#it's a lot milder now but thats the problem

[bipolarmoss]

maybe i still do like my manic crush even though im now medicated. im doomed

[pixeljade]

Oh I definitely believe the metaphor is incredibly poorly-formed, but still stands in a lot of good ways. That's kinda the problem with metaphors, they cant ever be a 1-to-1 representation of the situation they represent, because if they were...they'd be that situation, not a metaphor.

But I digress, regarding the X-men, I think they are overall a really good metaphor, but the metaphor really REALLY falls apart when placed within the greater Marvel Universe. When theyre in their own universe, its easy to see them as outcasts, with a massive debate over whether or not they should be given rights. Little details about their powers really lend themselves to it, like, I'm sure we all know the post thats like, "Of course Storm thinks their powers are a gift, Rogue kills everyone she touches". That post can be used metaphorically as an example of how oppression and privilege affect people differently, it could be seen as a discussion between a trans person who fully passes and someone who doesnt, or it could be between someone with a debilitating disability versus a milder one, etc etc. And of course, these kinds of debates are useless when considering that we all face a common enemy, but the discussion eventually settles on that fact too. There's good parallels everywhere.

But like you say, there's nothing in real life that parallels PERFECTLY with superpowers! The supposed threat trans people pose to society is an existential one, but Rogue can *literally* kill people with a touch! But see, I think that serves perfectly into another form of parallel, which is exemplified in another comic series: Maus. In Metamaus, Art Spiegelman admits that he really played up his father's "Jewishness", turning him into almost a direct stereotype. The Vladek we meet in the comic speaks broken english, is miserly and penny-pinching, worries over everything, etc. The real Vladek spoke nearly perfect english and was much less concerned about money than we're shown. Art played up these stereotypes, though, to ask us a question: Even if he WAS a stereotype, does he deserve the hell that he suffered through?

Rogue serves a similar purpose, she parallels fears about the AIDS crisis. Back then, many ignorant people believed they could catch AIDS by being around them, and the AIDS wards were largely abandoned by folks, including the very nurses who were supposed to be caring for them. Some even feared a touch could kill them. Rogue, though, is that fear realized, and begs us the question: Does she not deserve care? Does she not deserve a place of love? And as such, does it even matter if queer folks DO represent a threat? Do they not deserve our love as well?

And ultimately, the X-Men is all about presenting those extreme examples, and asking us if they deserve our love. Magneto wants to rule over humanity for much of his early story, and has the capability to do so. Magneto is basically a worst-case representation for an oppressed person! But the stories make it clear that he only has the desire to take over because the world has been so utterly cruel to him and those around him. And even if he has this darkness to him now, Xavier wants to bring him back from his supremacist ways, show him that he's become what he hated. And eventually, he does, and Magneto leads the X-Men. And so, while the metaphor is hardly 1-to-1, it presents enough of a metaphor to set up that sort of thought experiment, and so, I think the metaphor doesnt need to be 1-to-1.

our modern society really needs to start understanding that a solid chunk of superhero media is straight up right wing propaganda. and no i dont just mean in the "MCU has a partnership with the military" way, I mean in the hyper-individualist "Some People Are Just Born Better" way.

[anaxgardner]

Couple #1: Ian and Jamie

Jamie Wilkinson

James- who goes by Jamie(and gets flustered and irritated when called his full name especially by Ian)  is a shy, introverted character who tends to over analyse things and aire on the side of caution; his personality parallels his boyfriend Ian, who is much more spontaneous and outgoing, Jamie prefers to meticulously plan out things to avoid mishaps. This is not to say that he doesn’t get caught short (as you’ll see he often does) but he tries his best due to his anxious nature to be prepared in any given situation.

He loves everything and anything creative from art and music, to books and film, not least of all video games. He was raised by a loving (if not somewhat over bearing) single mother and is the youngest of three,  having two older sisters. He’s also obsessed with his dog, Cookie, a three year old golden lab.

Age: 19

Ethnicity: Caucasian.

Nationality: Third generation Irish-American.

Eye color: Light Blue.

Hair Colour and Style: Light blond and shaggy.

Height: 5ft 4in.

Tattoos/Piercings: None. (His mother would kill him, though secretly he wants a tattoo for Cookie.)

Kinks/Fetishes: He’s very private about his desires, especially when it comes to the bedroom, but secretly he wants to be tied up and forced to wet himself by his significant other...

Bladder stuff: Jamie has a rather...unimpressive bladder size and capacity. Due to his nervous nature and love for caffeine he needs to visit the restroom frequently. Growing up he had accidents often because he was too shy to admit his needs, now his older he’s equally as shy but manages to avoid a lot of scenarios by taking frequent potty breaks and planning his schedule down to a T. When his plans are interrupted however thats when it causes problems..

