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NEWS YOU CAN USE: Is your meth contaminated with coronavirus? This Florida police dept. will test it for free.

The post President Trump Refuses Reauthorize Surveillance Laws Without FISA Reforms appeared first on The Bongino Report.

Alan Reynolds

Assuming the number of people who have reportedly died from COVID-19 is reasonably accurate, then the percentage of infected people who die from the disease (the death rate) must surely have been much lower than the 2–3% estimates commonly reported. That is because the number of infected people is much larger than the number tested and reported.

The triangle graph, from a February 10 study from Imperial College London, shows that most people infected by COVID-19 are never counted as being infected. That is because, the Imperial College study explains, “the bottom of the pyramid represents the likely largest population of those infected with either mild, non‐​specific symptoms or who are asymptomatic.”

As the Director General of the World Health Organization (WHO), Tedros Adhanom, explained in his February 28 briefing, “Most people will have mild disease and get better without needing any special care.” Several studies have found that about 80% of all the COVID-19 cases have relatively minor symptoms which end without severe illness and therefore remain unreported.

A Chinese study in the Journal of the American Medical Association, February 20, found a “case‐​fatality rate” of 2.3%, meaning 1,023 died out of 44,672 cases. But the total sample in that study (72,314) included an additional 27,642 non‐​confirmed cases, and simply including cases (let alone unreported minor cases) would have reduced the fatality rate to 1.4%. China‐​based estimates are largely confined to cases with the most severe symptoms, so it should be no surprise that the reported death rate among severe cases is much higher than it would be if the data also included “most people” who “have a mild disease and get better.” The risk of infecting more people is also more severe in China data, since severe cases are concentrated and transmitted in hospitals. This can also lead to overstated estimates of how many people are infected by someone with COVID-19, including the WHO “reproduction number” estimate of 1.4–2.5, which is mainly based on evidence from China.

As the graph indicates, other countries include more non‐​severe cases than China does, notably by testing incoming travelers who arrive with a cough and fever. Even after casting a slightly wider net, however, the number of confirmed cases probably captures only about 30% of the actual number.

By the morning of March 2, there had been 89,253 confirmed cases of COVID-19 reported around the world, with about 96% of those in Asia. For comparison, the were an estimated 37.9 million people living with HIV in 2018.

It is worth noting that have also been 45,393 known recoveries from COVID-19 (compared to 3048 cumulative deaths) and, importantly, recoveries have been outnumbering new cases.

What about the relatively small number of COVID-19 cases outside China? In his February 28, the Director General of WHO reported that “Outside China, there are now 4351 cases in 49 countries, and 67 deaths.” Deaths of 67 divided by 4351 seems to demonstrate a death rate of 1.5%. But such calculations are highly misleading. They assume the denominator of that ratio (4351) is as accurate as the numerator (67). Yet people with “mild cases who get better” are unlikely to ever be included in the denominator.

If the WHO estimate of 4351 confirmed cases amounted to 30% of the actual number infected outside of China at that time, for example, then the combined total of both unreported and confirmed cases would be 4351 divided by 0.30 or 14,503. In that case, the actual death rate would 67 divided by 14,503, or less than one half of one percent (0.46%). Also, such death rates in the recent past are likely to come down over time, because they happened before promising new clinical trials of antiviral drugs that proved effective against more deadly viruses such as SARS, HIV and Ebola.

For perspective, the SARS coronavirus killed 774 people out of 8096 known cases in 2003, which was a death rate of 9.6% before it vanished the next year. Bird flu in 1997 was predicted to be a deadly pandemic, but it killed very few people before it disappeared. In its February 22 U.S. Influenza Surveillance Report, “CDC estimates that so far this season there have been at least 32 million flu illnesses… and 18,000 deaths from flu.” Dividing 18,000 by 32 million implies a low U.S. death rate of .0138% from the flu. Looking at the death rate alone is obviously not enough: We also have to look at the numbers of people infected, and the duration of the epidemic, which is why the flu killed so many more people than SARS. Still, it is important to avoid scaring people about the risk of death from COVID-19 by continuing to ignore the fact that the vast majority of cases “have mild disease and get better without needing any special care.”

