The Union health ministry said in a statement that 21,387 samples were collected in accordance with laboratory standards and were tested between June 27 and July 10 to determine the extent of the spread of the coronavirus disease in Delhi.
“Nearly six months into the epidemic, only 23.48% of the people are affected in Delhi, which has several pockets of dense population,” the Union health ministry, which commissioned the study, said in a statement.
https://www.hindustantimes.com/delhi-news/over-23-of-delhi-s-population-affected-by-covid-19-shows-serosurvey-results/story-Sq1XXdPkfmDdggyNwGdlSK.html
As on July 28, Mumbai has recorded 1,10,846 [sic] COVID-19 cases and 6,184 deaths.
A sero-surveillance study done in Mumbai has revealed that 57% of slum population and 16 per cent of non-slum residents in three civic wards had developed antibodies, indicating many people would already be affected by COVID-19 than the official tally suggests.
The Serological Surveillance for SARS-CoV2 infection was jointly commissioned by NITI Aayog, the BMC and the Tata Institute of Fundamental Research (TIFR).
The sero-surveillance started on June 3 and 6,936 samples out of an estimated 8,870 were collected from slum and non-slum population of three civic wards — R-North, M-West and F-North — in the first half of July.
https://www.thehindu.com/news/national/coronavirus-57-of-mumbai-slum-population-has-developed-antibodies-study/article32216939.ece
As of today, India has had 1,582,028 confirmed cases and 34,956 deaths, with 1,019,740 people recovered from the virus.
These reports are taken from Indian newspaper websites and published July 29. According to Wikipedia, the average age is 29 in India and more than 50% of the population is under 25. This is the youngest average for all countries in the world, according to this 2017 article in Financial Express of India.
For comparison, the median age is 38.2 in the US as of 2018; Maine has the highest median at 45 and Utah the lowest at 31.
The penetration of coronavirus is intense in the slums of Mumbai, yet the youth of the population seems to have reduced morbidity and mortality. Testing rates have been very low, although no exact data is available, only totals for the country. Authorities are freely admitting that funds for testing and treatment are simply not available in the needed amounts.
This article in the Washington Post on July 17 argues that India’s low death rate is due to under-reporting. The article also states that the pandemic is spreading unchecked throughout the country.
The hospital situation in India is surely as bad as that in Mexico. Fortunately for those who wish to know, there is better reporting about what is going on there. I was unable to locate any seroprevalence studies for Mexico at all.
Another statistic, not quite relevant but of interest: life expectancy at birth in India in 2020 for men is 68.4 and for women 71.2– while in the US, for men it is 76.2 and for women 81.2. For Mexico, men’s numbers are 72.12 and women’s 77.84. For Japan, the numbers are: 81.25 years for men and 87.32 years for women in 2018. (Numbers from Wikipedia and Google.)
COVID-19 in Mexico: unreported suffering
Mexico has seen 408,449 COVID-19 cases confirmed, with 45,361 deaths– 11% of cases are deaths, according to Worldometer. There are reports that testing is extremely limited by government policy in Mexico. According to Wikipedia, a government agency estimated that there were actually over 2.8 million cases, although their methodology is unknown.
If the death rate were only 1%, which would be low, that would mean that there would be 28,000 deaths. If there were 45,000 deaths, at a death rate of 1%, there would be 4.5 million cases… so your guess about the true figures is as good as mine.
Searching in Google, I was unable to find much recent information about Mexico’s COVID-19 problems. This Vox article from May 13 states that the pandemic in Mexico is being deliberately undercounted.
This article in the Yucatan Times from July 29 details the financial toll that is exacted from patients trying to get treatment for the virus in Mexico. There is, theoretically, public health care there, but the public hospitals are overwhelmed. Private hospitals demand pre-payment of large fees before even accepting patients at all.
This article in the Washington Post from July 2 says that Mexico City’s death rate tripled from March through May. The article includes figures stating 27,394 people died in Mexico City during that period, although the government reported only 4,000 coronavirus deaths. This would suggest that they are reporting less than half of deaths due to coronavirus.
