The Pandemic of Politics

Kenn Brody, Broken Symmetry Publishing

April, 2023

 

The business of changing our government leadership happened on a schedule, like football playoffs or tax filings, take your pick.  Outside of that time frame our attentions and donations were applied to other things, such as family life, work and life goals.  This is what we are used to.  This is the regular change of guard in a democratic republic.

 

Not anymore.

 

The virus of politics has invaded every aspect of our lives from what we eat to what kind of car we drive to what words we use.  Do you understand how absurd, how invasive, how unhealthy this is?  Politicians are media gods (small g).  Singers, actors and others are subordinate, angels or demons as they may be inscribed in the political pantheon.  Sex is now a political act between an oppressor and an oppressed, unless you are LGBTQ+, then it’s a furtive act among the oppressed.

 

The political season has grown to include each and every day of the week, all 24 hours, and all 12 months.  You can tell if there is an election is coming by a slight increase in the number and desperation of the calls.  Email, flyers, ads to hurry and contribute your wages to some person’s election.  You know, that person probably makes 5 times your salary and needs your vote, not your money.  What do you think he/she/ze does with your money?  Why, he/she/ze uses it to harass you for more, with more emails, more ads, more ghost-written self-serving memoirs.  It’s a hyperbolic assault on your mental immune system.

 

Do you really welcome this bizarre infection, or do you think, like a bad cold, it will go away?

 

It persists, tainting the world and the words around us, like the faint smell of mold and piss in the subway.

 

Please consider that this is a disease caused by an environmental hazard.  You don’t lick lead paint.  You use repellant to keep mosquito bites down.  You wash you dishes and pots.  Why not sanitize your home and your life against the pandemic of politics?

 

I will not excoriate the media here, even though they are the prime carriers of this infection, like rats in the Plague.  They are also infected.  

 

There is an organism, Toxoplasma gondii, that infects rats.  A healthy rat avoids cats in order to, um, stay healthy.  Once infected with Toxoplasma gondii the rat finds cats attractive, sniffs their urine to find a hungry cat, which, of course, leads to the terminal effect of the virus: munched rat.  The virus now has a cat host that roams around leaving things that can infect more rats.

 

That, in a nutshell, is how the media works.  They are cats.  Hello, Rats!

 

Infected with story line, true or false, the media excretes it en masse..  Their readers absorb it, spread it and come back for more.  A good story has emotional impact.  It is dramatic, triggering.  It gets legs.   There are reactions of the people in the streets, celebrities,  commentators who sprout like weeds from sidewalk cracks.  Maybe there is a reference, a fact that disproves the initial story, but it happens so long after the initial meme-virus that it is hardly noticed at all.

 

One of the effects of this infection is to cripple the brain.  Certain words cannot be uttered.  Some feelings must be swallowed without expression.  The uninfected cannot mingle with the infected for fear of rejection.  This goes so far as to label whole groups of people, states for example, with racial colors, red and blue.  Blue people consider reds as violent tribal subhumans.  Reds consider blues to be stupid lemmings.  No healthy person can see these racial colors at all.

 

Basic sanitation is the best cure for pandemic politics.  Get rid of your TV.  It is the open funnel right into your brain.  Read books, you can put them down when you feel like it and they do not, usually, have commercials.  Rent videos and good movies, not what the TV has on that night.  With the money you save buy a bicycle or invite your real friends over for supper on Friday nights. 

 

If the discussion turns to the latest viral meme, stuff airpods in your ears and listen to music. 

 

A funny thing will happen.  When you get your head out of the TV and political email and get a real life, you will be more interested in real issues instead of personalities.  You will develop a tolerance for ideas that may not be the same as yours.  You will recognize the infected and develop a thick skin against their jibes.

 

Cover your mouth, bite your tongue and stay 6 feet away.

 

 

 

A Basic Guide to Drug Studies

Kenn Brody August 14, 2021

In this pandemic age, every pundit and panic-monger has an opinion. Masks or no masks for kids? Vaccine or not for COVID survivors? Lockdowns or no lockdowns? Who is right? What is the best thing to do?

