Wednesday, October 21, 2020

Possible role for the element tellurium in weight loss

As I've studied molybdenum over the past few years, one thing that I keep noticing is how elements tend to displace and disrupt the function of elements over and under them in the periodic table of elements. For instance, tungsten administration is used to create a functional molybdenum deficiency. Calcium can have effects in the body that oppose magnesium, while strontium can displace calcium in bones. 

Selenium has an important role in thyroid hormone function. Being in a state of low-selenium can increase activity of certain thyroid hormones and lead to weight loss. A 2003 study of human males fed controlled diets found the following:

Decreases of serum T3 and compensatory increases in thyrotropin suggest that a subclinical hypothyroid response was induced in the high selenium group, leading to body weight increases. Increases of serum T3 and serum triacylglycerol accompanied by losses of body fat suggest that a subclinical hyperthyroid response was induced in the low selenium group, leading to body weight decreases.

https://academic.oup.com/jn/article/133/11/3443/4817951 

How can one temporarily get into a state of functional low-selenium status? Perhaps by intake of the element below it, tellurium. Tellurium is reportedly found in meat, seafood, dairy, and cereals, and the best source appears to be seafood. I suspect heavily farmed soil is often tellurium-poor, which would make it harder to obtain tellurium from grain. I've been tracking my food intake/activity/weight for some time, and I see the best results from intermittent fasting and exercise when I eat a diet that is high in seafood and relatively low in selenium (much as I love my whole grains, consumption of high-selenium wheat germ while trying to lose weight "protects" my status quo). 

Tellurium is actually already in our bodies in minute amounts, and scientists have been investigating what biological functions it might have in various compounds. Possibilities include anti-cancer and anti-inflammation. See https://pubmed.ncbi.nlm.nih.gov/20205748/ and https://pubmed.ncbi.nlm.nih.gov/22202556/. I don't see why it couldn't end up being something that helps fight obesity. Here are my reasons for thinking that:

1) The "ketogenic" diet also happens to be one that would promote a relatively high intake of tellurium, especially when one is eating wild-farmed seafood and grass-fed-source dairy and meat.

2) If thyroid hormones are involved, that would help explain why widespread use of measures to sanitize food production seem to go along with increased obesity; chlorine can interfere with iodine, and iodinated proteins are important to thyroid function. It's worth noting that the Netherlands, the European country that is resisting the "globesity" trend, also eschews chlorination of water. 

3) I have noticed that I do better at losing weight when I include foods that are good sources of kaempferol, which has been observed to increase the activity of an enzyme that activates thyroid hormone T3. See https://diabetes.diabetesjournals.org/content/56/3/767/

4) The state of Colorado has mysteriously low obesity rates (see https://www.denverpost.com/2018/09/12/colorado-least-obese-state/) and coincidentally is one of the major known sources of tellurium in the world. In fact, that's where the name of the Colorado city Telluride comes from.

I know the world is busy figuring out what to do about a new virus, but perhaps someone will take this hypothesis and look further into it. If "dust we art," we ought to find out more about what various kinds of dust do in our bodies.

Thursday, September 24, 2020

Another reason to investigate glucosamine in connection with Covid-19

As one can read in my prior posts, I think glucosamine (bioavailable in the human diet via fermented shrimp paste) is helping protect the regions that eat it regularly from high Covid-19 mortality burdens. I think it does so via protection of cartilage and via inhibition of interleukin-6 activity. Based on the very low numbers of Covid-19 cases seen in the Indochinese peninsula, I'm beginning to suspect that glucosamine not only lessens symptom severity but might even be helping stop transmission of the virus. A study I cited before about glucosamine indicates that it stops N-glycosylation in a manner similar to tunicamycin.

In DU145 cells glucosamine reduced the N-glycosylation of gp130, decreased IL-6 binding to cells and impaired the phosphorylation of JAK2, SHP2 and STAT3. Glucosamine acts in a very similar manner to tunicamycin, an inhibitor of protein N-glycosylation. Glucosamine-mediated inhibition of N-glycosylation was neither protein- nor cell-specific. Sensitivity of DU145, A2058 and PC-3 cells to glucosamine-induced inhibition of N-glycosylation were well correlated to glucosamine cytotoxicity in these cells.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4057579/

An interesting thing about tunicamycin is that it can prevent some coronaviruses from producing any infectious virions.