Actually, it is worse than that, because according to the article, it takes at least a year for the government to finish totalling up all deaths for any given period. Add a few thousand more, but at this point, the exact number matters less than the overall picture of devastation.
With the border closed, there is little chance of spillage of Mexican cases into the US. Untold suffering is going on there, and if you think the US has problems, I am sure Mexico’s problems are worse. Our government is not handling the pandemic well, but Mexico’s government is doing very poorly.
I’m not going to look at the numbers from Canada (I’m tired), but all reports are that they are doing far, far better than we are. Fortunately, that border is closed as well.
This editorial published in JAMANETWORK today, July 29, discusses a research article also published today that estimates a roughly 60% reduction in COVID-19 cases and deaths due to school closures in March.
The implications are that re-opening schools will lead to a dramatic increase in cases during an uncontrolled outbreak due to SARS-COV-2. We can’t afford to increase cases, despite the economic and scholastic impact of keeping them closed.
Here are the statistics quoted in the editorial:
Auger et al4 found that school closure was associated with a −62% (95% CI, −71% to −49%) relative change in COVID-19 incidence per week, corresponding to an estimated absolute difference of 423.9 (95% CI, 375.0 to 463.7) cases per 100 000. The authors also reported that school closure was associated with a −58% (95% CI, −68% to −46%) relative change in mortality per week, corresponding to an estimated absolute difference in mortality of 12.6 (95% CI, 11.8 to 13.6) deaths per 100 000. Extrapolating these results to the US population, the authors estimate that school closure may have been associated with 1.37 million fewer cases of COVID-19 over a 26-day period and 40 600 fewer deaths over a 16-day period during the spring of 2020. It is important to emphasize these are estimates.
JAMA. Published online July 29, 2020. doi:10.1001/jama.2020.13092
It is not yet time to re-open schools. I suggest that we wait until January, when it will become clear in what direction this country is heading. Either things will be worse or better. They can’t stay the same.
The reason “He who must not be named” needed to take the screening test for dementia is that His father died of Alzheimer’s Disease (AD.) This disease runs in families to a very large extent (see below for explainer.)
The reason He brags about it is that he misunderstands or chooses to misinterpret the reason he had the test. I think that fundamentally, he misunderstands for two reasons: he wasn’t told the truth about why he was given the test, and/or he doesn’t have the intellectual capacity to make the distinction between dementia and personality disorder.
He doesn’t admit that dementia has nothing to do with his mental “problems”– his problem is what we call personality disorder, meaning there’s something wrong with his personality. What’s wrong? He has sociopathy and malignant narcissism, which are the problems causing the decline of our country.
Not to mention the deep roots of sadism, misogyny, xenophobia, and racism, which go along with his identification with the Republican Party and its nativist wing. I’ll set those things aside today and concentrate on dementia and personality disorder.
Let us not forget Ronald Reagan, who had AD while he was president and died of it. His entire staff knew that he was losing it, but they covered it up because he pushed the right buttons when it came to policy.
What is sociopathy? In basic terms, it’s the lack of a conscience, that thing inside you that makes you do right when other people aren’t looking or don’t stand in your way.
What is malignant narcissism? It is the concentration of your entire being on yourself and the complete absence of interest in anything other than yourself. Other people are only of concern to the extent that they validate you by praising you and doing what you want.
Every subject is of interest only to the extent that it reflects on your glory and your complete mastery. Nothing can be allowed to get in the way.
To a malignant narcissist, anyone who questions or criticizes is automatically an enemy to be destroyed. There is never any sense that one might be wrong or imperfect, or if there is, it must be immediately negated by praise from another or complete destruction of the critic.
To diagnose sociopathy and narcissism, there is the Minnesota Multiphasic Personality Inventory, but He wouldn’t take it– it’s way too long. Instead, one can make these diagnoses on the basis of spontaneous statements and behavior outside of the exam room, as His niece Mary Trump has done.