There is rarely any evidence presented. It all comes down to which authority we trust, as if authorities had no political biases. But they do. They all claim “science” as if it was a religion. Science is not an article of faith.

 

Science is based on evidence, not opinions and not on authorities. Evidence in COVID research is presented in published papers generally reviewed by panels of experts prior to publishing. Not everyone is going to be able to read these papers. But it is now necessary for at least SOME of us to be able to read and understand what a scientific study is, and whether it is good evidence that supports some policy. At least a few people in every community should have this level of understanding and then interpret it for the rest of us. That is the only way we are going to overcome the mainstream narrative.

The goal of this article is to give you a start on this understanding, some of the methods, some of the terminology and some of the sources of data. You, the reader, will form your own opinions about the issues after you read a few scientific papers.

Unlike physics or mathematics, medicine relies less on fundamental theory and more on comparisons. What works versus what does not work seems like a simple concept, but untangling the threads of causes and effects takes a bit of cleverness.

Charlatans all know that giving you a sugar pill with a fancy name and a rigmarole will cure aches and pains, at least for a short time. This is the placebo effect. In order to be an effective drug, it has to be better than a placebo. So we have two- branched, double blind, placebo controlled studies. What this means is that a study population is divided roughly in half. One half gets the drug, the other gets the placebo. Now imagine running such a study with thousands of subjects,

dozens of nurses and data collectors, over months of time, under the supervision of doctors and academic specialists approved by a institutional study committee. It is a significant task, not something done on a whim.

There are two branches. In one branch subjects get the drug, in the other branch subjects gets the placebo. Neither the subjects nor the administrators know which person is getting the drug or the placebo. It is blind to the subjects and blind to the administrators. It is double blind. Each subject is assigned a random number. Half the numbers selected at random get the drug, the rest get the placebo, or some equivalent arrangement.

The administrators follow the subjects until some pre-selected effect is observed, or some time limit is reached. That pre-selected effect is called the endpoint. It may be the onset of a measurable response such as a negative blood test for COVID. Or a release from an ICU. The design of the study and the endpoint is critical. It isn’t always possible to find a perfect endpoint. For example, we cannot always determine which variant of the virus was involved in particular subject, so we may use a proxy endpoint. In the U.K. they used a general test for COVID, the paqPCR,to distinguish between the original alpha variant and the delta variant. The paqPCR detected a spike protein for the alpha and no spike protein but other virus parts for the delta variant. Was this appropriate to the purpose of the study? Did the paper clearly explain why they used a proxy endpoint? You read and decide.

Sometimes you will find that the endpoint has little or no relation to the purpose of the study. This is a big red flag.

The number of subjects is referred to as n. A study with a small n is going to yield a less reliable result. Larger studies are not always better, though. Results can get messy. What you’re looking for is n in the range of thousands of subjects, not tens or even hundreds in most cases. The reliability of a study, the length of the error bars, is proportional to the square root of n. Larger studies have smaller error bars.

Some math is unavoidable here.

Suppose you take a list of all the subjects of some study with their endpoint virus clearance results. This might be the number of virus particles detected per nanoliter of saliva sampled. It might range from 0 to 1000. You add them all up and divide by n. This gives you an average. But how good is that average? It might be all 0 and 1000s and nothing in between, or it might be a good distribution of numbers. So you do another calculation, the standard deviation. The raw numbers, if you plot then on a graph, will give you a curve. You are hoping for a normal distribution curve with a single hump in the middle pretty close to the average. The standard deviation then gives you the slope of the skirts of this curve. The result of the measurement is properly represented as the average plus or minus three standard deviations. Another way of saying this is that the average, say 55, is likely to be accurate to within plus or minus (=/-) 1.2 for 3 sigma. Sigma is one standard deviation. The higher n, the small sigma will be.

Remember we have TWO branches. We have to reduce each branch to a separate standard deviation and sigma, and compare the two results. Suppose we find that the drug branch has an average of 22 with a sigma of 2 and the placebo has an average of 43 with a sigma of 3. These ranges do not overlap. We can say that the drug, whatever that is, is effective with a ratio of 43/22 or 1.95. This is the OR the odds ratio.

