancy called brain-predicted age difference (brain-PAD) has been found to be consistently higher in schizophrenic patients compared to healthy individuals. The studies have also shown that the gap between the two ages mainly widens during the first years after the onset of the illness.

On a larger scale

Recognizing the importance of examining whether these findings can be generalized through large-scale studies, the research team investigated brain age in more than 5,000 individuals from 26 international cohorts from the Enhancing NeuroImaging Genetics through Meta-Analysis [ENIGMA] Schizophrenia working group. The study included data from 2,803 schizophrenic patients and 2,598 healthy individuals aged 18 to 73 years.

“Brain-predicted age was individually estimated using a model trained on independent data based on 68 measures of cortical thickness and surface area, seven subcortical volumes, lateral ventricular volumes and total intracranial volume, all derived from T1-weighted brain magnetic resonance imaging (MRI) scans,” the study reports.

This shows a brain
Schizophrenia is associated with an increased risk of premature death, partially as a result of suicide or poor physical health.

On average, people with schizophrenia were found to have a higher brain-PAD compared to healthy controls, with a discrepancy between their brain-predicted age and their chronological age being about 3.5 years larger.

The team also investigated whether a higher brain-PAD in schizophrenic patients was linked to specific clinical characteristics: the age of onset of the illness, how long the patient has had schizophrenia, the severity of the symptoms, and the use and dosage of antipsychotic drugs. They found no association between brain-PAD and these characteristics.

“This suggests that a greater brain-PAD in schizophrenia may not be primarily driven by disease progression or treatment-related effects on brain structure that have been reported elsewhere. This is in keeping with previous studies showing a greater brain-PAD already present in first-episode schizophrenia and first-episode psychosis patients,” the authors state.

The study concludes that longitudinal studies with more in-depth clinical characterization are needed to establish whether a brain-age predictor such as brain-PAD could be a useful tool in early prevention or intervention strategies for the disease.

A New Way to Monitor Blood Flow in the Brain


Summary: A newly developed technique called parallel near-infrared interferometric spectroscopy (πNIRS) significantly improves the monitoring of cerebral blood flow throughout the brain.

Source: Institute of Physical Chemistry of the Polish Academy of Sciences

Monitoring the proper blood supply to the brain is crucial, not only to prevent neurological diseases but also to treat them. The parallel near-infrared interferometric spectroscopy technique, or simply πNIRS, could make life easier for doctors and patients worldwide.

Blood drives our entire body and is especially important for brain function. On average, about 50 ml/min/100 g flows through brain tissue – about 80-90 ml/min/100 g through the gray matter and 20-30 ml/min/100 g through the white matter. When there is a lack of oxygen and, therefore, a lack of proper blood supply, the death of nerve cells occurs – then we speak of a stroke. It affects about 70,000 people every year in Poland.

This is why it is essential to monitor cerebral blood flow in disease prevention and treatment. Neurology knows many effective methods for doing so, but many of them have their weaknesses. Now a team of neuroscientists led by ICTER researchers has developed a technique that can significantly improve the monitoring of cerebral blood flow in vivo.

It is described in a paper titled “Continuous-wave parallel interferometric near-infrared spectroscopy (CW πNIRS) with a fast two-dimensional camera,” by Saeed Samaei; Klaudia Nowacka; Anna Gerega; Zanna Pastuszak; Dawid Borycki, which appeared in the journal Biomedical Optics Express.

How to monitor cerebral blood flow?

Cerebral blood flow (CBF) uses about 15% of cardiac output to deliver the essential substances (oxygen and glucose) to the brain and take away the unnecessary ones (products of metabolism). Any deviation from the norm can cause temporary brain dysfunction and irreversible trigger diseases, with Alzheimer’s disease at the forefront. That’s why non-invasive monitoring of CBF is so important – we have several practical tools for doing so.

The first that comes to mind is functional magnetic resonance imaging (fMRI), probably the most widely used diagnostic test in the world, which also works well here. It allows monitoring local changes in brain blood supply and associated fluctuations in neuronal activity in vivo. The technique offers high-resolution images but is quite expensive and difficult to use in young children, for example. This is where optical methods come to the rescue.

Brain oxygenation can be assessed using functional near-infrared spectroscopy (fNIRS). This technique allows non-invasive measurement of regional cerebral oxygenation by using selective absorption of radiation of electromagnetic waves in the range of 660-940 nm by chromophores in the human body. It is often used as a tool to help monitor a patient’s condition, including during neurosurgery.

On the other hand, blood flow can be continuously monitored by diffuse correlation spectroscopy (DCS). Their most advanced modifications are based on continuous-wave (CW) lasers, which prevent absolute measurements. Interferometric near-infrared spectroscopy (iNIRS) can help here.