The post After Failed Gun Ban, Virginia to Pass “Red Flag” Laws appeared first on The Bongino Report.

HIGHER EDUCATION BUBBLE UPDATE: UC Santa Cruz fires 54 graduate student workers striking for higher pay.

NICE WORK, GUYS: China officials knew of coronavirus in December, ordered cover-up, report says.

In late December, several genomics companies tested samples from sick patients in Wuhan — the center of the coronavirus outbreak — and noticed alarming similarities between their illnesses and the 2002 SARS virus, the Sunday Times of London reported, citing Chinese business news site Caixin Global.

The researchers alerted Beijing of their findings — and on Jan. 3, received a gag order from China’s National Health Commission, with instructions to destroy the samples.

Rather than hunkering down to contain the virus, Wuhan officials went ahead with their annual potluck dinner for 40,000 families.

The alleged cover-up continued when representatives from the US Centers for Disease Control and Prevention visited Wuhan Jan. 8, where officials intentionally withheld information that hospital workers had been infected by patients — a telltale sign of contagion.

China really isn’t ready to join the family of civilized nations.

SOCIALIST FAUX PAS OF THE WEEK: Bernie Sanders boards the wrong private jet. “Mistakes like this (getting on the wrong Gulfstream) are bound to happen.”

Plus: “It’s a 2 hr drive from Charleston to Myrtle Beach & locals do it all the time – Not @BernieSanders- He & his entourage flew from Charleston to Myrtle Beach in not 1, not 2, but 3 Gulfstream Jets today. It took them 10 minutes to fly. Who is the elitist??”

I don’t know, but I don’t want to hear another goddamn thing about my carbon footprint.

FISA TO BE RE-UPPED, SPYGATE REFORMS DELAYED: Careful reading of the coronavirus emergency funding bill that will pass Congress soon will likely also uncover a reauthorization provision for the Foreign Intelligence Surveillance Act (FISA).

Just don’t expect to see any of the reforms Republicans say must be enacted to prevent future recurrences of the FBI surveillance abuses against the Trump campaign in 2016.  Most important among those reforms is a ban on bulk metadata collection derived from telephone calls by individuals within and without the country.

BERNIE SANDERS PRAISES SLAVE OWNERS FOR FREE HOUSING PROGRAM.

From the Babylon Bee, America’s Newspaper of Record.

REST IN PEACE: Renowned Mathematician And Physicist Freeman Dyson Has Died At Age 96. From an era when great scientists were rebels. Nowadays they’re more likely to be organization men and women.

New York Times columnist Thomas Friedman, who admires what a single-party autocracy such as China's can accomplish when it is "led by a reasonably enlightened group of people," praised that country's "one child" policy in a 2008 book, saying it "probably saved China from a population calamity."

In the Amazon Prime Video documentary One Child Nation, the Chinese-American filmmaker Nanfu Wang lays bare the brutal reality of the oppressive regime that was so glibly endorsed by rich Westerners who take their own reproductive freedom for granted. She shows that the one-child policy, in force from 1979 to 2015, routinely relied on extortion, assault, kidnapping, and infanticide.

Returning to the farming village in Jiangxi province where she was born and raised, Wang talks to an uncle and an aunt who mournfully remember the infant daughters they felt compelled to abandon. Wang's grandfather says he had to dissuade local officials from sterilizing her mother after Wang was born.

One of those village leaders tells Wang "the one-child policy was very difficult to implement" because "people resisted." If they couldn't be persuaded by propaganda, they would be punished by confiscation of their possessions or demolition of their homes. Recalcitrant women were physically forced to undergo sterilization. "It was really fucked up," the former official says. "We below didn't want to do this, but we had no choice."

A local midwife estimates that she performed 50,000 to 60,000 sterilizations and abortions. "Many I induced alive and killed," she says. "My hand trembled doing it."

A former family planning official recalls that "sometimes pregnant women tried to run away" from forced abortions, often performed at eight or nine months, and "we had to chase after them." Unlike the midwife, she is proud of her work, agreeing with Thomas Friedman that "the policy was absolutely correct."