There is one other test that is common in medicine. It is possible that the result we got, 1.9 OR, is just an accident. Maybe some other effect is hidden here. So, we ask, what is the possibility that the same lists of numbers could yield this result? So we mix up the results in the two branches, randomly, do the averages and sigmas again and compare this mixed, random result with the result we got before. Do the error bars overlap? We want them to be separated by more than two sigma. In ordinary medical parlance, this gives us an acceptable p-value l of .02. In plain language, the chance that some weird random data error caused our OR is less than 1 chance in a fifty.

Beware of sources that quote something like, “Your chances are 26% better with our product.” Better than what? Suppose your chances of getting across a highway without being hit is 26% greater if you wear a red shirt than a blue shirt. OK, I’d better wear a red shirt all the time, you say. But they never gave you the incidence of people with blue shirts getting hit on that highway. It turns out to be

12 in 100,000 crossings. Hardly anything to be concerned about no matter what color shirt you wear.

Anytime you are given a percent improvement without both a comparison and an incidence you are getting propaganda, not data.

Let’s do a quick review here:

• -  Is the study from a peer reviewed journal

• -  Is it double-blind placebo controlled?

• -  Is the endpoint or the proxy endpoint reasonable for the purpose?

• -  Is n a reasonably high number?

• -  Is the OR significant?

• -  Is the p-value good enough?

  It is customary for the researchers to make their raw data available for further analysis by other researchers. I would be somewhat concerned if this data was being withheld. In for-profit Big Pharma, this is not uncommon. However, since we are talking among us amateurs, this is a nit.

  Let’s take a look at some of the complications of studies and how they can be designed to correct for other factors.

  Usually, a well-designed study looks for one effect as determined by a single endpoint. There are such things as trial and error studies, but the expense and difficulty of doing a large enough study with a significant n makes such trials uncommon. We won’t consider them here.

  How much drug do we give? How much is needed to work? What are the safe limits and side effects? FDA requirements separate new drug studies into three phases: Phase 1 is for the safety of the drug. Phase 2 is for the effectiveness of the drug. Phase 3 is a mass study for dosage, tolerance and side effects. You can get more details here:

https://www.fda.gov/drugs/information-consumers-and-patients-drugs/fdas- drug-review-process-continued

Each phase has a separate set of statistics, endpoints and results. You should get the Phase 3 study if you want the best picture. The earlier phases are usually too small to be of benefit to a casual reader.

What about confounding factors? Suppose we look at studies to determine whether masks work for COVID. How would you design such a study? Not all masks are equal. An N95 mask filters out particles down to 300 nanometers in diameter. Who knows what your hankie-gater filters? How often do you wash that mask in your pocket? How susceptible are you to COVID? Do you have natural immunity? Did you take the shots? Are you outside in sunlight or trapped in an elevator? Age and access to health care are significant in COVID infections. How do you sperate out those factors?

What would you choose for an endpoint? Whether you get sick, go to the hospital, get put in an ICU or die?

It’s a mess. Here’s how you begin to separate this out. It’s called a cohort- matched multi-phasic study.

Get a lot of subjects together. Thousands. You’ll need a lot. For each subject gather the following data: mask vs no mask; age; co-morbidities like cancer or heart disease that may make them ineligible; economic sector; sex; ethnicity, geographic location.

You take all this data and separate the subjects into the usual two branches, call them A and B. What are you looking for? Mask efficacy. So you start with masks users vs no maskers. Then, within each branch you try to match subjects in A with subjects in B that have the same data: the same geographic location, age, etc. You need a significant number of subjects in each data classification. These are your matched cohorts.

The simple idea is that if two people with the same age, location, etc. differ only in mask usage, than looking at how many in each branch get COVID will tell you something about how well masks work. You cannot just see how many people in Florida get sick vs how many people in New Jersey get sick. There are too many confounding factors, such as weather, population age, economic sector, etc.

At this writing, there is no such cohort-matched study on masking. Finally, let’s mention other types of studies.

A retrospective study is done on other studies that are all relevant to a single determination. Instead of a new study, the researchers are effectively mining previous studies for new insights. This can be done by looking at older studies and reviewing newer results, a retrogressive study. Or it can combine the data of several studies and attempt to winnow out confounding factors using a linear analysis.

