Science Monitor | 21.03.2020

coronavirus:social distancing

In the latest attempt to curb the corona virus crisis, schools and major public events are shutting down, and seniors have been encouraged to self-quarantine.

what you need to know about social distancing

what you need to know about social distancing.

The Potential of Coconut Oil and its Derivatives as Effective and Safe Antiviral Agents Against the Novel Coronavirus (nCoV-2019)

The Potential of Coconut Oil and its Derivatives as Effective and Safe Antiviral Agents Against the Novel Coronavirus (nCoV-2019)

Read the research of Professor Emeritus Dr. Fabian Antonio Dayrit (GS'67, HS'71, BS Chemistry '75) and Dr. Mary Newport of Spring Hill Neonatolody, Inc. on the potential use of coconut oil as a safe antiviral agent against the novel coronavirus. 

As we write this, the World Health Organization has declared a global emergency over the novel coronavirus, nCoV-2019, that has spread beyond China. There is still no cure for nCoV-2019. nCoV-2019 has been shown to be related to SARS (Zhou et al., 2020), a coronavirus which caused an outbreak in 2003. Several researchers have been designing drugs to specifically target protease enzymes in coronavirus, but testing for these drugs is many months away. What if there is a treatment candidate against the coronavirus that might already be available and whose safety is already established?

Lauric acid (C12) and monolaurin, its derivative, have been known for many years to have significant antiviral activity. Lauric acid is a medium-chain fatty acid which makes up about 50% of coconut oil; monolaurin is a metabolite that is naturally produced by the body’s own enzymes upon ingestion of coconut oil and is also available in pure form as a supplement. Sodium lauryl sulfate, a common surfactant that is made from lauric acid, has been shown to have potent antiviral properties. Lauric acid, monolaurin, and sodium lauryl sulfate (which is also known as sodium dodecyl sulfate) are used in a wide range of products for their antiviral properties.

Mechanisms of action

Three mechanisms have been proposed to explain the antiviral activity of lauric acid and monolaurin: first, they cause disintegration of the virus envelope; second, they can inhibit late maturation stage in the virus replicative cycle; and third, they can prevent the binding of viral proteins to the host cell membrane.

1. Disintegration of the virus membrane. The antiviral activities of lauric acid and monolaurin were first noted by Sands and co-workers (1979) and later by Hierholzer & Kabara (1982). In particular, Hierholzer & Kabara showed that monolaurin was able to reduce infectivity of 14 human RNA and DNA enveloped viruses in cell culture by >99.9%, and that monolaurin acted by disintegrating the virus envelope. Thormar and co-workers (1987) confirmed the ability of lauric acid and monolaurin to inactivate viruses by disintegration of the cell membrane. Sodium lauryl sulfate has been shown to be able to solubilize and denature the viral envelope (Piret 2000, 2002).
2. Inhibits virus maturation. The Junin virus (JUNV) is the causative agent of Argentine hemorrhagic fever. In a comparison among the saturated fatty acids from C10 to C18 against JUNV infection, Bartolotta and co-workers (2001) showed that lauric acid was the most active inhibitor. From mechanistic studies, it was concluded that lauric acid inhibited a late maturation stage in the replicative cycle of JUNV. From transmission electron microscope images, JUNV is an enveloped virus featuring glycoproteins that are embedded in the lipid bilayer forming viral spikes (Grant et al., 2012); this is similar to nCoV-2019.

3. Prevents binding of viral proteins to the host cell membrane. Hornung and co-workers (1994) showed that in the presence of lauric acid, the production of infectious vesicular stomatitis virus was inhibited in a dose-dependent and reversible manner: after removal of lauric acid, the antiviral effect disappeared. They observed that lauric acid did not influence viral membrane (M) protein synthesis, but prevented the binding of viral M proteins to the host cell membrane.

Although lauric acid accounts for much of the reported antiviral activity of coconut oil, capric acid (C10) and monocaprin have also shown promising activity against other viruses, such as HIV-1 (Kristmundsdóttir et al., 1999). Capric acid accounts for about 7% of coconut oil. Thus, at least two fatty acids in coconut oil, and their monoglycerides, have antiviral properties. Hilarsson and co-workers (2007) tested virucidal activities of fatty acids, monoglycerides and fatty alcohols against respiratory syncytial virus (RSV) and human parainfluenza virus type 2 (HPIV2) at different concentrations, times and pH levels. They reported the most active compound tested was monocaprin (C10), which also showed activity against influenza A virus and significant virucidal activities even at a concentration as low as 0.06-0.12%.