‘BDS THIS:’ Israel Makes ‘Exciting Breakthrough’ In Race For Coronavirus Vaccine.

AMERICA’S PAPER OF RECORD:  Joe Biden Claims He Is Only Human Left On Earth Not Killed By Gun Violence.

The post A Number of Swing States Have “Suspiciously High” Levels of Voter Registration appeared first on The Bongino Report.

SENSIBLE:  Let’s talk about coronavirus.

Look, guys, as with Ebola this coronavirus is almost certainly being spread by certain cultural practices.  What Bookworm calls “toilet hygiene” is completely different in much of the world. And we DO know some of the transmission is through fecal matter.

I will be honest, I and most of the people I talk to online have been sick (up and down) with never-get-well since early January. We were joking that we’re not sure this is not coronavirus, because it keeps returning.

It probably isn’t. But it could be. Not enough people have been tested to know where and if there’s community transmission.

What we do know, though, is that so far the deaths in the US are of people who contracted the virus abroad. If people are sick in the US, it’s manifesting as a series of very bad colds or a returning virus. We’ve had these before, at least in military towns. Remember early 2000s when they were sending contractors back from Iraq when they couldn’t treat them? Fun times. I don’t remember what year it was everything in Colorado Springs closed, including the churches and the schools. I don’t remember, because I was sick over and over again, each time a weaker attack, till it passed. But none of us died. It was just truly annoying.

There are other factors than cultural practices. For instance, the population of Wuhan was under stresses we can’t even imagine.

Our particular issue is how enmeshed we allowed our economy to become with theirs. It’s time to split the sheets. The sooner, the better.

Meanwhile take sensible precautions, work from home if you can, and wash your hands. Oh, and don’t panic over the stock market. Killing the economy will only elect Bernie who’ll turn us into what China is.

A SMALL VICTORY FOR FREEDOM: Illinois House passes bill to tear down nearly 100 red-light cameras.

YET ANOTHER MASSIVE TIME-SUCK: Smithsonian Releases 2.8 Million Images Into Public Domain. “For the first time in its 174-year history, the Smithsonian has released 2.8 million high-resolution two- and three-dimensional images from across its collections onto an open access online platform for patrons to peruse and download free of charge. Featuring data and material from all 19 Smithsonian museums, nine research centers, libraries, archives and the National Zoo, the new digital depot encourages the public to not just view its contents, but use, reuse and transform them into just about anything they choose—be it a postcard, a beer koozie or a pair of bootie shorts.”

Nice.

THE BUDGET PROBLEM WASHINGTON DARE NOT MENTION: It’s the unfunded future obligations under Social Security, Medicare and other entitlements that make the national debt $122 trillion, not the officially cited figure of $23 trillion.

The Committee for a Responsible Federal Budget (CRFB) had an otherwise-excellent summit on the budget Tuesday that featured Senate Budget Committee Chairman Mike Enzi (R-WY), Sen. James Lankford (R-OK) and Sen. Sheldon Whitehosue (D-RI), plus key Senate and House budget panel staffers going back to 1985.

But nobody said anything about that $122 trillion monster lurking in the “out years” that won’t be out sooner than anybody thinks.

AND HE’S RIGHT! HAVING MINORITIES, WOMEN, AND THOSE NORMALLY LESS ABLE TO DEFEND THEMSELVES IS EXTREMELY DANGEROUS TO WOULD-BE TOTALITARIANS, LAW BREAKERS AND RAPISTS:  Gun-Control Exec Says Attempts to Sell Guns to Minorities, Women ‘Incredibly Dangerous’ .

YEAH, PRETTY MUCH:

THE ENTIRE NONPROFIT WORLD IS A CESSPIT OF SLUSHFUNDS AND LIMITED ACCOUNTABILITY: ‘So shady and disgusting’: Florida’s nonprofit pay scandal is worse than you think.

I’ve been blogging about the sleaziness of the nonprofit world for a long time.