The kinds of ways studies can be designed varies with the science. Physics is different from medicine. Medicine is different from biology. In each science a researcher must apply cleverness to yield insight to some natural phenomenon, and that is a creative thing.

I hope you have found this guide useful. I welcome your feedback.

Where to find COVID data:
World-wide COVID data on WorldOmeter:

https://www.worldometers.info/coronavirus/

COVID deaths by age in US:

https://www.statista.com/statistics/1191568/reported-deaths-from-covid-by- age-us/

Children state by state COVID report:

https://www.aap.org/en/pages/2019-novel-coronavirus-covid-19- infections/children-and-covid-19-state-level-data-report/

Deaths per Million Population by Country:

https://www.worldometers.info/coronavirus/

scroll down on this page
New York City COVID statistics by age, sex, morbidity:

https://www.worldometers.info/coronavirus/coronavirus-age-sex-demographics/

P-values, confidence intervals and odds ratios:

http://www.bandolier.org.uk/painres/download/whatis/What_are_Conf_Inter.pd f

Standard deviation calculator:

https://www.calculator.net/standard-deviation-calculator.html

 Herd Immunity is Important

level 1

kenlbear

· 15m

From Reddit:

Herd immunity has to work if the vaccine works due to the simple mechanism that the number of susceptible individuals goes down.

Michelle, a friend, had a genetic deficiency. Her doctor says she should not risk the vaccine. She is a certified nurse, and her hospital fired her for refusing. This is not that uncommon. There are some people with good and valid reasons not to be vaccinated. That's why herd immunity is important. You can never vaccinate everyone, and SARS-COVID-2 has a reservoir of infection in animals that never get vaccinated.

The formula for herd immunity is V = 1-1/(R0), where V is the required level of herd immunity given R0, the spread rate. According to most sources, R0 for the Delta variant is 5, twice as high as for the Alpha variant. So V is .8 or 80%. That is pretty high, but not a high as mumps, with an R0 of 10.

Also, people who have recovered fro COVID have lasting immunity, including from delta. There are perhaps 100 million in the US with natural immunity. Add this to the 150 million who have had the vaccines.

The unvaccinated are at risk, but COVID is treatable. It should rarely require hospitalization. Johns Hopkins and University of Texas are publishing lists of treatments that work. This is a void in the system right now.

Caution is useful. Panic is irresponsible. I got my shots. Talk to your doctor.

https://covid.cdc.gov/covid-data-tracker/#datatracker-home

https://covid.cdc.gov/covid-data-tracker/#trends_da

 

Virus Evolution and Delta Variant

Kenn Brody

August 3, 2021

 

 

Evolution is an inexorable process that changes everything that can reproduce and exists in a competitive environment.  I’m using this definition to avoid the question of whether a virus is a living thing or just a self-serving collection of organic material.  Evolution doesn’t care either way.  A virus evolves whether you call it alive or not.

 

How and why does a virus evolve? 

 

Corona virus is an old species with hundreds, perhaps thousands, of members, many of which infect the cells of mammals.  It is an obligate parasite.  Without infection, without getting inside host cells, a virus does not have any activity.  You can think of it as a seed in a suspended state.  When it meets a nice, juicy mammal, however, it attaches itself to a cell though a spike mechanism.  SARS-COVID-2 attaches to ACE2 receptors in human lungs and elsewhere.  That attachment is like a key-and-lock mechanism, where a part of the virus actually locks onto a part of the ACE2 protein. 

 

Once the attachment is made, the virus inserts its DNA into the cell.  It looks like a molecular mosquito, injecting its replicating code into the host cell.  That code takes over the machinery of the host cell to make more virus proteins, which assemble themselves into virions (virus particles).  The cell soon explodes, releasing the new virions to infect other cells and repeat the process.  The virus explodes so quickly in the host that the immune system cannot keep up.  In a few hours there will be as many as 100 billion virions produced from just a few hundred invaders.  Each virion is a somewhere between 50 and 100 nanometers in size, much smaller than the pores on a cloth mask. 