To examine these possibilities, we analyzed the oligosaccharide moieties of the membrane proteins of the avian coronavirus infectious bronchitis virus. In addition, we determined the effect of inhibiting the glycosylation of these proteins on viral maturation and infectivity. Infectious bronchitis virus virions contain nine proteins. Four of these proteins, GP36, GP31, GP28, and P23, are closely related structurally and appear to be homologous to the E1 proteins of murine coronaviruses. We found that the oligosaccharides of GP31 and GP28 could be removed with endoglycosidase H and that neither of these glycoproteins was detectable in tunicamycin-treated cells. These two results indicated that GP31 and GP28 contain N-linked oligosaccharides. Therefore, O-linked oligosaccharides are not a universal feature of the small coronavirus membrane glycoproteins. Tunicamycin inhibited glycosylation of all of the viral glycoproteins but did not inhibit production of virions by infectious bronchitis virus-infected cells. The virions released by these cells contained only the three non-glycosylated viral proteins P51, P23, and P14. These particles were not infectious. Therefore, it appears that glycosylated infectious bronchitis virus polypeptides are not required for particle formation. However, the viral glycoproteins are apparently indispensible for viral infectivity.

https://pubmed.ncbi.nlm.nih.gov/6294330/

The places that eat fermented shrimp paste the most regularly--Laos, Cambodia, Thailand, and Vietnam--appear to have aspects of their lifestyle that interfere with transmission of Covid-19. Perhaps shrimp paste-provided glucosamine is one of those aspects. Someone with more resources than I have should be investigating this possibility.

Friday, September 18, 2020

A contributory reason to why food supplements and vitamins are too often a waste of money: magnesium stearate

Fat cells secrete an enormously important protein called FABP4 (alternative name is aP2). It is involved in metabolic syndrome, obesity, heart disease, hypertension, diabetes, and cancer. (See https://journals.sagepub.com/doi/full/10.4137/CMC.S17067). When we start releasing stored fat from our fat cells, it goes up. When we fast, it goes up. It appears to me that it stands in the way of weight loss by working together with PPAR-gamma to store lipids (See https://www.biorxiv.org/content/10.1101/2020.01.03.894493v1 and https://pubmed.ncbi.nlm.nih.gov/11872365/). So targeting FABP4 with various compounds has been the subject of much research. 

Many compounds that can inhibit FABP4 naturally occur in various foods, herbs, and spices that often pop up as associated with lower fat gain from hypercaloric and/or high fat diets. These compounds are easy to find for sale online and in vitamin stores. But they usually are sold in capsules that include magnesium stearate, an additive used to improve "flow" and make encapsulation easier. Unfortunately for everyone who finds that they seem to be wasting their money on vitamins, prescription pills, and supplements in pursuit of better health, magnesium stearate is quickly turned into magnesium and oleic acid in their bodies. Oleic acid stimulates FABP4 in the liver (https://www.nature.com/articles/s41388-018-0597-1, Supplemental Figure 3). Magnesium stearate also typically contains some palmitic acid (http://library.njucm.edu.cn/yaodian/ep/EP5.0/16_monographs/monographs_l-p/Magnesium%20stearate.pdf), which increases FABP4 in macrophages (https://pubmed.ncbi.nlm.nih.gov/31363792/). Pill "fillers" aren't the inactive substances that people tend to view them as.

Thursday, August 20, 2020

Changing consumption patterns to confront Covid-19

Here is a meme summarizing some of the consumption patterns that seem to be associated with not being heavily burdened by Covid-19. This can be freely shared. I don't care about "getting credit" when people are suffering. Just don't alter it without basing the alteration on actual statistics and peer-reviewed, published findings, please.