Folks, I’m excited to bring you this book excerpt from The Carnivore Code. Author Dr. Paul Saladino is one of the best informed thought leaders and advocates of the carnivore diet. Paul uses his experience in functional and traditional medicine to devise a holistic picture of healing. I think you’ll appreciate his detailed, well-researched, and measured approach to presenting and analyzing evidence.

We’ve reviewed study after study that’s correlated red meat consumption with mortality risk, atherosclerosis, heart disease, and more. Paul takes the topic to task in The Carnivore Code, hopefully proving once and for all the true physiological cause of these conditions.

You can purchase a copy of The Carnivore Code here. From February 24, 2020 until February 26, 2020, you can enter for your chance to win a signed copy of The Carnivore Code. Simply follow @marksdailyapple and @carnivoremd on Instagram, tag some friends in the comments of the Instagram giveaway announcement, and you’ll be automatically entered to win a signed copy of the book plus a canister of Primal Kitchen Collagen Peptides. Five winners will be selected and notified via DM; U.S. entrants only. Good luck, and enjoy the excerpt.

Few things conjure more fear in the hearts and minds of the general population than the big, bad cholesterol monster and the associated trepidation that red meat will cause our arteries to become filled with plaque. After all, we’ve been told by cardiac surgeons that when they scoop plaque out of the arteries in our heart or neck, it looks just like animal fat, eggs, or butter.

In this excerpt, we’ll debunk the notion that eating animal meat, fat, or organs is bad for our heart and blood vessels and slay this final beast once and for all. We’ll see that these false notions have been based on more misleading epidemiological literature and how interventional and mechanistic studies tell a very different story. Come, brave adventurers, our destiny of discarding unfounded ideologies and reclaiming the vibrant health of our ancestors awaits!

The Basics of Lipoproteins and Cholesterol

The word “cholesterol” is often used colloquially to refer to all of the lipoproteins in our blood, but technically, cholesterol is a steroid backbone type of molecule that is used to make all sorts of vital compounds in human physiology. Our body makes around 1,200 milligrams of cholesterol every day for many important purposes, including the proper formation of all of our cell membranes.

The fat we eat is absorbed from our intestines and packaged as triglycerides with dietary cholesterol into a type of lipoprotein known as chylomicrons, marked with apolipoprotein B48. These particles circulate in the blood stream, dropping off their contents to cells of the body before becoming chylomicron remnants and being taken up by the liver.

In medicine, the term “total cholesterol” refers to the sum of all the cholesterol molecules in the blood and is usually measured directly in laboratory tests. In order to know how much of this cholesterol resides in the different lipoproteins, these must be measured individually. Most current lipid testing measures HDL, LDL, VLDL, and triglycerides directly, but older assays measure only some of these and must calculate LDL, which you may see written as LDL-C. For this reason, many previous research studies have looked at total cholesterol levels rather than LDL. Historically, elevated levels of total cholesterol have been assumed to correlate with elevated levels of LDL, and unless triglycerides are extremely elevated, this is generally a reasonable assumption.

The Vital Role of LDL in Our Body

Most of the cells of our body can make a bit of cholesterol from scratch, but they also rely heavily on the delivered supply of this molecule to build membranes and hormones. In addition to its vital role transporting building blocks and nutrients, LDL also serves important roles within the immune system. Yes, you read that correctly, LDL plays a valuable part in our response to assault by infectious invaders, as do many of the lipoproteins, including HDL. When gram-negative bacteria seek to invade our body, they release a cell wall component known as endotoxin, which is quite inflammatory and can strongly trigger the immune system. But don’t worry, friendly neighborhood LDL is around to bind-up this toxin and prevent things from getting out of hand.