The “Goldwater Rule” would normally prevent a professional from discussing diagnoses, especially mental, outside of the exam room and without the patient’s consent. There is another doctrine, the “duty to warn” if there is a danger to “self and others.” In this case, anyone who realizes how bad things are has a duty to tell everyone because this patient can be very dangerous.
G-d help this country if this man is re-elected.
Explainer: the causes of dementia, specifically Alzheimer’s Disease.
First, the symptoms: The most common early symptom is difficulty in remembering recent events. As the disease advances, symptoms can include problems with language, disorientation (including easily getting lost), mood swings, loss of motivation, not managing self-care, and behavioural issues.
(references for symptoms: British Medical Journal, 2009 Feb 5;338:b158. doi: 10.1136/bmj.b158. World Health Organization fact sheet.)
Second, the causes: the chance of inheriting (heritability) of AD is estimated between 49% and 79%. This means that AD is caused by problems with your metabolism that you are born with. Your chances of getting AD are less, even if you have metabolic problems, if you exercise (both body and mind) and eat a diet low in animal fat.
Most AD is called “sporadic” because it has not been identified in the patient’s relatives. If He were found to have AD, we would say it was inherited because His father has it.
In sporadic cases as well as inherited ones, the risks are higher with high cholesterol, fatty diet, inactivity, obesity, and lack of mental exercise. Sound familiar? All of these risk factors fit He-who-must-not-be-named.
Luckily for Him, risks are probably less with cholesterol-lowering drugs, which He is taking– but the risk is NOT eliminated just by taking a pill.
A small percentage (roughly 0.1%) of AD is caused by a dominant mutation on regular chromosomes (not X-linked.) These are interesting cases because they are traced to mutations in genes for amyloid precursor proteins (more on these below) or “presenilins” (proteins that sit in the cell membrane and control how calcium crosses into the cells– important in nerves that sit in the hippocampus, a brain region that controls memories.)
In most sporadic cases, like the inherited forms, there is an apolipoprotein called apo-E4 present. It is involved in cases of atherosclerotic heart disease as well as AD. This fat-binding protein is part of fat metabolism in the body and brain, but it may cause heart disease in different ways than it causes brain disease and AD.
In the brain, apolipoprotein E helps to break down amyloid deposits called plaques. When the E4 type malfunctions, especially when body cholesterol levels are high, these deposits can damage nerve cells. Over a lifetime, amyloid plaques that build up eventually kill nerve cells. This has a lot to do with AD, but it’s not the whole story.
Those amyloid precursor proteins mentioned above also play a role. These proteins, when broken down into amyloid beta, accumulate in sheets called amyloid plaques. These are metabolized and removed in the brain by apo-E. Certain types of amyloid beta are harder to break down than others– leading to more and bigger plaques and, eventually, brain damage… thus, AD.
There is actually a known mutation in amyloid precursor protein that protects against AD by reducing breakdown into amyloid beta. The “amyloid precursor proteins” play many physiological roles that are still being evaluated (see the Wikipedia article on these proteins.)
That’s enough science for one post. It all comes from Wikipedia, which is almost 20 years old and getting bigger by the day. I just gave them $5.35 because I was ashamed that they only asked for $1.75 …
This study, from JAMANETWORK on July 17, looked at blood antibody tests done in several large cities in late March of this year. The astounding finding: between 6 and 24 times more patients had antibodies than had been counted by nasopharyngeal swab testing for SARS-COV-2:
In this cross-sectional study of 16 025 residual clinical specimens, estimates of the proportion of persons with detectable SARS-CoV-2 antibodies ranged from 1.0% in the San Francisco Bay area (collected April 23-27) to 6.9% of persons in New York City (collected March 23-April 1). Six to 24 times more infections were estimated per site with seroprevalence than with coronavirus disease 2019 (COVID-19) case report data.
JAMA Intern Med. Published online July 21, 2020. doi:10.1001/jamainternmed.2020.4130
This study has been widely reported recently. Its finding, that an average of ten to twelve times more patients with antibodies were present in each city than had been counted by antigen testing, has not been accounted for.