References:  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7267383/,  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7175868/,  https://www.ijidonline.com/article/S1201-9712(20)30568-3/fulltext,  https://academic.oup.com/ajcn/article/80/4/862/4690388,  https://www.cell.com/iscience/fulltext/S2589-0042(20)30068-7,  https://pubmed.ncbi.nlm.nih.gov/30121057/, https://www.tandfonline.com/doi/full/10.1080/13880209.2016.1214739, https://www.sciencedirect.com/science/article/abs/pii/S0944711320300684, https://pubmed.ncbi.nlm.nih.gov/30263705/, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4057579/, https://pubmed.ncbi.nlm.nih.gov/28558148/

Tuesday, August 18, 2020

Some of the most important dietary factors that appear to be involved in regional Covid-19 case/mortality variation

Levels of the immune system messenger (cytokine) named “interleukin-6” rise and fall together with severity of Covid-19 symptoms.  Interleukin-6 is involved in causing a feedback loop of inflammation.
The earlier patients with Covid-19 receive medications that interfere with interleukin-6 messaging, the better they do.
Regional diets and the varying Covid-19 burdens in different countries/regions point to what we can put in our mouths in order to keep interleukin-6 levels down and decrease Covid-19 severity:

o Avoid coffee and vaping. 
o Do eat/drink ginger, hibiscus, peppermint, and shrimp paste (a source of glucosamine).





References:  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7267383/, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7175868/, https://www.ijidonline.com/article/S1201-9712(20)30568-3/fulltext, https://academic.oup.com/ajcn/article/80/4/862/4690388, https://www.cell.com/iscience/fulltext/S2589-0042(20)30068-7, https://pubmed.ncbi.nlm.nih.gov/30121057/, https://www.sciencedirect.com/science/article/abs/pii/S0944711320300684, https://pubmed.ncbi.nlm.nih.gov/30263705/,  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4057579/, https://pubmed.ncbi.nlm.nih.gov/28558148/

Saturday, July 4, 2020

Why is Brazil being hit so hard by Covid-19?

Based on my investigations and observations over the past few years, I can point to three characteristics of the Brazilian diet that appear to me to be major contributors to Brazil's high death toll from this new virus:

1) High consumption of salty foods that contain free chondroitin sulfate, especially the national dish feijoada, a black bean stew that is typically made by boiling several cuts of meat--including cartilige-filled pig ears--for several hours. Chondroitin sulfate is an important structural component of cartilage. There is a case study of a man in Japan who induced the same respiratory tract symptoms as seen in Covid-19 cases merely by taking supplemental sodium chondroitin sulfate:
"A case of drug-induced pneumonia caused by sodium chondroitin sulfate"
T. Itoh, Y. Hamanaka,
Japanese Journal of Chest Diseases 71(6):593-598, June 2012
Abstract: A 49-year-old man was admitted to the hospital with complaints of fever and dry cough. Chest X-ray film revealed ground-glass attenuation in both lung fields, so he was transferred to our hospital for further examination. Chest CT film showed ground-glass attenuation in both lung fields. A transbronchial lung biopsy revealed infiltration of lymphocytes and neutrophils, thickening of alveolar walls and proliferation of type II pneumocytes. By careful history taking, he admitted he had taken sodium chondroitin sulfate for one month before admission. The lymphocyte-stimulation test was positive for sodium chondroitin sulfate. Based on the above findings, we diagnosed this case as drug-induced pneumonia caused by sodium chondroitin sulfate. He recovered after discontinuation of the drug without corticosteroid therapy.
https://www.researchgate.net/publication/287575000_A_case_of_drug-induced_pneumonia_caused_by_sodium_chondroitin_sulfate

A salty feijoada stew is full of both sodium and readily available chondroitin sulfate, which I suspect combine to form some sodium chondroitin sulfate. And it's not just feijoada. The Brazilian go-to food for treating colds is canja de galinha, which similarly involves boiling down cartilaginous chicken portions for a long time in salty water. (https://en.wikipedia.org/wiki/Canja_de_galinha)

(If my hypothesis about this connection is correct, then it could also be a small factor helping to explain the higher Covid-19 burden seen in Ecuador and Peru, where "seco" stews are popular, cooked for many hours, and frequently made with cuts of meat that include bones and connective tissue. But I suspect high starch consumption and resulting metabolic syndrome-related consequences are probably much more to blame in Ecuador and Peru.)