Favourite beverage (alcoholic and non alcoholic): If you ever see Jamie with a bottle of water in his hand there’s either something wrong or hes being forced to by Ian. Ian’s told him countless times his caffeine addiction is the cause of a lot of his...ah, ‘issues’, but this conversation always ends in an argument with Jamie sulking whilst angrily drinking red bull. As for alcohol...Jamie is a cheap date and that’s putting it lightly. He’ll drink almost anything but his quick metabolism and weak stomach have it hitting him an his bladder very quickly. Ian likes to recall the first time he saw Jamie drunk, which was off of rum and raisin ice cream, and teases him to no end much to Jamie’s annoyance. He also tends to lose all inhibition and a good chunk of his bladder control so fun often ensues when the boys drink...

How did he and his partner meet?: Ian found Cookie as a small puppy on the street and flagged down a car to take them to a vet, the driver happening to be Jamie. When it came time to pay the vet bill Ian couldn’t afford it but Jamie adopted Cookie  right there on the spot. They exchanged numbers so Ian could keep getting updates about Cookies health and wellbeing and the friendship grew from there. It wasn’t even two weeks when Ian asked Jamie out on a date.

Jamie: “How did you know I was gay?”

Ian: “Really? You had pink fluffy dice on in your car, your lockscreen was a selfie of you and your mom and you named our male dog Cookie.”

Jamie: “...shut up.”

Ian: “So, I take that as a yes?”

Jamie: “Yes.”

Jamie: “AND WHAT DO YOU MEAN OUR DOG?!”

Ian Devereaux

Ian is a loud, fun loving extrovert who can often be found doing something to make a sceptical of himself. He was the typical class clown in high school and never shied away from being the enter of attention. His spontaneous risk taking nature if what drew him to Jami in the first place, their personalities balancing one another. Ian helped Jamie come out of his shell and feel comfortable with his sexuality, which greatly helped his confidence and anxiety; while Jamie helps ground Ian and give him more direction in life.

Ian is also a creative soul and feeds off of Jamie’s artistic energy (and visa versa). He hopes one day to become and actor/film director or comedian...maybe a writer- something like that! He’s the middle child (no surprise there) of three boys and comes from a well off family- yet he’s still terrible with money and it often comes down to Jamie to stop him from impulse buying.

Age: 20

Ethnicity: Caucasian.

Nationality: Full blooded ‘MERICAN

Eye Color: Golden Brown

Hair Colour and Style: Dark brown but he dyes it black.

Height: 5ft 9in.

Tattoos/Piercings: Several ear piercings and a upper half sleeve on his right arm.

Kinks/Fetishes: He’s very open about his kinks once he’s comfortable with someone; he tends to play the dominant  but can switch if the rare opportunity arises. He’s into a range of things from bondage, and other ‘milder’ elements of BDSM but all of his interests tend to tie back into Omorashi in some way. For example he’d jump and the chance to indulge Jamie in his fantasy.

Bladder stuff: Ian’s always had a pretty average sized bladder and has never prided himself on an amazing holding capacity. Due to his extroverted nature he has no problem speaking up about his need which has saved him from a lot of predictiments (not to say he hasn’t come close in the past). In private he likes to engage himself in holds just to test his limits, but not often and he doesn’t particularly enjoy omo himself he enjoys spectating...unless he’s drunk then he enjoys getting a little squirmy.

Favourite beverage (alcoholic and non-alcoholic): He likes soft drinks mostly and he likes any kind of liquor but unlike Jamie he stays pretty well hydrated with water too.

How did he and his partner meet?: Ian found Cookie as a small puppy on the street and flagged down a car to take them to a vet, the driver happening to be Jamie. When it came time to pay the vet bill Ian couldn’t afford it but Jamie adopted Cookie right there on the spot. They exchanged numbers so Ian could keep getting updates about Cookies health and wellbeing and the friendship grew from there. It wasn’t even two weeks when Ian asked Jamie out on a date:

Jamie: “How did you know I was gay?”

Ian: “Really? You had pink fluffy dice on in your car, your lockscreen was a selfie of you and your mom and you named our male dog Cookie.”

Jamie: “...shut up.”

Ian: “So, I take that as a yes?”

Jamie: “Yes.”

Jamie: “AND WHAT DO YOU MEAN OUR DOG?!”

Ian: “I found her!”

Jamie: “HIM! HE’S A BOY!”

Ian: “You call a dog cookie I’m calling her she.”

[freenewstoday]

New Post has been published on https://freenews.today/2021/03/21/vaccines-are-here-thats-no-reason-to-call-off-the-hunt-for-effective-covid-19-treatments/

Vaccines are here. That’s no reason to call off the hunt for effective COVID-19 treatments.

Millions of Americans are getting their COVID-19 shots every day, but the U.S. is still going to need better treatments that can nip mild or moderate cases of COVID-19 before they become serious. 

There are a number of reasons that people could still get sick after they are vaccinated. There will be “breakthrough” cases, since the COVID-19 vaccines are not 100% effective. Some people won’t get vaccinated, putting others around them at risk. And new variants or mutations of the virus could make vaccines less effective than they are right now. 

Plus, people who have been vaccinated and then later undergo certain types of treatments such as for lymphoma could see their antibody-making B-cells wiped out.

As of Thursday, more than 12% of the U.S. population has been vaccinated, according to the Centers for Disease Control and Prevention. The U.S. is currently averaging about 53,000 new cases a day — a rate that, while far below January’s peak, is still high enough to worry public health authorities.