The conclusion is that many people either had asymptomatic infection or never went to be tested when they had symptoms. This has implications for preventive measures: everyone should be trying to prevent catching this disease all the time, even when they are not around people known to have been infected.
This means that you should be wearing a mask whenever you are around people you don’t know intimately. Even those you know well are potential vectors of disease: every non-household member and even those in your own household.
Previous studies have found ten to twenty percent of household contacts of people with proven COVID-19 become infected within ten days after the virus has been detected. What happens after ten days is unknown.
There have been very few reports of infections among children under ten, but this population has not been well-studied. If schools open next month, we should soon find out how many children have it and how well they pass it on. I would be extremely cautious about contacts with small children.
Children over ten years of age are likely to be just as infectious as adults. This age group includes a large proportion of school children– everyone in fifth grade and above. The vast majority of them will not get sick, even when they are infected, but they will be efficient vectors of disease to their parents, grandparents, schoolteachers, and staff.
The risks of open schools in the USA, with its environment of rapidly expanding infections, are great. For the last week or so, every day has brought over 50,000 new cases, and every day over a thousand people die. The actual number of new cases each day, with a broken testing system, is completely unknown.
Only in a state like Vermont would opening schools for in person attendance be even minimally acceptable.
SARS-COV-2 infects the heart and leads to lasting heart damage in many patients: JAMANETWORK.
This study from JAMA Cardiology posted on JAMANETWORK on July 27 looked at cardiac MRI scans of 100 people who had recovered from COVID-19. Their median age was 49; a third of them had been hospitalized, and all had been diagnosed between two and three months before they were examined. Many of these patients had been infected during a ski vacation, so they were not sedentary prior to their disease onset.
Only 5% of the patients had increased cardiac troponin T levels (a sign of heart damage often observed in myocardial infarction or “heart attack”) and none of them had active symptoms. This from the abstract:
Compared with healthy controls and risk factor–matched controls, patients recently recovered from COVID-19 had lower left ventricular ejection fraction, higher left ventricle volumes, higher left ventricle mass, and raised native T1 and T2. A total of 78 patients recently recovered from COVID-19 (78%) had abnormal CMR findings, including raised myocardial native T1 (n = 73), raised myocardial native T2 (n = 60), myocardial late gadolinium enhancement (n = 32), and pericardial enhancement (n = 22). … . Endomyocardial biopsy in patients with severe findings revealed active lymphocytic inflammation.
JAMA Cardiol. Published online July 27, 2020. doi:10.1001/jamacardio.2020.3557
In conclusion, the MRI findings showed: “cardiac involvement in 78 patients (78%) and ongoing myocardial inflammation in 60 patients (60%)…” This is astounding and indicates that most patients in this age group (roughly 50 year olds) had heart damage from COVID-19 that was not resolved 2-3 months after diagnosis.
The second heart study, of autopsies, was also from JAMANETWORK on July 27. 39 consecutive autopsies, with a median age of 85, were examined. The presence of SARS-COV-2 was documented in 24 patients, with elevated virus RNA in 16. From the results section:
SARS-CoV-2 could be documented in 24 of 39 patients (61.5%). Viral load above 1000 copies per μg RNA could be documented in 16 of 39 patients (41.0%). A cytokine response panel consisting of 6 proinflammatory genes was increased in those 16 patients compared with 15 patients without any SARS-CoV-2 in the heart. Comparison of 15 patients without cardiac infection with 16 patients with more than 1000 copies revealed no inflammatory cell infiltrates or differences in leukocyte numbers per high power field.
JAMA Cardiol. Published online July 27, 2020. doi:10.1001/jamacardio.2020.3551
This autopsy showed high levels of viral replication in heart tissue and definite signs that cells were “transformed” into virus factories, getting ready to die and release their viral loads. These results explain the frequent observations of acutely ill patients with elevated cardiac troponins and the 70% incidence of echocardiographic evidence of myocardial dysfunction (hearts not working right.)