Still, previous studies have shown that this method is too slow to detect immediate changes in blood flow that translate into neuronal activity. This is because it is a single-channel system, which measures the intensity of only the single-mode of the light collected from the sample.

Innovative πNIRS

A team of researchers at ICTER decided to modify iNIRS, relying on parallel near-infrared interferometric spectroscopy (πNIRS) for multi-channel detection of cerebral blood flow. To achieve this, it was necessary to alter the iNIRS detection system. In πNIRS, the collected optical signals are recorded with a two-dimensional CMOS camera operating at an ultrafast frame rate (~1 MHz).

Each pixel in the recorded image sequence effectively becomes an individual detection channel. With this approach, it is possible to obtain similar data as with iNIRS, but much faster – even by orders of magnitude!

This shows the researchers
In experiments conducted at ICTER, a team of researchers (Saeed Samaei, Klaudia Nowacka) led by David Borycki used laser light along with an ultrafast camera to measure blood flow in the brain. The measurements showed that this novel technique, called parallel interferometric (π) NIRS, is sensitive enough to non-invasively analyze prefrontal cortex activation while reading unfamiliar text. which contributes to the development of a non-invasive brain-computer interface. Which contributes to the development of a non-invasive brain-computer interface. Credit: ICTER, Karol Karnowski, PhD

Such an improvement, in turn, translates into greater sensitivity of the system and accuracy of detection itself. It is possible to detect rapid changes in blood flow related to the activation of neurons, for example, in response to an external stimulus or administered drug. The solution could be helpful for diagnosing CBF-related neuronal disorders and evaluating the effectiveness of therapeutic approaches, e.g., for neurodegenerative diseases.

  • This project will improve rapid, non-invasive systems for human cerebral blood monitoring in vivo. Continuous and non-invasive monitoring of blood flow could help treat significant brain diseases. In addition, quick detection of cerebral blood flow will bring us closer to developing a non-invasive brain-computer interface (BCI) that could help people with disabilities. Finally, our project will strengthen the tradition of Polish development in diffusion optics – says Dawid Borycki of ICTER.

Tests have confirmed that the technique used effectively monitors prefrontal cortex activity in vivo. Moreover, it can be further improved thanks to the development of LiDAR technology and ultrafast volumetric imaging of the eye, reducing the cost of CMOS cameras. Thus, the πNIRS technique can monitor cerebral blood flow and absorption changes from more than one spatial location.

The data obtained by the πNIRS technique can be applied to the diagnosis of cerebral circulatory disorders, which will facilitate the evaluation of the patient’s condition and allow the prediction of early and long-term treatment results.

Human-Approved Medication Brings Back ‘Lost’ Memories in Mice


Summary: Roflumilast, a drug commonly prescribed for the treatment of COPD and asthma helps retrieve learning memories following a period of sleep deprivation in mice.

Source: University of Groningen

Students sometimes pull an all-nighter to prepare for an exam. However, research has shown that sleep deprivation is bad for your memory.

Now, University of Groningen neuroscientist Robbert Havekes discovered that what you learn while being sleep deprived is not necessarily lost, it is just difficult to recall.

Together with his team, he has found a way to make this ‘hidden knowledge’ accessible again days after studying whilst sleep-deprived using optogenetic approaches, and the human-approved asthma drug roflumilast.

These findings were published on 27 December in the journal Current Biology.

Havekes, associate professor of Neuroscience of Memory and Sleep at the University of Groningen, the Netherlands, and his team have extensively studied how sleep deprivation affects memory processes.

‘We previously focused on finding ways to support memory processes during a sleep deprivation episode’, says Havekes. However, in his latest study, his team examined whether amnesia as a result of sleep deprivation was a direct result of information loss, or merely caused by difficulties retrieving information.

‘Sleep deprivation undermines memory processes, but every student knows that an answer that eluded them during the exam might pop up hours afterwards. In that case, the information was, in fact, stored in the brain, but just difficult to retrieve.’

Hippocampus

To address this question, Havekes and his team used an optogenetic approach: using genetic techniques, they caused a light-sensitive protein (channelrhodopsin) to be produced selectively in neurons that are activated during a learning experience. This made it possible to recall a specific experience by shining light on these cells.

‘In our sleep deprivation studies, we applied this approach to neurons in the hippocampus, the area in the brain where spatial information and factual knowledge are stored’, says Havekes.

First, the genetically engineered mice were given a spatial learning task in which they had to learn the location of individual objects, a process that heavily relies on neurons in the hippocampus. The mice then had to perform this same task days later, but this time with one object moved to a novel location. The mice that were deprived of sleep for a few hours before the first session failed to detect this spatial change, which suggests that they cannot recall the original object locations.