2) High coffee consumption. Coffee drinking raises levels of the cytokine interleukin-6, levels of which correlate with Covid-19 symptom severity, in otherwise healthy people.

3) Relatively low consumption of foods/spices that reduce the level and effects of the cytokine interleukin-6, particularly ginger, hibiscus, and fermented shrimp paste (glucosamine, which is found in shrimp shells, can prevent binding of interleukin-6 to cells).

Tuesday, June 2, 2020

2020 Summer Country Studies

Summer vacation has officially started for our family, and that means we'll be studying some countries in depth. We typically let the children pick them. In order, we'll be learning about Argentina, Norway, Samoa, Germany, and Finland. Technically, Samoa, or the Samoan Islands, is two different countries because the islands comprise the Independent State of Samoa and most of American Samoa.

I anticipate some tango dancing, science videos about the Northern Lights, rye bread, and lots of cooking with coconut. And Eurovision song videos again. My children really love those, which is why 3/5 of this summer's selected countries are in Europe.

Wednesday, May 6, 2020

Response to a press release that could be read to mean that glucosamine might exacerbate the "cytokine storms" seen in COVID-19

Tonight I came across this press release--https://www.eurekalert.org/pub_releases/2020-04/aaft-hbg041320.php--in which one of the authors of a 2020 paper on the influenza A virus said that their findings might be applicable to help understand why diabetes can lead to higher COVID-19 mortality. Unfortunately, one could come away from reading the press release with an impression that because glucosamine resulted in increased levels of inflammatory cytokines in mice infected with influenza A, glucosamine might do the same to COVID-19 patients. Here is a link to the actual study, "O-GlcNAc transferase promotes influenza A virus–induced cytokine storm by targeting interferon regulatory factor–5" by Wang et al.: https://advances.sciencemag.org/content/6/16/eaaz7086

While glucose metabolism issues can undoubtedly promote a state of inflammation in the body via a number of mechanisms, the Wang study does not appear to otherwise apply to COVID-19. Cytokine storms can result from a wide variety of infectious and noninfectious diseases. (See https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3294426/.) In 2017, Wang and his colleagues discovered that influenza A virus induces cytokine storms via interferon regulatory factor–5 (IRF5), (see https://www.jbc.org/content/292/52/21291), and their 2020 paper states, "results suggest that IRF5 is at least the major, if not the only, functional [O-GlcNAc transferase] target that promotes [influenza A virus]-regulated cytokine storm." A search in the PubMed database turns up 0 results for a search on "IRF5" combined with "COVID-19," even though there are currently 9509 papers about COVID-19 in the PubMed database.

Viruses differ. A study about influenza A virus does not necessarily advance our understanding of a different virus such as COVID-19.

I think that glucosamine is more likely to calm rather than exacerbate a COVID-19 cytokine storm because of its role in protecting cartilage. (See my previous post, https://petticoatgovernment.blogspot.com/2020/05/working-hypothesis-of-how-cartilage.html.) Moreover, glucosamine can suppress secretion of the inflammatory cytokine interleukin-6 in bronchial epithelial cells (see https://www.sciencedirect.com/science/article/abs/pii/S001429991000186X) and even keep interleukin-6 from binding to some cells (see https://cancerci.biomedcentral.com/articles/10.1186/1475-2867-14-45). Lastly, the extremely low COVID-19 case and death rates in regions that frequently eat fermented shrimp paste--the only widely eaten food source of appreciable, bioavailable glucosamine--are strong evidence in support of a hypothesis that glucosamine provides a net benefit to those infected with COVID-19.

Tuesday, May 5, 2020

Working hypothesis: how cartilage damage is connected to respiratory tract symptom progression, particularly within the context of COVID-19.