One difference in the autopsy study was that they didn’t see an “inflammatory cell infiltrate” whereas the MRI study mentioned a finding of “active lymphocytic inflammation”– perhaps this is a late finding, and the older autopsied patients died before this could occur.
A clinical presentation compatible with myocarditis or heart inflammation (abnormal heart rhythm, palpitations, swelling in ankles, increased shortness of breath on lying down) as opposed to the usual cough, headache, chest pain, shortness of breath, weakness, and dizziness, is unusual. This suggests that infection of the heart is relatively silent compared to the obvious lung infection.
This does account for the devastating presentations of patients with severe COVID-19 if both the heart and lungs are affected.
This heart damage is shocking but not really surprising, given that a large proportion of patients with even mild disease have prolonged symptoms of fatigue or weakness and dizziness. Patients who have recovered from COVID-19 often complain of symptoms compatible with “mild heart failure” like exercise intolerance and shortness of breath.
Only time will tell how long these lingering symptoms will last and whether they will lead to a large population of chronic heart failure patients.
We learn something new about SARS-COV-2 almost every day.
A report of severe COVID-19 cases in four young men with mutations in their TLR7 genes came out a few days ago.
That is significant because TLR7 is part of the innate immune system. It recognizes the single-stranded RNA that SARS-COV-2 uses. When the virus injects itself into a cell, it is this RNA which hijacks the cell’s processes to reproduce itself.
TLR7 starts an immune cascade that results in the production of large amounts of type 1 interferons and other responses that have not yet been fully characterized (TLR proteins were only discovered recently and TLR7 specifically in 2004.)
You can find all the details in the Wikipedia articles about “toll-like receptors” and “TLR7”. There are also some scientific articles of interest, like this one: “Toll-like receptor signalling pathways” from 2014 in the journal “Frontiers in Medicine.”
The Wikipedia article on TLR7 mentions the study on the four young men with severe COVID-19, so they are up to date as well.
This article in today’s LA Times tells of the new movement in the investor community that is beginning to take account of the damage that climate change will cause. There’s an unmet need to develop new industry based on new technology that adapts to and counters climate change.
I don’t know how you’ll view that article (it looks pretty strange to me when I clicked on that link– but you can read it!) so take a look.
It seems to me that smart people with money are coming to realize that the climate is changing for the worse and their money is at risk. Big companies that sell oil could find the value of their holdings bottom out when people stop burning oil– if internal combustion engines are replaced by electric motors that use renewable energy, for example.
A good use for “all that oil” would be to synthesize plastics– not flimsy plastic bags but structural components, like replacements for concrete blocks, for example. Another use for oil is to synthesize chemicals like pharmaceuticals (and many other chemicals too numerous to name.)
Even ramping up synthetics production won’t use much of the oil left over if you stop burning it in engines. The demand could plummet and the value will follow, leaving oil companies bankrupt.
Companies that are exploring for new oil fields won’t be needed. Spending a lot of money to extract in harsh environments offshore or in the Arctic would make no sense if there’s no market for their product.
So that may be a good reason to disinvest.
Thoughts like these are going through the minds of the people with money who don’t want to lose it and have some smarts. That’s what this article seems to be saying between the lines.
PS this new wordpress editor is not ready for prime time. It’s just not stable. What happened to the total word count, to mention one glaring omission? Why does the size of the part I’ve marked out with my mouse keep changing whenever I try to change the type size or italicization? Does anybody at wordpress read my blog?
This article in JAMANET released July 24 caught my eye because it ties in with something we’ve seen in this pandemic: men are more severely affected than women, and young people are less affected.
The article is a “case series”, an examination of 4 patients, young men with an average age of 26, who got severe COVID-19 and were on ventilators for an average of ten days; one died. Here’s what they found:
Rapid clinical whole-exome sequencing of the patients and segregation in available family members identified loss-of-function variants of the X-chromosomal TLR7. In members of family 1, a maternally inherited 4-nucleotide deletion was identified (c.2129_2132del; p.[Gln710Argfs*18]); the affected members of family 2 carried a missense variant (c.2383G>T; p.[Val795Phe]).