Is there evidence that higher levels of LDL could be protective against infection in us? You bet there is! There are many studies that show elevated levels of LDL are not a risk factor for increased all-cause mortality or cardiovascular mortality in the elderly.9 Furthermore, there are many studies suggesting that higher levels of LDL are protective as we age, which is most likely connected with its role in immune function.1,2,3-11

In a sample of 347 individuals over the age of sixty-five, those with low total cholesterol had a significantly higher risk of dying by non-vascular causes, while those with elevated total cholesterol had half the risk of the reference population.1 Another study of 105 individuals over the age of eighty living in Iceland found that those with the highest total cholesterol level had less than half the all-cause mortality of those with lower levels.12 An even larger investigation called the Leiden 85-plus study had even more striking results. This study included 724 elderly individuals living in the Netherlands in whom the correlation between total cholesterol and all-cause mortality was measured for ten years. The authors found that for every 38 milligrams per deciliter increase in the total cholesterol, there was a corresponding 15 percent decrease in the risk of dying over this time period.

Clearly, LDL is a valuable particle in our blood and serves many indispensable roles. How can LDL be both protective and harmful? This doesn’t seem to make any sense! The answer is that LDL itself is not harmful, but in certain situations, it can be involved in the process of responding to injury and inflammation—making it look like it’s a bad actor when it’s merely present at the scene of the crime.

So… What Causes Atherosclerosis?

There are more than a quintillion particles of LDL floating around in our bloodstream. If every LDL particle that entered the subendothelial space in our arteries led to the formation of a plaque, we’d be deader than a doornail long before our first birthday. Every second of every day, lipoproteins like LDL are moving in and out of the walls of both veins and arteries, delivering nutrients to the cells there for energy and the construction of membranes. Clearly, there must be another part of this equation that leads to retention of some of these LDL particles within the arterial wall.

Interestingly, HDL particles are smaller and ten times more numerous than LDL. They carry more cholesterol in our blood stream, but these particles do not participate in the formation of atherosclerotic lesions. Why not? Because they do not get stuck in the subendothelial space.

Within the arterial wall, it appears that only particles containing the APOB molecule are able to bind to the proteoglycans within the intima and be retained.13 It’s not the size of the particle, or the number of particles moving into the vessel wall that’s important, it’s how likely a lipoprotein is to be retained that determines whether or not it contributes to the process of plaque formation.

What determines how sticky the LDL particle and the intimal space are? Ah, my friends, this is truly the million-dollar question! There’s very good evidence that during the states of insulin resistance and inflammation, both the LDL particle and the intimal space get coated in “molecular velcro” and become more sticky.14,15,16-18

Specifically, studies looking at the arteries of diabetics and arterial wall injury have shown changes in the proteoglycan matrix that increase its affinity for LDL.19 Additional research reveals that the LDL particle becomes more likely to be bound to proteoglycans in the intimal space when it is enriched with apolipoprotein ApoC III—a process that occurs during states of insulin resistance—making for a dangerous combination that strongly predisposes to plaque formation. The risk of atherosclerosis is so high in diabetics that rates of heart attack are elevated in this population even with low levels of LDL.20

At this point, you may be saying, “Sure, I believe you on this, but doesn’t atherosclerosis occur in people without diabetes or pre-diabetes? How common is this scenario of insulin resistance?” Though diabetes and pre-diabetes are diagnosed in 35 percent of the American population, there’s strong evidence that insulin resistance is much more common than this! There is evidence that a whopping 88 percent of the American population has some degree of metabolic dysfunction.21 If the vast majority of people around us have insulin resistance, is it any wonder that some studies have shown a correlation between LDL levels and cardiovascular disease? Almost the entire population of the U.S. has velcro on their lipoproteins and within their arteries, and the tennis balls are getting stuck to the wall!

So to answer the previous question, there’s good evidence that when atherosclerosis does occur, it is almost always in the setting of insulin resistance and metabolic dysfunction.

One of the biggest mistakes Western medicine makes is to extrapolate these pathologies to the 12 percent of us who are not insulin resistant and not inflamed, warning us that certain cardiovascular disease will swiftly follow with an elevated LDL.

Those of us with good insulin sensitivity are essentially a different breed, and there are many striking stories of plaque regression among insulin-sensitive individuals with “elevated LDL” eating carnivore or ketogenic diets. In the absence of insulin resistance and inflammation, higher levels of LDL are probably protective because of their roles with the immune response. Want to live a long time? Eat in a manner that allows for insulin sensitivity, decreases inflammation, and leads to a robust amount of valuable LDL particles. Carnivore diet, anyone?