The body senses the presence of virus-infected cells, so the immune system starts to produce messenger molecules (cytokines) as part of its attack on those cells. Some of the cytokines--IL-1beta, IL-6, and TNFa--induce degradation of hyaline cartilage in the nose, larynx, trachea, bronchi, and other locations throughout the body. The degraded cartilage releases atypical or virus-bound forms of chondroitin sulfate or other glycosaminoglycans (GAGs) that the immune system perceives as a threat. The body then begins to have a delayed hypersensitivity reaction to those atypical or virus-bound GAG molecules. The hypersensitivity reaction increases the very cytokines that cause degradation of cartilage, thus creating a positive feedback loop, so symptoms--which include fever, pain, and increased secretions of protective and cartilage matrix reparative substances--continue to worsen. Underlying conditions that predispose to higher levels of those cytokines contribute to strengthening that feedback loop. The increased secretions of protective and reparative cartilage matrix substances contribute to "clogging" the lungs, some of which reparative substances have adhesive properties; their presence in the alveoli counteracts the surfactant that usually keeps the alveoli clear, and if they are not cleared, hyaline membranes--a characterizing feature of diffuse alveolar damage--form in the lung lobes. 

[I'll be returning to this post frequently over the next few days to post supporting evidence and explanations below. And likely to edit the paragraph above, for it is a work in progress. I apologize for any sloppiness of language. My formal educational/employment background is in law, computer programming, and math, so while I'm good at logic and analysis, my use of biology terms is sometimes imprecise.]

* A delayed hypersensitivity reaction to an atypical GAG is plausible and has been proven to happen. A 2012 case study reports how a middle-aged man inadvertently gave himself fever, dry cough, and lung congestion (the described symptoms are strikingly similar to the main ones seen with serious COVID-19 cases) merely by taking sodium chondroitin sulfate as a supplement:

"A case of drug-induced pneumonia caused by sodium chondroitin sulfate"
T. Itoh, Y. Hamanaka,
Japanese Journal of Chest Diseases 71(6):593-598, June 2012
Abstract: A 49-year-old man was admitted to the hospital with complaints of fever and dry cough. Chest X-ray film revealed ground-glass attenuation in both lung fields, so he was transferred to our hospital for further examination. Chest CT film showed ground-glass attenuation in both lung fields. A transbronchial lung biopsy revealed infiltration of lymphocytes and neutrophils, thickening of alveolar walls and proliferation of type II pneumocytes. By careful history taking, he admitted he had taken sodium chondroitin sulfate for one month before admission. The lymphocyte-stimulation test was positive for sodium chondroitin sulfate. Based on the above findings, we diagnosed this case as drug-induced pneumonia caused by sodium chondroitin sulfate. He recovered after discontinuation of the drug without corticosteroid therapy.
https://www.researchgate.net/publication/287575000_A_case_of_drug-induced_pneumonia_caused_by_sodium_chondroitin_sulfate

* The envelope protein of the Zika virus (a flavivirus) was found to bind tightly to chondroitin sulfate and heparin sulfate. See https://pubmed.ncbi.nlm.nih.gov/28151637/. Like other coronaviruses, Covid-19 has a viral envelope. See https://cen.acs.org/biological-chemistry/infectious-disease/know-novel-coronaviruss-29-proteins/98/web/2020/04

* This hypothesis indicates two ways to interfere with symptom progression:

1) Protect the hyaline cartilage from damage, and
2) Reduce secretions of cartilage glycosaminoglycans that can contribute to covering the alveolar surfaces and, if atypical or virus-bound, increase the immune system's attacks.

COVID-19 researchers are already successfully investigating how to reduce cytokines that help cause degradation of cartilage, but I don't know if they are looking at which proteins are involved in secreting adesive molecules that could promote accumulations within the lung lobes; I recommend looking at reducing activity of SOX9, for it is increased by EGCG (found in tea) and pomegranate juice, which could partially explain the rapid increase in serious cases seen in Hubei (where panicked people contributed to damaging cartilage by spraying everyone down with bleach) and then Iran. Another possibility is temporary suppression of the body's own production of chondroitin sulfate, perhaps via an inhibitor of glycosyltransferases.