What does this mean? These men had two different mutations in the gene for the TLR7 (toll-like receptor 7) protein, which controls an important part of the immune system– one that is rarely needed. They had been perfectly healthy for an average of 26 years, until they came down with COVID-19.
This could have some implications for resistance to SARS-COV-2 infections: first, TLR7 seems to be vital for an innate resistance pathway to the virus. There could be other mutations that weaken this gene, which is on the X chromosome– meaning that men are more likely to be affected.
Since men only have one X chromosome, any defective gene on that chromosome will be automatically expressed throughout their bodies. Women who have a defect on one X chromosome could be less affected because that one is only expressed in half their body’s (bodies’?) cells.
In women, one of the two X chromosomes is inactivated in each cell early in development, apparently randomly. This creates a “chimera” (an organism that has a mixture of cells and DNA of two different individuals, like tortoiseshell cats) although not the kind of chimera you usually think of. This is only significant if one X has different genes from the other, say with mutations, that cause problems.
This may partially explain why men are over-represented among victims of severe COVID-19.
The second significance is that TLR7 is important, so boosting this pathway may lead to some form of treatment. People with deficiencies could receive something that makes up for it…
Finally, the TLR7 pathway may weaken with age, partially explaining why older people get sicker.
Look for more developments in this area in the (hopefully near) future.
One more point: I first read about this in “Scienmag”– and then lost it. It was on my iPhone news feed, along with a lot of other content from the same people. I didn’t pay much attention to the source until I looked up the reference on Google and got this hit (along with the journal paper I wanted, described above):
“Why I unfollowed Scienmag” from July 26, 2017, and lo and behold, it’s a wordpress blog!
It says that they got tired of looking at its articles (and twitters) because they never linked to their original source– the scientific paper they were based on. The reason? Greed for eyeballs. Unless you go to a sponsored link they lose you, and scientific journals don’t sponsor/be sponsored by scienmag.
Finally, the very name is an attempt to feed off of “Science” magazine, an already trusted source, which posted this article way back in 2015:
“Who’s in your tribe?” which is about being very selective about who and what you follow…
There’s a word for the falsehoods/lies/confusion in “Plandemic”– what it is, it involves throwing up so many different things, under different headings, making implications, direct statements, negations, mentioning two things and implying there’s a connection between them, etc. that you just can’t keep up.
There was a lady (sorry, it was a guy) who used to do this, and her (his) name stuck to the technique. It’s called “the Gish Gallop.” From the RationalWiki, which I’ve never used before:
The Gish Gallop is the fallacious debate tactic of drowning your opponent in a flood of individually-weak arguments in order to prevent rebuttal of the whole argument collection without great effort. The Gish Gallop is a conveyor belt-fed version of the on the spot fallacy, as it’s unreasonable for anyone to have a well-composed answer immediately available to every argument present in the Gallop. The Gish Gallop is named after creationist Duane Gish, who often abused it.
Anyway, in all the excitement of finding the many, many fallacious arguments, specious statements, outright falsehoods, and so on in “Plandemic”, I forgot to mention that Judy Mikovits pushes hydroxychloroquine (HCQ) !
Now, right there, you know there’s a problem, because everybody who claims to have “the answer” to this pandemic pushes HCQ.
I won’t get into it with references and all right now, but there’s no accepted, good study of HCQ that shows any benefit to it. The latest popularized study had a major problem: many of the people who got HCQ also got a steroid, which we already know helps a lot in coronavirus (when it’s severe, anyway) and saves lives in ventilator cases.
So anyone who says it’s great right now isn’t listening to Tony Fauci and/or isn’t carefully reading the studies that are coming out/have recently come out.
So I call BS on Judy Mikovits (again!)
Conrad Theodore Seitz 