“A lot of people have the impression that vaccination is going to solve the problem,” said Dr. John Brooks, a medical epidemiologist at the CDC. “But just look at influenza. We know that every year there are people who are breakthrough infections, and that is if they had the vaccine.”

When it comes to the flu, there are four treatments that can be prescribed to patients, including GlaxoSmithKline’s GSK, +0.41% Relenza and Roche Holdings AG’s ROG, +0.57% Tamiflu, an oral antiviral approved by the Food and Drug Administration in 1999.

Having Tamiflu-like medications at the ready to treat people with mild to moderate forms of COVID-19 and keep them from getting so sick they end up in the hospital or die could go a long way toward slowing the pace of the virus and moving the U.S. back toward normalcy.

Preventing hospitalization and death from COVID-19 are two endpoints that companies like Eli Lilly & Co. LLY, +0.20% and Regeneron Pharmaceuticals Inc. REGN, -0.21% have focused on while testing their monoclonal antibodies in clinical trials.

Lilly got its first emergency-use authorization for a stand-alone antibody treatment, bamlanivimab, and then another one for bamlanivimab and etesevimab together, while Regeneron’s antibody cocktail, called REGEN-COV, is authorized for teens and adults who are at high risk for hospitalization.

From the archives (October 2020): Regeneron CEO cautions Trump’s results are ‘a case of one,’ and coronavirus drug needs more testing

But there have been road bumps when it comes these therapies. They may not be as effective against variants like the B.1.351 strain, which was first identified in South Africa. And patients have had to go to infusion centers to receive those treatments as it’s not scientifically possible to package monoclonal antibodies into the kind of oral medicines one can pick up at a local pharmacy. (This part of the equation may soon change, with the White House on Wednesday announcing $150 million in funding to ensure more equitable access to these therapies.)

“The ideal therapy would be one that’s easy to take, easy to get a hold of, and not expensive,” Brooks said. “Monoclonals are wonderful. They really do seem to help people. But they require an intravenous infusion.”

‘The mere existence of a vaccine is not enough’

Monoclonal antibodies, which have been the only authorized treatment options for people with milder forms of COVID-19 during the course of the pandemic, show tons of promise, both as treatments for patients who have tested positive for the virus and also to prevent infections. (None of the antibody treatments has been authorized to prevent COVID-19 for instances of pre- or post-exposure at this time.)

Several drug makers beyond Lilly and Regeneron are currently running clinical trials for antibody-based treatments, including Vir Biotechnology Inc. VIR, +3.71%, in partnership with GSK and AstraZeneca AZN, -0.24%, which announced Tuesday that the U.S. just bought a half-million doses of its still-experimental antibody cocktail. 

“The mere existence of a vaccine is not enough,” a spokesperson for Vir said in an email. “It has to be available, widely taken, and effective year after year after year, even against emerging variants. Now more than ever, we need treatments that are active against currently circulating variants of concern, as well as any new variants that emerge.”

But executives at Lilly and Regeneron say they have seen limited utilization of their antibody treatments since the first authorizations were handed out back in November.

A Lilly spokesperson confirmed that only about one out of every seven qualified people with COVID-19 is being prescribed an antibody treatment. And a Regeneron executive in February said that prescribing guidelines may have been written too narrowly to ensure widespread access to the company’s antibody therapy. (The National Institutes of Health and the Infectious Diseases Society of America both updated their guidelines this week to recommend use of the monoclonal antibody treatments.)

“We as a country are not using these antibodies properly,” said Dr. David Weinrich, Regeneron’s head of global clinical development. “Generally, there are pockets where physicians have realized the value of these things, but it’s not universal. And that is, unfortunately, creating disproportionate access to the drug based upon where you are in the country and who your physician is — that’s not a good scenario.”

Bernstein analyst Ronny Gal’s hunch is that lower-than-expected utilization of these drugs has had more to do with physician expertise or lack thereof. “I suspect the main reason is that folks being diagnosed with mild cases have low overlap with physicians who often use infusions,” he said in an email. 

Toward a Tamiflu for COVID-19

Then there are antivirals, which are the same type of drug as existing flu treatments, but those options are limited at this time.

The Gilead Sciences Inc. GILD, +0.59% antiviral treatment Veklury is only indicated for people who are sick enough to be hospitalized, and clinical trials have been limited to testing the drug in people who have been hospitalized.

It’s not the only antiviral candidate undergoing testing, however. Ridgeback Biotherapeutics and Merck & Co. Inc. MRK, +0.31% have an experimental oral antiviral treatment, molnupiravir, that reduced infection times in about 200 nonhospitalized COVID-19 patients, according to preliminary findings from a Phase 2 clinical trial that were announced in March.

“It is going to be the combined approach of vaccines and antivirals,” said Dr. Bruce Polsky, an infectious-disease physician at NYU Langone Hospital on Long Island. “Ideal would be to be an oral medication — an oral medication that you could give to someone when they first present to you with symptoms.”