Excerpted (in a summarized format) from The Carnivore Code by Paul Saladino, MD. 

References

1. Raiha, I., Marniemi, J., Puukka, P., Toikka, T., Ehnholm, C., & Sourander, L. (1997). Effect of serum lipids, lipoproteins, and apolipoproteins on vascular and nonvascular mortality in the elderly. Arteriosclerosis, Thrombosis, and Vascular Biology, 17(7), 1224-1232. doi:10.1161/01.atv.17.7.1224

2. Forette, F., De la Fuente, X., Golmard, J., Henry, J., & Hervy, M. (1982). The prognostic significance of isolated systolic hypertension in the elderly. Results of a ten year longitudinal survey. Clinical and Experimental Hypertension. Part A: Theory and Practice, 4(7), 1177-1191. doi:10.3109/10641968209060782

3. Forette, B., Tortrat, D., & Wolmark, Y. (1989). Cholesterol as risk factor for mortality in elderly women. The Lancet, 333(8643), 868-870. doi:10.1016/s0140-6736(89)92865-1

4. Risk of fatal coronary heart disease in familial hypercholesterolaemia. Scientific Steering Committee on behalf of the Simon Broome Register Group. (1991). BMJ, 303(6807), 893-896. doi:10.1136/ bmj.303.6807.893

5. Weijenberg, M. P., Feskens, E. J., & Kromhout, D. (1996). Total and high density lipoprotein cholesterol as risk factors for coronary heart disease in elderly men during 5 years of follow-up: The Zutphen elderly study. American Journal of Epidemiology, 143(2), 151-158. doi:10.1093/oxfordjournals.aje.a008724

6. Weuenberg, M. P., Feskens, E. J., Bowles, C. H., & Kromhout, D. (1994). Serum total cholesterol and systolic blood pressure as risk factors for mortality from ischemic heart disease among elderly men and women. Journal of Clinical Epidemiology, 47(2), 197-205. doi:10.1016/0895-4356(94)90025-6

7. Zimetbaum, P., Frishman, W. H., Ooi, W. L., Derman, M. P., Aronson, M., Gidez, L. I., & Eder, H. A. (1992). Plasma lipids and lipoproteins and the incidence of cardiovascular disease in the very elderly. The Bronx Aging Study. Arteriosclerosis and Thrombosis: A Journal of Vascular Biology, 12(4), 416-423. doi:10.1161/01.atv.12.4.416

8. Abbott, R. D., Curb, J., Rodriguez, B. L., Masaki, K. H., Yano, K., Schatz, I. J., … Petrovitch, H. (2002). Age-related changes in risk factor effects on the incidence of coronary heart disease. Annals of Epidemiology, 12(3), 173-181. doi:10.1016/s1047-2797(01)00309-x

9. Chyou, P., & Eaker, E. D. (2000). Serum cholesterol concentrations and all-cause mortality in older people. Age and Ageing, 29(1), 69-74. doi:10.1093/ageing/29.1.69

10. Menotti, A., Mulder, I., Nissinen, A., Feskens, E., Giampaoli, S., Tervahauta, M., & Kromhaut, D. (2001). Cardiovascular risk factors and 10-year all-cause mortality in elderly European male populations. The FINE study. European Heart Journal, 22(7), 573-579. doi:10.1053/euhj.2000.2402

11. Krumholz, H. M. (1994). Lack of association between cholesterol and coronary heart disease mortality and morbidity and all-cause mortality in persons older than 70 years. JAMA: The Journal of the American Medical Association, 272(17), 1335-1340. doi:10.1001/jama.272.17.1335

12. Jónsson, Á., Sigvaldason, H., & Sigfússon, N. (1997). Total cholesterol and mortality after age 80 years. The Lancet, 350(9093), 1778-1779. doi:10.1016/s0140-6736(05)63609-4

13. Hurt-Camejo, E., & Camejo, G. (2018). ApoB-100 lipoprotein complex formation with intima proteoglycans as a cause of atherosclerosis and Its possible ex vivo evaluation as a disease biomarker. Journal of Cardiovascular Development and Disease, 5(3), 36. doi:10.3390/jcdd5030036