‘However, when we reintroduced them to the task after reactivating the hippocampal neurons that initially stored this information with light, they did successfully remember the original locations’, says Havekes.

‘This shows that the information was stored in the hippocampus during sleep deprivation, but couldn’t be retrieved without the stimulation.’

Memory problems

The molecular pathway set off during the reactivation is also targeted by the drug roflumilast, which is used by patients with asthma or COPD.

Havekes: ‘When we gave mice that were trained while being sleep deprived roflumilast just before the second test, they remembered, exactly as happened with the direct stimulation of the neurons.’

As roflumilast is already clinically approved for use in humans, and is known to enter the brain, these findings open up avenues to test whether it can be applied to restore access to ‘lost’ memories in humans.

This shows neurons in the hippocampus
High magnification image showing part of the mouse hippocampus in which a sparse population of neurons encoding a specific learning event are labelled in red. Neurons that are not activated by the learning event are shown in blue.

The discovery that more information is present in the brain than we previously anticipated, and that  these ‘hidden’ memories can be made accessible again – at least in mice – opens up all kinds of exciting possibilities.

‘It might be possible to stimulate the memory accessibility in people with age-induced memory problems or early-stage Alzheimer’s disease with roflumilast’, says Havekes.

‘And maybe we could reactivate specific memories to make them permanently retrievable again, as we successfully did in mice.’

If a subject’s neurons are stimulated with the drug while they try and ‘relive’ a memory, or revise information for an exam, this information might be reconsolidated more firmly in the brain. ‘For now, this is all speculation of course, but time will tell.’

At this time, Havekes is not directly involved in such studies in humans. ‘My interest lies in unravelling the molecular mechanisms that underlie all these processes’, he explains.

COVID-19 Skin Effects Can Precede or Follow the Infection


Skin effects like hives and rashes are an underreported symptom of COVID-19

(pumatokoh/Shutterstock)

The common symptoms of COVID-19 are familiar to most people—many having experienced them more than once—and can include fever, cough, runny nose, loss of taste or smell, fatigue, and other flulike affections.

Less commonly known are the skin changes that may occur both before and after the infection sets in. According to Massachusetts General Hospital, skin symptoms may be the only or first sign that someone has contracted COVID-19.

In a study by the American Academy of Dermatology, more than half of the patients with pernio-like lesions and COVID-19 were otherwise asymptomatic. A woman in her fifties, who spoke anonymously to The Epoch Times, said an itchy red rash on her chest was her only COVID-19 symptom and neither she nor her dermatologist related it to the virus until she tested positive.

Such skin eruptions can resemble prickly heat and chickenpox rashes or present as hives and red, scaly rashes. A registry created by Massachusetts General Hospital, Harvard Medical School, along with the American Academy of Dermatology and International League of Dermatologic Societies, found the most common skin effect was a measles-like rash called morbilliform.

Doctors and scientists are still learning about COVID-related dermatological effects but say they come in many forms—some harmless and others consequential. For example, a skin condition called retiform purpura can be linked to blood clots and be life-threatening in those who are critically ill according to researchers at Massachusetts General Hospital. COVID-19 has been reported to reactivate the varicella-zoster virus, which causes chickenpox and shingles. “Both of these viruses are in the herpes family, persist indefinitely in the body after infection, and can start to multiply again after a period of quiescence,” wrote researchers in Nature.

Long COVID-19 and Long Haulers

Skin reactions associated with COVID-19 may appear after the infection and manifest as symptoms of long COVID-19, which affects up to half of those who originally get the virus. “Many long-haulers are reporting dermatological problems including hives, lesions, and red, scaly rashes,” reported Business Insider. “Sometimes, these issues appear in conjunction with early symptoms; in other cases, it can take weeks or months for skin problems to manifest after a person is diagnosed.”

Seven weeks after testing negative for COVID-19, the woman who spoke to The Epoch Times says she is still experiencing intermittent hives and rashes, a phenomenon reported in medical literature.

Recognition of long COVID-19 skin conditions is growing in the pandemic’s aftermath as symptoms are starting to emerge in those who had the virus. “Studies showed that the most common sequelae were those linked to the lungs, followed by skin, cutaneous, and psychiatric alterations,” found researchers in the Journal Healthcare (Basel) in 2022.