Norbert Bischofberger — one of the inventors of Tamiflu, which generated nearly $3 billion in peak sales during 2009’s swine flu pandemic — is CEO of a biotech startup called Kronos Bio Inc. KRON, +4.91% and had previously worked at Gilead when the company first began developing Veklury, then called remdesivir, as an Ebola treatment. Bischofberger sees a parallel between how a drug like Tamiflu is used against the flu and what is needed for this coronavirus.  

“In the old days, over the winter season, I always traveled with Tamiflu in my luggage,” he said. “When you encounter somebody in the elevator or somebody coughs and sneezes in your face, I go to my hotel room and take Tamiflu. It’s very, very effective.”

‘Imagine’ bespoke antibodies

It’s unknown at this time how many people will be at risk for contracting the virus even after they have been vaccinated. And even as public health experts applaud the arrival of COVID-19 vaccines, they do not shy away from making the case for more effective treatments, both now and in the future.

That we’re already seeing variants that may lessen the effectiveness of vaccines and monoclonal antibodies is a primary reason to maintain focus on therapeutic products alongside preventative ones. Already the U.S. is no longer allowing orders of bamlanivimab in Arizona, California and Nevada over concerns about its effectiveness against a newly emerging variant there, Lilly confirmed Thursday.

Looking ahead, as new variants emerge, a set of personalized treatment options could be indicated, according to the CDC’s Brooks. If a person’s test for the virus comes back positive, that sample may be sequenced to search for any variants of concern, and then a specific antibody treatment that is effective against that variant would be the medicine that gets prescribed.

Many of the pharmaceutical industry’s breakthrough therapies over the last decade have done just that. AstraZeneca’s ovarian cancer treatment Lynparza requires a test for the BRCA1 or BRCA2 gene mutations, while a prescription for Gilead’s Biktarvy is dependent on HIV-1 expression levels.

But for now the technology and medical practice haven’t caught up to the unruliness of this virus. Some regions are still experiencing COVID-19 testing delays, genomic sequencing can take five or six days, and the antibody treatments that we have are very new — and very underutilized.

“Imagine,” Brooks said. “I’d like to be able to give the person the monoclonal antibody that I know is going to work — for two reasons: one, if they’ve got a resistance, I want to avoid a drug. But if they don’t, then let me use the least expensive, most available drugs. It’d be nice to be able to use direct therapy. Right now, we are not there yet.”

Source

[kansascityhappenings]

Joe’s Weather Blog: 40s to 20s…and that’s a problem (TUE-1/22)

Good Tuesday morning…I may try and get an update out later this afternoon or this evening as time permits because from 7PM to 12AM or so things may start happening…the temperatures will be crashing and whatever moisture we have out there will start switching to some sort of freezing rain/drizzle/sleet/snow thing…and it may get messy on the roads tonight.

You should be fine for the evening rush hour in my opinion but we’ll watch that carefully for you.

Forecast:

Today: Cloudy with developing light rain/mist/drizzle. Highs 37-45° in the early afternoon then falling later this afternoon into the 30s. The cooler weather will be north of I-70 and the milder air will be south of KC.

Tonight: Falling temperatures and gusty NW winds of 15-25 MPH will allow whatever is falling to transition over to a winter mess of ice/sleet and some snow at times. Temperatures tumbling into the teens overnight. Slick roads are possible to likely depending on the treatments out there. There are two issues…1) the flash freeze issue and 2) an accumulating snow potential. I’m sort of in the dusting to 2″ potential for KC. 

Wednesday: Cold in the morning with lows 10-15° to chilly in the afternoon with highs rebounding into the 28-33° range. Skies should be clearing out so it will be a brighter day (finally)

Discussion:

It’s a complicated forecast for sure. Last night some model data, not all of it, jumped aboard the NAM solution which was to drop the developing surface low to the west of the region…and take it considerably farther south. It was a solution that I didn’t have a ton of confidence with because we were at the time, and still this morning, seeing a lot of warm air getting pulled northwards. This would keep the surface low from tracking as far south as the NAM though. The NAM model also had temperatures today in the mid 30s…essentially keeping the cold air in place. That too probably won’t work. IF you jumped on that outcome and jerked the forecast, today you would’ve predicted 35° for a high. As I start typing this…we’re into the upper 30s. That won’t work. I didn’t jump on that outcome. The thing is the surface low will be tracking towards the south of KC in the end it appears…which is a favorable snow track, BUT I’m still seeing somethings not coming together fast enough for a big snow in KC. It’s something to monitor though for the rest of the day.

With all that said you can see the changes coming…here is the 8AM surface map…the low itself should come towards the ENE…and allow the 40s to the south of KC early this morning to creep north of I-70 early this afternoon.

The thin colored lines are the isotherms…lines of equal temperatures…you can see the drop off from the 50° temperature in Wichita (red numbers) to the 15° temperature in far NW KS.

Here is a close up of KS…via the KS Mesonet…and you can see the change in temperatures at 8AM from the southeast to the northwest.

52° in Sedan to 14° in Sherman and Cheyenne.

Nice front.