Monday, May 4, 2020

A preliminary finding that highlights the important role of interleukin-6 in causing COVID-19 symptoms

A few days ago, researchers out of China announced some good news about their preliminary trials of tocilizumab, an interleukin-6 (IL-6) blocker used to treat arthritis:

The drug is a monoclonal antibody -- a cloned immune cell -- that is intended to bind to interleukin-6, or IL-6, a type of cytokine protein research suggests is part of an overactive immune response that causes serious illness in some of those infected with the new coronavirus.
By binding to IL-6, the researchers said, tocilizumab effectively works to disrupt this immune response, allowing patients to recover.
***
After treatment with tocilizumab, all patients' body temperatures returned to normal on the first day and remained stable thereafter. Within five days of treatment, 15 patients were able to reduce oxygen intake, and lung lesions were resolved in 19 patients after treatment, the study's authors wrote.
All participants were discharged between 10 and 31 days after treatment, and no side effects were reported.

https://www.upi.com/Health_News/2020/04/30/Monoclonal-antibody-used-for-arthritis-may-help-severe-COVID-19-study-suggests/1791588189875 Yale Health System is now recommending tocilizumab as the second-line treatment (right after hydroxychloroquine) for COVID-19 cases.

Guess what else inhibits IL-6 and is used for arthritis? Yes, glucosamine. Which I've been trying, with little effect, to tell people about as a potential preventive for pneumonia for over two years (see https://petticoatgovernment.blogspot.com/2018/02/glucosamine-to-protect-cartilage-during.html and https://youtu.be/JnN_OL1J8Vw).

These past three months have been extraordinarily stressful as I've watched evidence for my cartilage damage-pneumonia hypothesis mount in connection with this new virus amidst a relentless death toll that has hit my country and a former home in Ecuador especially hard. I was not able to get this idea to a wider audience (my blog is quite obscure) because I am hampered by a lack of professional connections in medical research fields. I have decided to seek a degree in an appropriate field, for being a "lawyer-housewife who is good at research and math and knows regional cuisines" is not sufficient to allow me effectively to spread information about my discoveries.

Tuesday, April 21, 2020

A study supporting a link between insults to tracheal cartilage and development of pneumonia

As I've blogged a few times now, I think there is an overlooked component of respiratory tract cartilage harm contributing to who develops pneumonia in many contexts, including that of infection with the current headline-making virus. Here is the abstract of a 2019 study out of Saudi Arabia that supports such a hypothesis because it found that moving an endotracheal tube around after an initial placement thereof approximately tripled the risk of developing ventilator-associated pneumonia:

Repositioning of endotracheal tube and risk of ventilator-associated pneumonia among adult patients: A matched case-control study

Taha Ismaeil, Latifah Alfunaysan, Nouf Alotaibi, Shatha Alkadi, and Fatmah Othman
Ann Thorac Med. 2019 Oct-Dec; 14(4): 264–268. doi: 10.4103/atm.ATM_26_19 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6784441/)

Abstract:

INTRODUCTION:
Ventilator-associated pneumonia (VAP) is one of the most serious hospital-acquired infections to occur among mechanically ventilated patients. Many risk factors for VAP have been identified in the literature; however, there is a lack of studies examining the association between endotracheal tube (ETT) repositioning and an increase in the risk of VAP. The aim of the present study, therefore, was to investigate the effect of ETT repositioning and the risk of developing VAP.

METHODS:
Matched case-control studies were conducted among mechanically ventilated patients admitted to the intensive care unit (ICU) at King Abdulaziz Medical City from 2016 to 2018. Patients who had a documented VAP diagnosis were identified and matched to four controls (within a 10-year age band). The history of ETT repositioning (defined as changes in the positioned ETTs from the first reading at the time of ETT insertion) was explored in the medical files of the sample, as were other demographic and comorbidity risk factors. Logistic regression analysis was used to test the association between ETT repositioning and VAP.

RESULTS:
A total of 24 cases were identified with documented VAP diagnosis during the study. Those cases were matched to 81 controls. The mean age was 55 (standard deviation 21) for both cases and controls. VAP patients had a greater history of ETT repositioning (46%) compared to controls (29%). Patients who had a history of ETT repositioning were twice as likely to develop VAP as patients who had no history of ETT repositioning (P = 0.13). After adjustment of a potential confounder, the results showed evidence of an increased risk of VAP after ETT repositioning (odds ratio 3.1, 95% confidence interval 1.0–9.6).

CONCLUSION:
Reposition of ETT considers as a risk factor for VAP in ICU patients, and appropriate measures should be applied to reduce movements of the ETT tube.