Early and Later COVID-19 Skin Effects

COVID-19’s ability to cause some skin effects such as “COVID toes” and “COVID arm” was seen early in the pandemic. Toes that adopt a bright red or purplish color, blister, itch, hurt or swell were described by the American Academy of Dermatology early in the pandemic adding that fingers can also be affected. The Academy also noted, early in the pandemic, the existence of “COVID arm” or “COVID vaccine arm”—a large rash that appears at the vaccine injection site.

“Rashes that appear more than four hours after getting the COVID-19 vaccine are not a sign of a severe allergic reaction,” the Academy wrote, and are no reason to skip your COVID-19 vaccine.”

Conversely, awareness of the existence of dermatological conditions that appear weeks, months, and even years after a COVID-19 infection is only now emerging. According to the U.S. Centers for Disease Control and Prevention, people who had severe COVID-19 or overall body inflammation (multisystem inflammatory syndrome) with the virus, those who have underlying health problems, or are unvaccinated are the most likely to have lasting effects.

Where does vaccination fit into the picture when it comes to COVID-19 skin effects? A study by the British Journal of Dermatology found that “there was no difference in skin-related symptoms between infected vaccinated and unvaccinated users,” except that “burning rashes, which were less common after vaccination.” A clear connection between receipt of a COVID-19 vaccine and the development of shingles has been established but the disease itself can also activate shingles and therefore is also seen in the unvaccinated according to medical research.

What Causes COVID-19 Skin Effects?

The jury is still out on the cause of COVID-19 skin effects. The most common explanation is that the aggressive immune response to the virus causes persistent inflammation. Yet it is also possible “that rashes and lesions could result from tiny blood clots in the skin,” according to Business Insider. “Some research has indicated that COVID-19 is a vascular disease instead of a respiratory one, meaning it can travel through the blood vessels.”

It is also possible that the virus is “transferred to the skin from respiratory sites by the lymphocytic cells” and causes “ballooning degeneration of the keratinocytes,” postulated researchers in the Journal of Family Medicine and Primary Care.

Speculating about the appearance of shingles following COVID-19 infections, the researcher wrote in the journal Cureus that T-cell and CD8 levels were “significantly decreased” in such patients, “indicating a possibility of SARS-CoV-2 directly infecting lymphocytes, which can eventually present in dysfunctional cells due to direct viral effects. These outcomes create optimum habitat for HZ [herpes zoster/shingles] emergence during an active COVID-19 infection but do not explain the emergence of HZ after clinical and functional recovery.”

Scientists at Mount Sinai Hospital and Mount Sinai School of Medicine found that opposing gene expressions create two molecularly distinct subsets of long COVID symptoms in plasma cells and that multiple and independent processes produce vastly different long COVID symptoms.

What Kinds of Treatments for COVID-19 Exist?

According to research published in the journal Viruses, itchy red patches in patients with COVID-19 are a “consequence of inflammatory processes in the skin,” and can be treated with antihistamines and painkillers like Tylenol. Lesions like COVID toe that resemble chilblains may be treated with, “topical corticosteroids alone or in combination with topical antibiotics.”

The researcher wrote in the journal Cureus that they treated a patient with a COVID-19-related morbilliform rash with oral diphenhydramine (an antihistamine) and topical triamcinolone 0.1% cream (a corticosteroid).

One should consult a doctor for concerning rashes, however, for slight itching, the website Altea lists several at-home and natural treatments that can be tried for relief:

  • Do not take hot showers and baths.
  • Moisturizing care (e.g., aloe vera gel or Polidocanol-based lotion) to be used daily, 1-2 times a day.
  • Store care products in the refrigerator.
  • Bath with moisturizing additives, max. 15 min. (e.g., St. John’s wort oil, has anti-inflammatory, antibacterial and analgesic effects).
  • Dab areas of skin several times a day with a mixture of apple cider vinegar and water (1: 1).
  • Do not scratch, better rub or pinch (bacteria under the nails can lead to further infections).
  • If the rash worsens, short-term cortisone-based creams will help.
  • For advice on which products to use, contact your dermatologist.

The COVID-19 sufferer who spoke to The Epoch Times found that cromolyn, an ingredient contained in some allergy preparations, took her skin eruptions away. “Mast cells which release histamine are found all over your body not just in the sinus areas and cromolyn is a mast cell stabilizer,” she said.

“Cromolyn sodium differs from antihistamine medications, which reduce the action of histamines following the release from mast cells,” says StatPearls research published in the U.S. National Library of Medicine. “Unlike corticosteroids that inhibit the late response of antigen-induced asthmatic reactions, cromolyn sodium inhibits immediate and late reactions.”

Conclusion

The state of medical care during the COVID-19 pandemic has been compared to “building a plane while flying it.” Trust in the mainstream medical system waned as it seemed unprepared and unable to offer advice and treatments to effectively address the pandemic.