So when it moves through…the temperatures will start crashing.

We should be in the upper 30s-45° range early this afternoon…there will be quite the variation from northern Platte County to Cass County it appears.

Here is the HRRR forecast for 2PM today.

Now the same thing for temperatures at 6PM tonight.

See the drop that’s occurring…

Teens coming after 12AM.

In terms of the wintry set-up for precipitation. We will be liquid for awhile today…probably into rush hour.

Then we’ll see a switchover from the west to the east. Here is the HRRR model for 6PM…

Then for 9PM…

We may see some decent snow rates for awhile…so that’s why last night I mentioned the potential for a dusting to 2″ for tonight combined with the flash freeze scenario.

The NAM models are both somewhat more aggressive with the snow overnight. Cranking out 2-4″ worth. I see that option on the table more towards the NW part of the region…up towards NE KS and NW MO. Areas off towards the east of KC will have a tough time getting a lot of snow I think. Why? Well look at the temperatures a bit higher than the surface…towards 5,000 feet or so. Those values in are °C…but the freeze line at that level is still near the I-35 corridor. So you can see how complicated this is, especially from the State Line eastwards. Oh the map below is for 10PM tonight!

That’s why I don’t want to go too crazy with snow amounts in KC just yet…because the wintry mix of whatever…sleet/ice/snow…may complicate snow totals.

Regardless don’t discount the flash freeze potential from this scenario…especially on untreated surfaces.

The NAM model is much more aggressive with this..cranking out about 3″ for KC and close to 8″ towards the IA border…even as I time the switch more towards 7PM for the accumulating snow potential. However that is an issue because it too has above 32° above us through 7-8PM or so…at least from I-35 eastwards

Boy there is a lot of cold air getting into the pattern over the next 10+ days. There will be all sorts of gyrations coming…and we may be seeing some near 0° mornings too depending on a few things.

So let’s go with dusting to 2″ potential for this at this point.

Our feature photo is from ‎Sarah Holloway‎ towards the NW of Trenton, MO of the Super Blood Wolf Moon. At least someone saw it! I thought they were stuck in the clouds too…I guess not.

Joe

from FOX 4 Kansas City WDAF-TV | News, Weather, Sports https://fox4kc.com/2019/01/22/joes-weather-blog-40s-to-20s-and-thats-a-problem-tue-1-22/

from Kansas City Happenings https://kansascityhappenings.wordpress.com/2019/01/22/joes-weather-blog-40s-to-20sand-thats-a-problem-tue-1-22/

[dreamwriting-things-blog]

DEPRESSION AND ANXIETY DREAMS

Depressed people dream much more on average. It shows that they cannot get negative thoughts off their mind.

This article will look at specific dreams from people who are depressed. But, first it is perhaps best to look at the dreams of depressed people generally. Modern psychologists have started to view dreams in a new way. It has been known for a long time that depressed people dream much more often than those who are not depressed. Time after time depressed people report how they wake up tired and exhausted. That they have spent the whole night dreaming. That they wake up more depressed than they went to sleep.

Nightmares at one time were thought of in a positive light. Those such as Freud argued that depression can be traced back to things that happen in childhood. In confronting our anxieties we can start to deal with the source of our illness.

Yet its more likely that many bad dreams simply reinforce the dreamers state of mind. Talking about traumas from the past simply fuel the fire. Deeply depressed people can simply wallow in their own anxiety.

It has been noticed that victims of trauma can be those who have the most developed imaginations. They allow their worries to get out of control.

Just how accurate is this modern view of depression? Yes depressed people certainly dream more. But if you stop them dreaming will this cure them? Thats not likely to be the case. Their dreams merely play out the waking anxieties. The heart of the problem is that depressed people get into a cycle. They simply cannot break out of their problems. They simply go round in circles feeling resentful. Therapy may allow them to hopefully view their situations from a new and fresh perspective.

In many ways it is pointless to study the dreams of depressed people as a separate group. But this article brings together dreams from people who have openly stated that they were very depressed at the time or were suffering from deep trauma or depression.

Dreams are by their nature metaphors for your life. All metaphors will tend to be exaggerations from the truth. So depression dreams will not differ that much from those people who have much milder forms of depression - those who are simply bored or fed up. Both will choose extreme metaphors to express their feelings.

Having said that - here is a selection of dreams from people who were severely depressed, paranoid or traumatised.

DEPRESSED DREAM I am on a bridge which is known for people jumping off committing suicide. I am without hope and feeling paralysed. I slowly edge down the path. There seems nowhere left to go.

THE REALITY The dreamer had felt seriously depressed over a long period of time. The dreamer mentioned that he had felt extremely depressed and on the point of suicide. Clearly the dream captures this. In the dream he does not jump but is simply edging towards suicide. It shows that his is the direction he is heading.

PARANOID DREAM - There is a man pointing at me. He is moving about frantically and is pointing right in my face.

THE REALITY Recently the dreamer had been very depressed. The day before he was also very paranoid. He had walked into town and was very nervous walking along. He felt people were looking at him. The dream emphasises that feeling that he is being targeted and looked at. This resulted in an extreme anxiety attack. ------------------ THE DREAM - I was in a building with gangsters. I suddenly realised that I was in danger so I started to shoot the gangsters. It was kill or be killed. I managed to kill them all.