Use of coconut oil and C12 derivatives in animals and humans

Coconut oil and its derivatives have been shown to be safe and effective antiviral compounds in both humans and animals. Because of the antiviral and antibacterial protection that it provides to animals, coconut oil, as well as lauric acid and monolaurin, is used in farm animals and pets as veterinary feed supplements in chicken, swine and dogs (Baltic et al., 2017). Monolaurin has been shown to effectively protect chicken against avian influenza virus (van der Sluis, 2015). Li and co- workers (2009) prepared a gel containing monolaurin and found it to be highly active against repeated high viral loads of Simean immunodeficiency virus in macaques and Kirtane and co- workers (2017) developed a 35% gel of monolaurin for application in the female genital tract to protect against HIV. Sodium lauryl sulfate (SLS) has been used at low concentrations to inactivate viruses in milk of farm animals (de Sousa et al., 2019). SLS is the active constituent in commercial disinfecting wipes and standard laboratory disinfectants, and is an emulsifying agent and penetration enhancer in pharmaceutical preparations.

Professor Emeritus Dr. Fabian Antonio Dayrit

Coconut oil itself has been shown to have anti-HIV properties in small clinical studies. The first clinical trial using coconut oil (45 mL daily) and monolaurin (95% purity, 800 mg daily) against HIV-AIDS was conducted in the Philippines. This study involved 15 HIV patients, aged 22 to 38 years, 5 males and 10 females, for 6 months. There was only one fatality and 11 of the patients showed higher CD4 and CD8 counts after 6 months (Dayrit, 2000).

In another study, 40 HIV subjects with CD4+ T lymphocyte counts less than 200 cells/microliter were divided into a virgin coconut oil (VCO) group (45 mL daily) and control group (no VCO). After 6 weeks, the VCO group showed significantly higher average CD4+ T lymphocyte counts versus control (Widhiarta, 2016).

Conclusion

Several in vitro, animal, and human studies support the potential of coconut oil, lauric acid and its derivatives as effective and safe agents against a virus like nCoV-2019. Mechanistic studies on other viruses show that at least three mechanisms may be operating.

Given the considerable scientific evidence for the antiviral activity of coconut oil, lauric acid and its derivatives and their general safety, and the absence of a cure for nCoV-2019, we urge that clinical studies be conducted among patients who have been infected with nCoV-2019 (see below). This treatment is affordable and virtually risk-free, and the potential benefits are enormous.

On the other hand, given the safety and broad availability of virgin coconut oil (VCO), we recommend that VCO be considered as a general prophylactic against viral and microbial infection.

A proposed clinical study

We can propose that a clinical study be conducted on patients infected with nCoV-2019 accordingly:

• Group 1: Control group, standard care
• Group 2: standard care + VCO (45 mL, approx. 3 three tablespoons, daily or higher,)
• Group 3: standard care + Monolaurin (95% purity, 800 mg daily). Monolaurin is recognized as GRAS by US FDA.
• Group 4: standard care + Monocaprin (95% purity, 800 mg daily). Monocaprin is recognized as GRAS by US FDA.
• Group 5: standard care + SLS (pharmaceutical grade, 100 mg/kg/day). SLS toxicity: lowest NOAEL (repeated dose, rat): 100 mg/kg/day (hepatotoxicity) (Bondi et al., 2015).

News Source: https://www.ateneo.edu/ls/sose/sose/news/research/potential-coconut-oil-and-its-derivatives-effective-and-safe-antiviral

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When should you clean your hands? - BEFORE, DURING and AFTER preparing food. - BEFORE eating food. - BEFORE and AFTER caring for a sick person. - AFTER using the toilet. - AFTER changing the diapers or cleaning up a child who has used the toilet. - AFTER blowing your nose, coughing or sneezing. - AFTER touching animal, animal feed, or animal waste. - AFTER touching garbage.

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Time-Restricted Eating May Reverse Diabetes & Obesity

Another case against the midnight snack

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LA JOLLA–These days, with the abundance of artificial light, TV, tablets and smartphones, adults and children alike are burning the midnight oil. What they are not burning is calories: with later bedtimes comes the tendency to eat.

A new study by researchers at the Salk Institute cautions against an extended period of snacking, suggesting instead that confining caloric consumption to an 8- to 12-hour period–as people did just a century ago–might stave off high cholesterol, diabetes and obesity.

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How caloric restriction prevents negative effects of aging in cells

A new study provides the most detailed report to date of the cellular effects of a calorie-restricted diet in rats. While the benefits of caloric restriction have long been known, the new results show how this restriction can protect against aging in cellular pathways.