That’s why knowing the possible skin effects of a COVID-19 infection is valuable as the virus persists and evolves. If you have an unexplained rash or hives, they could be your first—or only—sign that you have contracted the condition and should get tested. If, on the other hand, you already had a COVID-19 infection (or several), lingering skin conditions are more common than is widely known and that knowledge might put you at ease. The Epoch Times will keep you informed as more information on COVID-19-related skin conditions becomes available.

The Fundamental Substances: Essence


(Shutterstock)

Traditional Chinese medicine (TCM) is built on a foundation of more than 2,500 years of Chinese medical practice. TCM is a holistic practice that treats the system as a whole, rather than alleviates specific symptoms of illness.

Within the TCM, there is a substance called “essence.”

According to TCM, “essence, qi, blood, and body fluid” are the four basic substances that make up the human body and maintain the latter’s vitality. The viscera, meridians, internal organs, and other tissues of the human body are composed of these four basic components and rely on the nourishment of essence, qi, blood, and body fluid to conduct normal physiological activities.

Essence

  1. The basic concept of essence

In TCM, “essence” means focus and subtlety, and refers to all the subtle substances that comprise the basic components of the body.

Essence can have various names and imply different things according to its various sources, distribution, and functions. Most encountered are:

  • Congenital Essence: Inherited and derived from the parent’s prenatal. It is innate in nature and is the most primitive substance that constitutes the embryo and from there the origin of life.
  • Reproductive Essence: is stored in the kidneys and comes from the kidney essence. It is transformed from the congenital essence and with the help of the acquired essence, performs the function of reproducing the next generation’s offspring. The male and female reproduction essence comes together to form an embryo as a product of reproduction.
  • Water and grain essence: is also known as “acquired essence.” and is formed after absorption by the spleen and stomach and other viscera through the metabolism of water and grain after birth. It is an important essence to maintain all human life activities.
  • Viscera and internal organs essence: is the essence stored in the five viscera and six internal organs. The functional activities of all visceral and internal organs need not only to be stimulated and promoted by the innate essence but to be nourished by the acquired essence. Therefore, the essence of viscera and internal organs contains both congenital, as well as acquired essence. Essence derived from these two primitives is needed to maintain the functional activities of the five visceral and six internal organs.
  1. Generation of essence

The source of essence can be divided into congenital (innate) essence and acquired essence.

The innate essence is endowed by the parents, derived when the reproductive essence of the parents is combined into one. When the preliminary embryo is formed, the pre-natal essence is transformed to become the primary essence of the embryo (the next generation). The fetus, while still inside the amniotic sac during pre-natal development phases, is dependent entirely on its mother’s energy and blood for nourishment. Therefore, the innate essence also includes the nutrients that the fetus received from its mother.

Acquired essence comes from water and grain. After birth, the spleen and stomach work in unison to transport and absorb the subtlety of water and grain and distribute it to the five viscera and six internal organs to become the essence of them and maintain their physiological activities. Those of the best quality are stored in the kidneys to keep the essence in the kidneys full.

In other words, the source of the essence of the human body starts with the innate essence, which is continuously nourished after birth by the acquired essence. This combination of the essence of the past and present work in harmony, enhancing and assisting each other to maintain the full capacity of essence within the body at all times.

  1. The general function of essence
  • Reproduction
    “Reproductive essence” is the most primitive substance of life, which has the function of reproducing offspring.
  • Growth and development
    Essence is the material basis for human growth and development.
  • Marrow production for making blood
    Kidneys store essence, which in turn produces marrow. The marrow is further subdivided into the brain, spinal cord, and bone marrows, all of which are based on kidney essence. Essence is the main substance that makes blood, and it is done by transforming water and grain essence into blood, and by the transformation of kidney essence (generating marrow) into blood. When the essence is full, there will be sufficient blood supply.
  • Humidification
    Essence has the effect of moistening and nourishing all the viscera and internal organs, as well as other tissues within the human body.

One of the Most Harmful Ingredients in Processed Foods


When taken together, partially hydrogenated GE soybean oil becomes one of the absolute worst types of oils you can consume (Zoran Zeremski/Shutterstock)

When taken together, partially hydrogenated GE soybean oil becomes one of the absolute worst types of oils you can consume

It’s found in nearly everything you eat, but there are very good reasons to steer clear of it. This ‘homegrown’ oil creates chaos and dysfunction in your cells, and studies link it to tumors, diabetes, decreased immune function, obesity, asthma, heart disease, and more.