Monday, April 13, 2020

Why are Laos and its neighbors faring so well during the COVID-19 pandemic? A consideration of diet factors

Laos had COVID-19 cases very early in this pandemic. Laos neighbors China and has many commercial ties to it. Yet Laos has had only 19 known cases and no deaths. Vietnam and Cambodia, which border Laos to the south and east, have had 387 cases total but also no deaths. And Thailand, at around 2500 known cases, has only seen 40 deaths. What is different about the Indochinese peninsula that could be protecting them from the case numbers  and death rates being experienced in Italy, Spain, and the USA?

I will leave the specialized research into biomedicine to the experts right now and focus on dietary differences. Food choices often make an enormous difference in health issues, and I don't see them getting much attention right now.

What do people eat in Laos? The main starches appear to be rice (especially glutinous rice) and fruit (especially papaya and banana). The primary dietary fats appear to be palm oil and coconut. Stir frying at a high temperature in a wok, grilling, and deep frying are the main ways in which food is cooked. Typical condiments include fish sauce, fermented shrimp paste, and soy sauce. While meals are often accompanied by many fresh greens, Laotians also eat sweet snacks throughout the day. Galangal (a close relative of ginger) is a heavily-used spice, along with garlic, shallots (a type of onion), and lemongrass. Green tea and coffee are common beverages.

How does the Laotian diet differ from the Italian diet? Ginger is not very popular in Italy. The main dietary starch is wheat. Green tea tends to be reserved for weight loss and fighting colds. Wine is commonly consumed. Olive oil is a cornerstone of the Italian diet. A variety of cooking methods is used, but wok usage is rare.

These are just some of the differences between typical Laotian and Italian diets. Which ones could be relevant to COVID-19? I want to point out three differences that I think should be investigated:

1) Ginger/galangal consumption.

Ginger is an anti-inflammatory spice. Ginger has repeatedly been shown to reduce the levels of both interleukin 1 beta (IL-1β) and tumor necrosis factor alpha (TNF-α), cytokines which are involved in the destructive immune reaction to COVID-19. (See https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7103735/.)

2) Fermented shrimp paste. 

Shrimp shells are a good source of glucosamine, and the fermentation process breaks down the shell and thus makes the glucosamine more bioavailable. As I've discussed before on my blog, glucosamine appears to help protect against developing pneumonia, which I hypothesize is a result of its protecting cartilage cells from attack by the immune system. 

3) Lauric acid and myristic acid intake.

The "tropical oils," i.e., coconut oil and palm oil, contain lauric acid and myristic acid, which can help protect cartilage. (See https://www.oarsijournal.com/article/S1063-4584(18)30141-9/fulltext.) Lauric acid is relatively uncommon outside of coconuts.

Until recently, the Mediterranean diet was touted as one of the heathiest in the world. As seen in the past two months, it did not appear to protect the relatively wealthy countries of Italy and Spain from COVID-19, especially when compared to some financially-challenged countries in southeast Asia. I hope to see more attention paid in the coming weeks to possible dietary factors behind that unexpected outcome.


(My apologies for having almost certainly missed some other important dietary factors that could end up being relevant to the fight against COVID-19. The above is what I have put together from having lived in Europe and the Philippines and read a lot about southeast Asian and European cuisines. I even had an Italian live with our family recently, who made it clear that ginger was not a favorite with her!)

Saturday, April 11, 2020

Hypothesis: Cartilage protection is connected to preventing development of pneumonia, especially that caused by COVID-19

I think there is an overlooked cartilage connection to the development of fatal pneumonia. Below I will point to how this hypothesis is supported by the current COVID-19 epidemic.

First, why a cartilage connection? Because in the 1918 influenza epidemic, a doctor's record indicates that those recovering influenza patients who sat up, ate solid food, and brought on coughing by being in smoke-filled rooms, quickly relapsed and died of pneumonia while patients who stuck to liquid diets and lay flat survived. (See https://www.archives.gov/exhibits/influenza-epidemic/records/visiting-doctor-letter.pdf) Hyaline cartilage is found in the trachea, larynx, and bronchi.