THE REALITY The dreamer was prone to depression. She tended to lack trust in people. She had recently become more withdrawn and paranoid. She was not willing to trust anyone. The world of the gangster is a sordid one where you can trust no one. The dreamers own life had become like this and she was unable to trust anyone. ------------------ THE DREAM - I am then in some swamp area. There is a slug moving around me. A bee comes near me but I avoid it. I am in some long room. It appears to have lots of people. There is Terry Marsh there. He is dressed in some very odd clothes. He has a jumper on and a weird hat. I am then in some car in the back seat. There are some TVs there. There are three of them(reminds me of an old and out of shape Elvis Presley who watched a bank of TV's).

THE REALITY The dreamer had been sat at home for too long. He had been watching TV and just not doing anything and felt depressed. The symbols of the dream caught this mood:Elvis getting old and out of shape watching a bank of TVs; Terry Marsh a play on words linking to swamp like territory and with that a mood stuck in the mud. The weird clothes was symbolic of how the dreamer saw himself - worrying that he looked weird. All this showed how low and isolated the dreamer felt. ------------------ INTRUDER DREAM - I am in in my home. Suddenly the people are within it. They are intruding right into it. There seems to be a partition within the house and the intruders are in this part and have every right to be there.

THE REALITY The dreamer had been very ill. He had the opportunity to move into sheltered housing with a warden. He was worried that his independence would go. Obviously psychiatric help can be very intrusive. If you are taken into psychiatric hospital this is obviously a very intrusive act. A patient has to deal with their own depressive thoughts along with a sense of trauma at their lives being taken over. This dreamer had lived life independently and now felt he may have to give up that independence. ------------------ DREAM I was with my best friend from school(I haven't seen him for many years). I am pleased that he has returned. I keep enthusiastically talking to him. I am asking him what his music tastes are now. He doesn't answer.

THE REALITY The dreamer had had a very hard life and had recently sought psychiatric help. He was now starting to respond to treatment. He woke up feeling thankful of the help he was receiving and felt he had come to a turning point. He felt more able to talk openly about his problems. What struck him about the friend in the dream was that he never spoke when he asked a question. This reminded him of his therapist who never really engaged in conversation. She merely asked questions. The dream shows that the dreamer was trusting in the process. His therapist had effectively become his best friend.

If your dream is like a nightmare then the dream probably reflects your current emotional state. The nightmare being symbolic of your negative feelings and state of hopelessness.

THE DREAM I dreamed about a primary school teacher. She had a rapport with her children. She managed to make them eat up "all their food" so as to make them healthy and strong. Then in the school he was playing some sort of game. The game involved handling a snake. I knew that this snake was not too dangerous as you could tell by looking at it. At the back of my mind I felt it could be dangerous but still I was holding it.

THE REALITY The dreamer was receiving therapy to help overcome strong phobias and paranoia. He was very scared in many social situations. The day before he saw his therapist and immediately after leaving he set about a task which he had been putting off. He had been encouraged by his therapist and had realised that he was starting to overcome his phobias. The snake represented his ability to handle difficult and highly phobic situations. The snake was dangerous(like the challenges he had set himself) but was not THAT dangerous. His goals were achievable. The teacher, of course represents the dreamers therapist who was encouraging him. ------------------------ CONCLUSIONS The dreams of mentally ill people compared to those not suffering are not substantially different. It is not helpful to study the dreams of the depressed. Suicide often appears as a common symbol in dreams. Most of those are highly symbolic. Suicide often appears when a dreamer simply wants to give up in despair. Yet dreams do not say if the dreamer has given up generally or if they have merely given up on something very specific (eg "I simply cannot do maths - I have totally given up").

Dreams do not so much link to reality but rather the reality of your emotions. If you feel really negative then your dream reinforces that negativity. Someone who is depressed may experience a dream which places them in some worst possible scenario and so brings to life their most negative fears. This is not truth - its just the reality as that person sees it.

Mental illness is not something that you either have or do not have. It is more like a sliding scale. People can be depressed in very mild ways. Their dreams will be remarkably similar to those who are deeply depressed and in need of treatment. In the same way all people have mild paranoia's which result in remarkably similar dreams to a deeply paranoic person.

If you are severely mentally ill then this can affect your life in many ways. It may involve intrusive questioning and hospitalization. Expect dreams to link to the loss of independence which serious mental illness can result in.

Expect dreams at crucial moments. Changes in the severity of the illness will result in dreams. A dream notes noticeable improvements and setbacks in the dreamers health. Dreams will also show how the dreamer is dealing with and interacting with their treatment. If they are thinking negatively about the treatment. If they are enthusiastic about help and embracing the possibility of change.

Interpreting dreams does not really help you. So do not try to cure mental health conditions by studying your dreams. Dreams can easily be misinterpreted. They can be used to get patients talking about themselves. Many psychologists ask a dreamer what their dreams mean. They are not interesting in the dreams themselves they are simply trying to get a patient to open up about their feelings.