 

In time, the immune system will search out and destroy infected cells.  Lymphocytes will remember parts of the invading virus for a faster defense in the future.  This is called “natural immunity”.

 

In order to eliminate infected cells the immune system triggers cytokines in the cells.  Cytokines trigger cell dissolution.  Cytokines order the cell to commit suicide, or apoptosis.  However, with COVID, the cytokines destroy much tissue and do not always stop with infected cells.  A cytokine storm is the hyperactive immune system damaging tissue after the virus has been cleared.  It’s the cytokine storm that kills lung tissue, heart linings and other organs.  It’s the cytokine storm that kills patients in the IC wards.

 

This life cycle and the conditions inside a host are the things that define whether a virus is successful at reproducing itself or whether it fizzles out as isolated infections.  A map of the world a virus competes in is called a fitness map.  The fitness map has peaks and valleys.  Fitness includes characteristics like how contagious it is (R0), how resistant it is to antibiotics, antiviral agents and vaccines, and how fast it is at creating new virions.  Obviously, any successful virus needs a lot of hosts.  Therefore, killing a host is not a benefit to a virus, like COVID, that needs a living host to reproduce.  A virus evolves to reach the highest peak in that fitness map.

 

Every virus is competing on that fitness landscape to reach the peaks, where it will have the most offspring, not the most host deaths, not the worst host symptoms. 

 

The entire genome is about 30,000 base pairs, tiny compared to mammalian cells.  Virions outside the host are very fragile.  COVID survives perhaps an hour in air, less in sunlight.  Virions are also subject to bombardment by radiation, ultraviolet, and chemical agents.  These cause random changes in the viral DNA.    Most of these mutations are neutral or fatal for the individual virion, but there are so many virions that by the odds some mutations are beneficial to the virus.  So we get lots of variants.  WHO and CDC classify variants of note, listing about 20 of them in categories according to levels of concern.  They are now labelled with Greek letters: alpha, delta, lambda, etc.  Alpha is the initial variant.  Delta evolved from Alpha.  The difference between apha and delta is only a handful of mutations, or SNPs.

 

Now alpha and delta are competing variants in the same fitness landscape.  But that landscape has changed.  Most human hosts are now immune to apha, either due to vaccines or natural immunity.  We are slightly less immune to delta, so delta has the advantage in available hosts and rapidly overtakes alpha as the predominant variant.   Delta is also more contagious and much less likely to kill its hosts, both significant advantages if you are a virus.  This is the usual way a virus evolves – more contagious, less lethal.

 

The current high level of vaccinations and the huge population of humans creates an ideal situation for COVID mutations.  The older variants die out for lack of easily infectable hosts, but there are so many quintillions of particles out there the possible mutations are high and each gets a chance at finding a peak in the fitness landscape.  So the number of variants will continue to increase.

 

The usual rtPCR test that is currently the gold standard for COVID testing cannot distinguish among these variants.  Neither can the rapid tests.  A small sampling of tests is sent to specialized labs for sequencing, a two-week process.  Only sequencing can determine which variant is most common in a region.  Th United States has sequenced only 51,000 out of about 400 million COVID tests.  It does not yield a very detailed picture of variant spread.  This is the entire basis for making decisions about masking, vaccination mandates and lockdowns. 

 

Will COVID mutations stop?  Not as long as the virus persists in the population.  Not as long as evolution of the fitness landscape closes old niches and opens new ones.  There will be ever newer variants and possibly new vaccines to answer them until the virus simply becomes one more flu-like nuisance. 

 

References:

 

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7224694/

 

https://www.cdc.gov/coronavirus/2019-ncov/variants/variant-info.html

 

https://www.nature.com/articles/s42003-021-01754-6

 

https://www.washingtonpost.com/world/2020/12/23/us-leads-world-coronavirus-cases-ranks-43rd-sequencing-check-variants/

 

 

 

Are Humans So Special? Guest blog

Guest Blog by Noted SF Author Steve McEllistrem

What does it mean to be human?