14. Hiukka, A., Stahlman, M., Pettersson, C., Levin, M., Adiels, M., Teneberg, S., … Boren, J. (2009). ApoCIII-enriched LDL in type 2 diabetes displays altered lipid composition, increased susceptibility for sphingomyelinase, and increased binding to biglycan. Diabetes, 58(9), 2018-2026. doi:10.2337/db09-0206

15. Olsson, U., Egnell, A., Lee, M. R., Lunden, G. O., Lorentzon, M., Salmivirta, M., … Camejo, G. (2001). Changes in matrix proteoglycans induced by insulin and fatty acids in hepatic cells may contribute to dyslipidemia of insulin resistance. Diabetes, 50(9), 2126-2132. doi:10.2337/diabetes.50.9.2126

16. Hulthe, J., Bokemark, L., Wikstrand, J., & Fagerberg, B. (2000). The metabolic syndrome, LDL particle size, and atherosclerosis. Arteriosclerosis, Thrombosis, and Vascular Biology, 20(9), 2140-2147. doi:10.1161/01. atv.20.9.2140

17. Wasty, F., Alavi, M. Z., & Moore, S. (1993). Distribution of glycosaminoglycans in the intima of human aortas: Changes in atherosclerosis and diabetes mellitus. Diabetologia, 36(4), 316-322. doi:10.1007/ bf00400234

18. Rodriguéz-Lee, M., Bondjers, G., & Camejo, G. (2007). Fatty acid-induced atherogenic changes in extracellular matrix proteoglycans. Current Opinion in Lipidology, 18(5), 546-553. doi:10.1097/ mol.0b013e3282ef534f

19. Srinivasan, S. R., Xu, J., Vijayagopal, P., Radhakrishnamurthy, B., & Berenson, G. S. (1993). Injury to the arterial wall of rabbits produces proteoglycan variants with enhanced low-density lipoprotein-binding property. Biochimica et Biophysica Acta (BBA) – Lipids and Lipid Metabolism, 1168(2), 158-166. doi:10.1016/0005-2760(93)90120-x

20. Howard, B. V., Robbins, D. C., Sievers, M. L., Lee, E. T., Rhoades, D., Devereux, R. B., … Howard, W. J. (2000). LDL cholesterol as a strong predictor of coronary heart disease in diabetic individuals with insulin resistance and low LDL. Arteriosclerosis, Thrombosis, and Vascular Biology, 20(3), 830-835. doi:10.1161/01. atv.20.3.830

21. Araújo, J., Cai, J., & Stevens, J. (2019). Prevalence of optimal metabolic health in american adults: National health and nutrition examination survey 2009–2016. Metabolic Syndrome and Related Disorders, 17(1), 46-52. doi:10.1089/met.2018.0105

The post Will Red Meat Cause Your Heart to Explode? appeared first on Mark's Daily Apple.

WEIRD SCIENCE:

● Microdosed LSD: Finally A Breakthrough For Alzheimer’s Disease?

—Forbes, yesterday.

● This Is What Happens When You Take 550 Doses of LSD At Once. Accidental LSD overdoses are not fun. But for some, they can have a bizarrely beneficial effect.*

—Vice.com (appropriately enough), yesterday.

* Or it could get you sacked from Pink Floyd. Don’t try this at home, kids.

ORAL TRADITION: This Legend of a Volcano Erupting 37,000 Years Ago May Be The Oldest Story on Earth.

INTENSIVE TESTING to develop better jackets and outdoor clothing. “The chamber needs just two hours to go between its maximum temperature (122°F) and its minimum (–58°F, wind chill –85°F, in full blizzard conditions), although it uses about two thirds of the entire building’s power capacity to make this drastic temperature change.”

OUT: FAKE NEWS. IN: FAKE SCIENCE. A Major Study That Fueled National Vape Panic Has Been Retracted.

CORONAVIRUS: China deploys 40 incinerators to Wuhan amid fears of coronavirus death toll ‘cover up.’