If you want to reduce levels of inflammation throughout your body, delay the onset of age-related diseases, and live longer, eat less food. That's the conclusion of a new study by scientists from the US and China that provides the most detailed report to date of the cellular effects of a calorie-restricted diet in rats. While the benefits of caloric restriction have long been known, the new results show how this restriction can protect against aging in cellular pathways.

"We already knew that calorie restriction increases life span, but now we've shown all the changes that occur at a single-cell level to cause that," says Juan Carlos Izpisua Belmonte, a senior author of the new paper, professor in Salk's Gene Expression Laboratory and holder of the Roger Guillemin Chair. "This gives us targets that we may eventually be able to act on with drugs to treat aging in humans."

Aging is the highest risk factor for many human diseases, including cancer, dementia, diabetes and metabolic syndrome. Caloric restriction has been shown in animal models to be one of the most effective interventions against these age-related diseases. And although researchers know that individual cells undergo many changes as an organism ages, they have not known how caloric restriction might influence these changes.

In the new paper, Belmonte and his collaborators -- including three alumni of his Salk lab who are now professors running their own research programs in China -- compared rats who ate 30 percent fewer calories with rats on normal diets. The animals' diets were controlled from age 18 months through 27 months. (In humans, this would be roughly equivalent to someone following a calorie-restricted diet from age 50 through 70.)

At both the start and the conclusion of the diet, Belmonte's team isolated and analyzed a total of 168,703 cells from 40 cell types in the 56 rats. The cells came from fat tissues, liver, kidney, aorta, skin, bone marrow, brain and muscle. In each isolated cell, the researchers used single-cell genetic-sequencing technology to measure the activity levels of genes. They also looked at the overall composition of cell types within any given tissue. Then, they compared old and young mice on each diet.

Many of the changes that occurred as rats on the normal diet grew older didn't occur in rats on a restricted diet; even in old age, many of the tissues and cells of animals on the diet closely resembled those of young rats. Overall, 57 percent of the age-related changes in cell composition seen in the tissues of rats on a normal diet were not present in the rats on the calorie restricted diet.

"This approach not only told us the effect of calorie restriction on these cell types, but also provided the most complete and detailed study of what happens at a single-cell level during aging," says co-corresponding author Guang-Hui Liu, a professor at the Chinese Academy of Sciences.

Some of the cells and genes most affected by the diet related to immunity, inflammation and lipid metabolism. The number of immune cells in nearly every tissue studied dramatically increased as control rats aged but was not affected by age in rats with restricted calories. In brown adipose tissue -- one type of fat tissue -- a calorie-restricted diet reverted the expression levels of many anti-inflammatory genes to those seen in young animals.

"The primary discovery in the current study is that the increase in the inflammatory response during aging could be systematically repressed by caloric restriction" says co-corresponding author Jing Qu, also a professor at the Chinese Academy of Sciences.

When the researchers homed in on transcription factors -- essentially master switches that can broadly alter the activity of many other genes -- that were altered by caloric restriction, one stood out. Levels of the transcription factor Ybx1 were altered by the diet in 23 different cell types. The scientists believe Ybx1 may be an age-related transcription factor and are planning more research into its effects.

"People say that 'you are what you eat,' and we're finding that to be true in lots of ways," says Concepcion Rodriguez Esteban, another of the paper's authors and a staff researcher at Salk. "The state of your cells as you age clearly depends on your interactions with your environment, which includes what and how much you eat."

The team is now trying to utilize this information in an effort to discover aging drug targets and implement strategies towards increasing life and health span.

Other researchers on the study were Shuai Ma, Shuhui Sun, Lingling Geng, Moshi Song, Wei Wang, Yanxia Ye, Qianzhao Ji, Zhiran Zou, Si Wang and Qi Zhou of the Chinese Academy of Sciences; Xiaojuan He, Wei Li, Piu Chan and Weiqi Zhang of Xuanwu Hospital Capital Medical University; Xiao Long of Peking Union Medical College Hospital; and Guoji Guo of Zhejiang University School of Medicine.

The work and researchers involved were supported by grants from the National Key Research and Development Program of China, the Strategic Priority Research Program of the Chinese Academy of Sciences, the National Natural Science Foundation of China, Beijing Natural Science Foundation, Beijing Municipal Commission of Health and Family Planning, Advanced Innovation Center for Human Brain Protection, the State Key Laboratory of Membrane Biology, the Moxie Foundation, and the Glenn Foundation.

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Story Source:

Materials provided by Salk Institute. 

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