We like to think we’re special, we’re different than the rest of the animal kingdom. We can reason and communicate and imagine and empathize and manipulate our world in a way no other creatures can. We have consciousness, self-awareness. All these attributes allegedly make us human.

But what does that mean?

Other animals, like dolphins and elephants, are self-aware. They communicate and reason and empathize and even occasionally manipulate their habitat. Do they imagine? Probably. So what makes us special?

The truth is: We make us special. We’re special because we say we’re special, not because of any inherent quality or virtue we possess. We observe the world around us and note that no other species does quite what we do, even though many species do similar things.

And up until relatively recently, we didn’t even appreciate the similarities that other creatures have to us. We thought: Isn’t it cute that the crow over there is playing with a coin? or Look at my cat toying with that mouse.

But the more we’ve studied the animal kingdom, the more we’ve come to appreciate how little difference there is between humans and many animals. We have an evolutionary advantage in that we developed all these wonderful abilities at a high level whereas most animals can claim only one or two of these attributes.

Dogs, for example, can communicate, empathize and reason, but not to the same level and not in the same way we do. At least, that’s what we think. But we might be wrong. 

Dogs can communicate by sense of smell in addition to vocally but we didn’t understand that until recently. For instance, dogs can tell time by using their noses. They know that when the number of “owner” molecules in the air decrease to a certain level, their owner is going to return. That’s why they’re often waiting by the door when we come home from work.

Monkeys have a sense of justice and will scream in outrage if they’re treated unfairly. No different than us. Deer and cows can sense magnetic north; dolphins and bats use sonar; people can’t do either of those things. 

So why do we think we’re better than them? Mostly, because we have power over them. It’s not that different than white privilege or Nazi superiority. If you look at the historical record, you see that the people claiming whites were somehow better than blacks were white people. The blacks didn’t think of themselves as inferior. It was the people who had the power who made that determination.

The same thing is happening still, with the folks in power (humans) claiming that they’re superior to the folks not in power (animals). Yes, humans are different than zebras, but zebras are different than ostriches and ostriches are different than pumas. We all have our strengths and our weaknesses. It’s just that our strengths tend to be stronger than the rest of the world’s creatures and our weaknesses tend to be fewer.

So it’s okay to think of yourself as human. It’s okay to see yourself as a member of the dominant species on the planet. But I’m not certain it’s okay to think of ourselves as inherently superior to the creatures around us. We’re different, that’s all. 

_________________

Note from Kenn Brody:

Steve McEllistrem is a noted SF author whose “Devereaux” series covers themes of post human and trans human development, opposed by devastating forces that almost wipe us out.  He is also a futurist who writes on forthcoming trends and technologies. 

The opinions in this issue are entirely Steve’s.

We welcome feedback.  Email to Kenn@brokensymmetrypublishing.com.  The first hundred email responders will get a free copy of “The Sage of Sagittarius” in ebook form.  

You can look inside Steve's book here:  
http://smarturl.it/DECtg

Gravity Sucks

Gravity Sucks

Gravity always sucks, it has sucked since the Big Bang and it will suck until the whole shebang goes away.

This true statement has nothing to do with sex.  It simply means that the force of gravity is unipolar and cumulative.  There is no such thing a negative mass, and apparently no such thing as repulsive gravity.  Electrogravitics is probably not a gravity thing but an electromagnetic thing, if it exists.

Higgs Boson at CERN

Electrons and protons come in positive and negative, so, on the scale of the universe, the plusses cancel out the minuses.  This is a good thing, since the forces between them is much, much stronger than gravity.  

When enough mass gets together, their gravity gangs up on the stronger forces and overwhelms them.  Particles all have mass and therefore they have no choice but to clump up.  The other forces, electromagnetism, the weak and the strong nuclear forces, cancel each other out or cannot work at a distance.  They are handicapped when it comes to cooperation.  Not so with mass and gravity.  That’s how we get neutron stars and black holes.  Gravity wins the contest by sheer numbers.

But what about antimatter?  Exotic particles?  Could they have negative mass? 

There is a recent test, the Alpha Experiment, that has accumulated some antimatter in a “box” of laser beams.  The amount is tiny but enough to weigh.  Damn it, they weigh the same as their normal particles.  Science Fiction does’t get a break there, either.