[eurekakinginc]

"The 4 Epochs of longevity"- Detail: I have been studying Genomics for the last year, with a focus on longevity. I have come to the conclusion that there will be 4 distinct (although somewhat overlapping) epochs in the goal of living longer and healthier lives. I'd like to lay them out for you.This is a long article, and the last epoch has the most to read because it's about research that hasn't even started yet, and I have to talk about the science we know today that will lead to that research. let me also be clear, that while this is based on letitimate research I have read, some of this is SPECULATION. Although in a conversation with the guy that runs the lab I am in the other day, he endorsed my speculation has having solid logical roots.Epoch 1: Health Consciousness. This is the era that began as far back as we can imagine, and we are deeply into this today. This is the notion that (using the best current knowledge that) avoiding sugar, not smoking, eating well (more greens, more rawish foods, less processed stuff, less preservatives), not getting fat, and exercizing can all lead to longer healthier lives. This is undoubtably true. My local PBS station has shows that basically advertize programs (books, videos, you name it) detailing all the things you should do. This is at the rate of about one of these shows a week. I guess, as a species, we got serious about this when the surgeon general banned advertizing of cigarettes in 1970, and as time has passed, we have gotten more serious about it. Lets note, no matter how far forward we go with this process, these fundamental understandings of how NOT to abuse our bodies will always be good advice.Now, an argument can be made that Mary-Claire King is singularly personally responsible for raising the average lifespan age by about 2 years worldwide based on her discovery of the BRCA1 gene - the breast cancer gene - allowing women to get screened and being able to largely avoid dying from breast cancer by knowing that they should get screened more often if they are at risk, and then getting treated early if something is detected. I believe this is true, and I mention it as a proxy for a whole host of life saving interventions (Seatbelts and airbags are two other technologies that are examples), but I don't see those as being DIRECTLY aimed at the issue of longevity, so... Even though that sort of thing is going on in the background, and they are all working in concert to increase the average lifespan, I am going to choose to not count them here. What DO I count then? Well...Epoch 2. Longevity drugs. Starting as far back as 1999 (the earliest paper >I< have seen, though there are certainly earlier ones that I don't know about), specific drugs are mentioned as increasing healthspan, and that implies not dying from age related diseases, and that implies living longer.A few people realize that we are in this epoch right now, and the awareness that we are in it is slowly dawning on the general public. I have 5 treatments that are the hallmarks of this age. 2 are diets and three are drugs. Buckle up, if you haven't heard about these they are becomming mainstream fairly quickly.Lets start with the diets. It's long been known that Dietary Restriction leads to an increase in lifespan. If you knock off about %15 of the calories that you "need" on a daily basis, you tend to live about %20 longer. This, to a person living in the west, means living like a supermodel, and avoiding all those yummy calories - forever. And it turns out that very very very few people are willing to do that. So, a guy named Valter Longo said something genius: What is the minimum thing we can do to get the same effect as Dietary Restriction? He found that for a large number of reasons, fasting sporadically could accomplish that. There are some rules, During the fast, you can eat some things every day for minimum nutrition, but intake of calories is limited to 700 calories per day. Secondly, the fast has to be 5 days long, as you need your body to go into ketogenesis (where weak cells die and break apart and get flushed out of your body). Thirdly, you need to do this at least 7 times in a year for the longer term effects to show up. (These effects also include weight loss, and if you have pre-diabetic readings on some levels, those go back into the normal range). In fact, he was able to get FDA approval for this diet based on these pre-diabetic symptoms disapearing. An FDA approved diet. In this world of fad diets, this is a rarity.Based on Valters work, I was told by a nutrition researcher at the Fred Hutch Cancer Research Center that someone said: Oh, this diet also has anti cancer benefits... What can we do thats the minimum possible that gives >those< benefits.... and based on that the 8/16 diet was born. Basically you eat normally for 8 hours a day, then you don't eat the rest of the time. Think about it... whats the job of a cancer cell? To grab nurients and replicate. But you have antibodies that go find cancer cells and tear them apart allowing those bits to get flushed from your body. (In fact it has been said that everyone has had cancer multiple times, it's just that the antibodies got rid of those cells before they could replicate. So? In that kind of war, if you don't eat for 16 hours a day, thats time for the antibodies to wipe these cells out when they aren't gathering nutrients and making more of themselves. It's about leveling the playing field. Seems legit to me. and if you don't die of cancer? That will certainly lead to a longer lifespan... right?Moving on to the drugs: Rapamycin: This trug targets a gene called mTOR (want to know something funny? the TOR stands for Target Of Rapamycin). Now mTOr regulates a pretty well known metabolic pathway, so it turns out that rapamycin provides benefits in sort of the same way as Dietary Restriction. Lets note that there is a healthspan study in dogs at the University of Washington right now run by Dr. Matt Kaeberlein, but it's not in any clinical FDA trials for longevity even though it's FDA approved for transplant patients, but a number of scientists swear by it.Metformin: This is an FDA approved drug used by diabetics. It works to lower the amount of sugar in the blood. It's milder in terms of effect than rapamycin, and it