STORY AT-A-GLANCE

  • Two of the most harmful ingredients in processed foods are high fructose corn syrup and soybean oil, whether partially hydrogenated, organic, or made from newer soybean varieties modified in such a way as to not require hydrogenation
  • Completely unnatural man-made fats created through the partial hydrogenation process cause dysfunction and chaos in your body on a cellular level, and studies have linked trans-fats to health problems ranging from obesity and diabetes to reproductive problems and heart disease
  • Besides the health hazards related to the trans fats created by the partial hydrogenation process, soybean oil is, in and of itself, NOT a healthy oil
  • Add to that the fact that the majority of soybeans grown in the U.S. are genetically engineered, and as a result saturated with dangerous levels of the herbicide glyphosate, which may have additional health consequences as there are no long term safety studies
  • When taken together, partially hydrogenated GE soybean oil becomes one of the absolute worst types of oils you can consume
  • The genetically engineered (GE) variety planted on over 90% of U.S. soy acres is Roundup Ready engineered to survive being doused with otherwise lethal amounts of Monsanto’s Roundup herbicide (glyphosate). GE soybeans have been found to contain residue levels as high as 17 mg/kg, and malformations in frog and chicken embryos have occurred at just over 2 mg/kg

Processed food is perhaps the most damaging aspect of most people’s diets, contributing to poor health and chronic disease. One of the primary culprits is high fructose corn syrup (HFCS), the dangers of which I touch on in virtually every article I write on diets. The second culprit is partially hydrogenated soybean oil.

These two ingredients, either alone or in combination, can be found in virtually all processed foods, and one can make a compelling argument that the reliance on these two foods is a primary contributing factor for most of the degenerative diseases attacking Americans today.

Part of the problem with partially hydrogenated soybean oil is the trans fat it contains. The other part relates to the health hazards of soy itself. An added hazard factor is the fact that the majority of both corn and soybeans are genetically engineered.

As the negative health effects from trans fats have been identified and recognized, the agricultural and food industry have scrambled to come up with new alternatives. Partially hydrogenated soybean oil has been identified as the main culprit, and for good reason.

Unfortunately, saturated fats are still mistakenly considered unhealthy by many health “experts,” so, rather than embracing truly healthful tropical fats like coconut oil, which is mostly grown outside the U.S., the food industry has instead turned to domestic U.S. alternatives offered by companies like Monsanto, now Bayer (which bought out Monsanto in 2018), which has developed modified soybeans that don’t require hydrogenation.

Why Hydrogenate?

Americans consume more than 16 million metric tons of edible oils annually, and soybean oil accounts for about 11,339 metric tons of it.1 Until Monsanto genetically engineered its seeds to produce plants lower in linolenic acid, about half of it was hydrogenated, as regular soybean oil is too unstable otherwise to be used in food manufacturing.

One of the primary reasons for hydrogenating oil is to prolong its shelf life. Raw butter, for example, is likely to go rancid far quicker than margarine. The process also makes the oil more stable and raises its melting point, which allows it to be used in various types of food processing that uses high temperatures.

Hydrogenated oil2 is made by forcing hydrogen gas into the oil at high pressure. Virtually any oil can be hydrogenated. Margarine is a good example, in which nearly half of the fat content is trans fat.

The process that creates partially hydrogenated oil alters the chemical composition of essential fatty acids, such as reducing or removing linolenic acid, a highly reactive triunsaturated fatty acid, transforming it into the far less reactive linoleic acid, thereby greatly preventing oxidative rancidity when used in cooking.

In the late 1990s, researchers began realizing this chemical alteration might actually have adverse health effects. Since then, scientists have verified this to the point of no dispute.

Be aware that there’s a difference between “fully hydrogenated” and “partially hydrogenated” oils. Whereas partially hydrogenated oil contains trans fat, fully hydrogenated oil does not, as taking the hydrogenation process “all the way” continues the molecular transformation of the fatty acids from trans fat into saturated fatty acids.

Fully hydrogenated soybean oil is still not a healthy choice, however, for reasons I’ll explain below. The following slide presentation explains the technical aspects relating to the hydrogenation process.

The Health Hazards of Trans Fats

The completely unnatural man-made fats created through the partial hydrogenation process cause dysfunction and chaos in your body on a cellular level, and studies have linked trans-fats to:

  • Cancer, by interfering with enzymes your body uses to fight cancer
  • Chronic health problems such as obesity, asthma, auto-immune disease, cancer and bone degeneration
  • Diabetes, by interfering with the insulin receptors in your cell membranes
  • Heart disease, by clogging your arteries (Among women with underlying coronary heart disease, eating trans-fats increased the risk of sudden cardiac arrest three-fold!)
  • Decreased immune function, by reducing your immune response
  • Increased blood levels of low density lipoprotein (LDL), or “bad” cholesterol, while lowering levels of high density lipoprotein (HDL), or “good” cholesterol
  • Reproductive problems by interfering with enzymes needed to produce sex hormones
  • Interfering with your body’s use of beneficial omega-3 fats

As usual, it took many years before conventional health recommendations caught up and began warning about the use of trans fats. Not surprisingly, as soon as the FDA notified them that it planned to require food manufacturers to list trans fat content on the label — which ultimately took effect January 1, 2006 — the industry began searching for viable alternatives to appeal to consumers who increasingly began looking for the “no trans fat” designation.