Standard Model

What about other exotic matter?

We are just about out of exotic particles.  The Standard Model shows everything we should expect to find, even the Higgs boson that gives all the other particles their masses.  Nothing new there.  

What about SUSY, supersymmetric particles?  There’s a whole ‘nother set of particles with weird names like squark, photino, selectron.  Problem is we haven’t seen any of those yet.  We don’t think they will have negative mass either.  Why?  If there was such a thing as negative mass, a particle that loses energy would go faster and faster, until it reached the speed of light.  Everything with negative energy would escape to c, and that is both chaos and the speed of light.   The universe would be a dangerous place for humans and aliens alike.

Supersymmetry Model

With my license to create “science” as an SF writer, I did create exotic particles with a negative mass in my (incomplete) novel, “The Curtain of Heaven”.  An ancient and extremely advanced alien race broadcast a complete description of the physics of this universe.  It went out in all directions from an untraceable source.  In it was the secret of unlimited power from the vacuum.  I called it a “Burgess Generator”.  As it runs and puts out stupendous power it also cooks up a batch of exotic matter.  One of my characters, a thief, accidentally discovers that an old Burgess Generator has negative mass in it.

Never letting such an opportunity go to waste, another character uses this exotic matter in an Alcubierre-Wilson Warp Drive (see last blog) and mankind goes to the stars.  

Otherwise, gravity only sucks.

Faster Than Light?

Faster Than Light?

Zila's Space Yacht in "Sage of Sagittarius"?

 Ever consider how dull it would be to read about the thousand year passage for some hero to join the war against the alien princess?  Yeah, I’ve tried that in “Cosmic Rift”, but I only managed 100 years.  

Science fiction at the speed of light is confining.  Read my last blog on the size of the universe and see why.  We are like ants crossing the Pacific.  Precisely like ants who can’t swim.

In my novel, “Sage of Saggitarius,” I invented a new method, the Allurion Seed, a 6-dimensional object with peculiar attributes, that enabled those few FTL ships that could afford one.  They cost about the same as a small country, but Zila, the protagonist, gets an FTL yacht and a crew for her adventures.  It’s made-up physics, sure, but at least I tried and it is plausible physics.  Most writers just hand-wave at the problem:  the Captain announces “Warp Speed” and the ship disappears in a cone of horizon lines.  

That’s cheating.  Why not just invoke the power of the charcoal yellow gemstone and go “POOF”?

But there is hope, all you star-farers.  Spanish physicist Miguel Alcubierre worked Einstein’s field equations for General Relativity backward and found that there was a math solution to go faster than light.  His ideas have been expanded by NASA’s Dr. Sonny White in his paper, “Warp Drive 101”.  

While no information, object or energy can travel faster than c (the speed of light in a vacuum), space itself can expand at unlimited speeds.  In fact it's doing that right now, out beyond the parts we can see with the most powerful telescopes, still stretching out after the Big Bang.  Of course, while a myriad of galaxies are retreating from us faster than c, we can never see them or have any causal interaction with them.  

Alcubierre calculated that a vehicle could stretch space behind it and compress space in front of it in such a way that it rode a wave of shaped space.  In this warp bubble, passengers would feel no acceleration and their watches would keep Earth time while the bubble traveled at, maybe, 1000 times c.

Of course there is a hitch.  Actually, a lot of serious hitches.  

The warp bubble requires negative mass, which may not even exist.  It requires so much of it that we would have to convert a moon to negative mass.  As an SF writer, I’ll call this one and just claim my people have access to “exotic matter”.  There may be such a thing.

No one has a clue as how to start a warp bubble without already having a warp bubble.  

The transition from warp to inertial motion may create a kind of Bremstrahlung, high energy rays caused by your slowing down, that would destroy your destination just as you reached it.  Imagine coming home after your successful space battle to a cooked Earth, all your fault.  

Still in all, I’ve done the research and some calculations and I’m using the Acubierre-White Warp Drive  (AWW Drive) in my new novel, the Curtain of Heaven.  I’m using the 6-dimensional version of it.  

I hope you like it!