A longitudinal study looking at glucosamine--a shellfish component that is taken to protect against cartilage damage--found that glucosamine supplementation was associated with reduction of mortality from all causes and was associated with a very marked reduction in mortality from respiratory illnesses. (See https://link.springer.com/article/10.1007/s10654-012-9714-6)

If such a cartilage connection exists, why has it not been noticed by medical researchers previously? Conventional wisdom until recently has been that cartilage is "immune-privileged," i.e., that it is not attacked by the immune system even when cartilage cells are infected with a virus. Recent arthritis research indicates that the immune system does sometimes attack and cause destruction of cartilage cells. (E.g., https://www.nature.com/articles/s41598-018-36500-2 and https://www.nature.com/articles/srep16674) This points to an overlooked research avenue for pneumonia researchers.

Why should COVID-19 researchers spend precious time looking into this possibility when there are so many research areas they could be focusing on? Because environmental clues are pointing us to glucosamine and have since Chinese New Year travelers first left Wuhan carrying COVID-19 with them. 

COVID-19 is a highly contagious virus. China is highly connected via established tourism, trade, and other travel patterns to the countries of southeast Asia. Thailand, the Philippines, Vietnam, and Cambodia all had COVID-19 contacts and cases early in this pandemic. All are countries with densely populated areas and very poor infrastructure to support sanitation measures and any widespread ventilator needs. Why do they still have so few deaths compared to European countries and the USA? Vietnam and Cambodia still have no fatalities at all. Consider that for a moment: Cambodia and Vietnam combined have had nearly as many cases but far fewer deaths (i.e., zero) than Hawaii.

One reason could have been that those four southeast Asian countries are warmer countries. But tiny Singapore is warm. Spain and Italy are not snowbound in March. Louisiana, one of the hardest-hit US states, is a warm place. And, of course, Hawaii is very warm.

These four southeast Asian countries share a common dietary element that is mostly unused outside of that region: fermented shrimp paste. Shrimp paste is a very good source of readily bioavailable glucosamine. Shrimp paste is integral to meals in both Cambodia and Vietnam. It is commonly, though not universally, used in Thai cooking. Shrimp paste is a frequently used condiment in the Philippines, especially as a companion to green mango slices. A survey of the COVID-19 statistics supports a conclusion that consumption of fermented shrimp paste in the national diet is inversely related to COVID-19 case and mortality burdens.

Glucosamine is a widely used supplement--so it has a track record for safety already--that can be easily administered. There is vegetarian glucosamine available for those with shellfish allergies. In order to maximize its absorption by the surfaces of the upper respiratory tract, glucosamine can be included in warm broths and/or sucked on in the mouth to permit it to be aerosolized to some degree. Nebulizer administration appears to be a possible option for administration of glucosamine directly to the bronchi.

It’s worth investigating this hypothesis. The cost to test glucosamine's helpfulness in controlling COVID-19 symptoms is as minimal as you can get for a medication, and the potential benefit is huge in light of Vietnam and Cambodia’s continuing lack of fatalities from COVID-19. 


Disclaimer: I have no profit motive in posting this. I am an independent researcher who has lived on four continents and researches how regional diet differences could be connected to the epidemiology of various health issues.

Friday, January 31, 2020

My two bits about the novel coronavirus from Wuhan

1) Please, won't someone pay attention to my hypothesis about hyaline cartilage damage being an important contributory element in the progression to pneumonia that is so often seen with upper respiratory infections, especially in elderly people who are already prone to cartilage deterioration? Running around hoping for impossible-to-get antivirals when the cartilage damage has already started setting in, as is apparently going on in China right now, appears to be exactly the wrong approach. The infected should protect their cartilage by lying flat and subsisting on a cartilage-protecting liquid diet while their body fights off the virus. They shouldn't be building hospitals or treating patients in back-to-back shifts. Per page 4 of this letter from an army doctor who treated Native Americans during the 1918 influenza epidemic, the people who survived were those who lay flat and stuck with a liquid diet, while those patients who kept shifting between vertical and horizontal positions and/or ate solid food tended to die. This is a hypothesis that deserves further investigation.



2) My prayers are with everyone dealing with this. Quarantines, isolation, fear, overwork, oppression, all of it.