It didn’t take long before Monsanto had tinkered forth a genetically engineered soybean that is low in linolenic acid, which we’ll get to in a moment.

Be aware that some food manufacturers have opted to simply fool buyers — a tactic allowed by the FDA, as any product containing up to half a gram of trans fat per serving can still legally claim to have zero trans fat.3 The trick is to reduce the serving size to bring it below this threshold. At times, this will result in unreasonably tiny serving sizes, so any time you check a label and a serving is something like 10 chips or one cookie, it probably contains trans fats.

The Health Hazards of Soybeans

Besides the health hazards related to the trans fats created by the partial hydrogenation process, soybean oil is, in and of itself, NOT a healthy oil. Add to that the fact that the majority of soy grown in the U.S. is genetically engineered, which may have additional health consequences. When taken together, partially hydrogenated GE soybean oil becomes one of the absolute worst types of oils you can consume.

Years ago, tropical oils, such as palm and coconut oil, were commonly used in American food production. However, these are obviously not grown in the U.S., as with the exception of Hawaii, our climate isn’t tropical enough. Spurred by financial incentives, the industry devised a plan to shift the market from tropical oils to something more “home grown.”

As a result, a movement was created to demonize and vilify tropical oils in order to replace them with domestically grown oils such as corn and soy.

The fat in soybean oil is primarily omega-6 fat. And while we do need some omega-6, it is rare for anyone to be deficient in it, as it is pervasive in our diet. Americans in general consume FAR too much omega-6 in relation to omega-3 fat, primarily due to the excessive amount of omega-6 found in processed foods.

Omega-6 fats are in nearly every animal food and many plants, so deficiencies are very rare. This omega-6 fat is also highly processed and therefore damaged, which compounds the problem of getting so much of it in your diet. The omega-6 found in soybean oil promotes chronic inflammation in your body, which is an underlying issue for virtually all chronic diseases.

What About Organic Soybean Oil?

Even if you were fortunate enough to find organic soybean oil, there are still several significant concerns that make it far from attractive from a health standpoint. Soy in and of itself, organically grown or not, contains a number of problematic components that can wreak havoc with your health, such as:

•Goitrogens — Goitrogens, found in all unfermented soy whether it’s organic or not, are substances that block the synthesis of thyroid hormones and interfere with iodine metabolism, thereby interfering with your thyroid function.

•Isoflavones: genistein and daidzein — Isoflavones are a type of phytoestrogen, which is a plant compound resembling human estrogen, which is why some recommend using soy therapeutically to treat symptoms of menopause. I believe the evidence is highly controversial and doubt it works.

Typically, most of us are exposed to too many estrogen compounds and have a lower testosterone level than ideal, so it really is important to limit exposure to feminizing phytoestrogens. Even more importantly, there’s evidence it may disturb endocrine function, cause infertility and promote breast cancer, which is definitely a significant concern.

•Phytic acid — Phytates (phytic acid) bind to metal ions, preventing the absorption of certain minerals, including calcium, magnesium, iron, and zinc — all of which are co-factors for optimal biochemistry in your body. This is particularly problematic for vegetarians, because eating meat reduces the mineral-blocking effects of these phytates.

Sometimes it can be beneficial, especially in postmenopausal women and in most adult men because we tend to have levels of iron that are too high, which can be a very potent oxidant and cause biological stress. However, phytic acid does not necessarily selectively inhibit just iron absorption; it inhibits all minerals. This is very important to remember, as many already suffer from mineral deficiencies from inadequate diets.

The soybean has one of the highest phytate levels of any grain or legume, and the phytates in soy are highly resistant to normal phytate-reducing techniques such as long, slow cooking. Only a long period of fermentation will significantly reduce the phytate content of soybeans.

•Natural toxins known as “anti-nutrients” — Soy also contains other anti-nutritional factors such as saponins, soyatoxin, protease inhibitors, and oxalates. Some of these factors interfere with the enzymes you need to digest protein. While a small amount of anti-nutrients would not likely cause a problem, the amount of soy that many Americans are now eating is extremely high.

•Hemagglutinin — Hemagglutinin is a clot-promoting substance that causes your red blood cells to clump together. These clumped cells are unable to properly absorb and distribute oxygen to your tissues.

Worst of All — Genetically Engineered Soybean Oil

The genetically engineered (GE) variety planted on over 90% of US soy acres is Roundup Ready — engineered to survive being doused with otherwise lethal amounts of Monsanto’s Roundup herbicide. The logic behind Roundup Ready crops such as soy is that you can decrease the cost of production by killing off everything except the actual soy plant.

However, animal studies reveal there may be significant adverse health effects from these GE soybeans, including progressively increased rates of infertility with each passing generation. By the third generation, virtually all the hamsters in one feeding study were found to be infertile. Second-generation hamsters raised on GE soy also had a fivefold higher infant mortality rate.

Are Low-Linolenic Soybeans the Answer?

We now also have other Monsanto-made soy crops to contend with. Responding to the growing demand for healthier diets, Monsanto launched Vistive low-linolenic soybeans in 2005. Most soybeans contain roughly 7% linolenic acid. The new varieties contain 1% to 3%, which reduces the need for hydrogenation.4 As explained by Monsanto:5

“Farmers are not the only beneficiaries of Monsanto’s efforts … Consumers will also benefit from the healthier crops that could result, such as soybeans that are low in linolenic acid. Linolenic acid, a precursor to trans fats, may contribute to cardiovascular disease … Low-linolenic soybeans reduce the need for hydrogenation in food processing, helping to reduce the amount of trans fats in processed foods.”

Yet another soybean variety created by Monsanto is the high stearate soybean, which also has the properties of margarine and shortening without hydrogenation. But are these soybeans any better or safer than either conventional soybeans or Roundup Ready soybeans, even though they don’t have to go through partial hydrogenation, and therefore do not contain trans fat? No one knows.

Another Hazard of GE Soybeans: Glyphosate

I keep stacking health risks upon health risks, and here’s another one: Research has shown that soybean oil from Roundup Ready soy is loaded with glyphosate, the main ingredient in Roundup — the broad-spectrum herbicide created by Monsanto.

According to a report in the journal Chemical Research in Toxicology, the highest MRL for glyphosate in food and feed products in the EU is 20 mg/kg. GE soybeans have been found to contain residue levels as high as 17 mg/kg, and malformations in frog and chicken embryos occurred at 2.03 mg/kg.6 That’s 10 times lower than the MRL.

This is an alarming finding because glyphosate is easily one of the world’s most overlooked poisons. Research published in 2010 showed that the chemical, which works by inhibiting an enzyme called EPSP synthase that is necessary for plants to grow, causes birth defects in frogs and chicken embryos at far lower levels than used in agricultural and garden applications.7 The malformations primarily affected the:

  • Skull
  • Face
  • Midline and developing brain
  • Spinal cord

When applied to crops, glyphosate becomes systemic throughout the plant, so it cannot be washed off. And, once you eat this crop, the glyphosate ends up in your gut where it can decimate your beneficial bacteria. This can wreak havoc with your health, as 80% of your immune system resides in your gut (GALT, or Gut Associated Lymph Tissue) and is dependent on a healthy ratio of good and bad bacteria. Separate research has also uncovered the following effects from glyphosate:

  • Endocrine disruption
  • DNA damage
  • Developmental toxicity
  • Neurotoxicity
  • Reproductive toxicity
  • Cancer

To Avoid Harmful Fats, Ditch Processed Foods

If you want to avoid dangerous fats of all kinds, your best bet is to eliminate processed foods from your diet. From there, use these tips to make sure you’re eating the right fats for your health:

  • Use organic butter (preferably made from raw milk) instead of margarines and vegetable oil spreads. Butter is a healthy whole food that has received an unwarranted bad rap.
  • Use coconut oil for cooking. It is far superior to any other cooking oil and is loaded with health benefits.
  • Be sure to eat raw fats, such as those from avocados, raw dairy products, olive oil, olives, organic pastured eggs and raw nuts, especially macadamia nuts which are relatively low in protein. Also take a high-quality source of animal-based omega-3 fat, such as krill oil.

Following my comprehensive nutrition plan will automatically reduce your trans-fat intake, as it will give you a guide to focus on healthy whole foods instead of processed junk food.

Remember, virtually all processed foods will contain either HFCS (probably made from genetically engineered corn) and/or soybean oil — either in the form of partially hydrogenated soybean oil, which is likely made from GE soybeans, loaded with glyphosate, or from one of the newer soybean varieties that were created such that the y do not need to be hydrogenated. They’re ALL bad news, if you value your health.