IS in human trials for healthspan improvement by the FDA at present. These trials are called TAME - Targeting Aging with Metformin. Again, a number of people swear by it.NMN or NR. If you look at a cells energy cycle, cells burn ATP. The make ATP by breaking up sugar that enters the cell, and using some of the parts to make ATP. But they also make NAD+ out of other parts of the sugar - and later on the NAD+ also gets turned into ATP. Now, NMN and NR are chemicals that are along the pathway that cells use to make NAD+ so it's very easy for cells to use this same pathway to make extra NAD+ from a supplement that you take and that NAD+ is then later used to make more ATP. It's well known that NAD+ levels go down as people age... so it makes sense to try to boost those levels right? There have been a few human trials although none were FDA sponsored. There is really solid laboratory evidence in mice these two molecules work AMAZINGLY well, there are ongoing human trials right now, and there is loads of anecdotal evidence. There are also shenanigans about how it's made (enzymatically is FAR preferred to the solvent based manufaturing process), and there are a few lawsuits between some of the companies that sell one or the other as a supplement. But it's the big stick of the current crop of Epoch 2, and it looks like keeping energy levels in cells up helps them function well for a LOT longer.Thats where we are today. There are a few drugs being tested, and in use by early adopters, and it looks very very promising. Where are we headed?Epoch 3: Stem cells and senescent cell removal.There are two breakthrus that will dramatically increase lifespan that are in the "actively being researched" but farther out than the drugs above which are already on the market.Lets tackle stem cells first. These are basically skin cells turned into stem cells that get injected into problem areas, but since they can multiply and become any kind of cell, they can be used to repair damage from any number of age related maladies. Also stem cells tend to decrease with age, so this forced replacement of them can be a good thing if done right. There are stem cell therapies today (things like repairing severed neurons, restoring heart muscle after a stroke, and maybe helping to repair joint function, and on and on and on), none of them were specifically engineered with aging in mind, adn so like above, I won't dwell on them. But... you ask... why did I mention stem cells? Well, there are folks working on aging specific stem cell therapies. These longevity related stem cell therapies tend to be in the realm that uses genetically engineered stem cells. Repairing macular degeneration, and tissue regeneration are two that are on the radar. Lets talk about the first: It turns out that in the eye, there is a specific protein that builds up, that our bodies can't get rid of, but with a 1 base pair change to our dna, there is a protein that CAN get rid of it. So, we take a sample, make a few stem cells, then edit the dna of those stem cells so that they can clear this protein out of the eye, and grow a large number of them, and inject THOSE stem cells back into the eye. This is the macular degeneration fix. It is NOT here today, but there are labs that have done this in mice. This is the exact same approach that is being talked about for arterial plaque buildup. This first use is really indicative of a larger "category" of age related diseases where the body has built up some gunk outside of the cells over time, and it needs to get removed, but it never gets built up too much until after we have kids, so evolution doesn't see it as a problem. (Since evolution only cares about the genes we pass on, adn thats already done by the time this issue crops up.) We who want to live longer, clearly DO think that this is an issue. Since I mentioned them, for muscle regenation or nerve regeration, it's basically a genetically edited stem cell where the appropriate growth factor is somewhat overexpressed, injected into the correct tissue to stimulate faster or more growth thats wanted.The first one of these stem cell therapies, if I have to guess is 5 to 7 years out since it is a new approach that the FDA has to approve. Thankfully they have approved stem cell therapies in the past, and they have approved genetic editing of single cells that get grown to a large number of cells in the past (the car-t lukemia treatment that got approved as of december 2017), so with the fundamental approaches being known it probably won't take them a full decade for us to start to see these uses for stem cells.Senescent cells. Also on the "getting rid of what we don't want vein". It turns out that all cells start as a stem cell then divide into a stem cell and a differentiated cell - one that has a specific function. Senescent cells are those that are doing their differntiated job but getting old (and probably starting to be bad at their job), and refusing to die.. They are just a hangin around. Now, the body knows how to handle small scale damage (As a single example - there is a signal called PDGF Platelet Derived Growth Factor) that some cells excrete as they die telling stem cells in the area that someone is gone, and maybe another cell is needed...) So, IF we can get weak differentiated senescent cells to die we can force nearby stem cells to divide and get a fresh cell thats new and NOT bad at it's job to take the place of the senescent cell. Turns out that Hydrogen sulfide (present in garlic) is a good chemical to trigger weak sensecent cells to die. But there are issues getting it to the right cells, not having it be toxic, and any number of other issues. There are folks that have done work in mice that shows DRAMATIC improvement of healthspan, and restoration of many weakened body functions due to "age" when senescent cells are removed. There are no human trials yet, but be sure that once there is a senescent cell removal therapy, you will want to go get it.I espect this to come about (given the state of research and published papers) within the next decade. These two technologies will make for a HUGE leap forward in both quality of life and longevity.And if this is going to make things so much better, what could possible be epoch 4?Epoch 4, Epigentic resetting.This is where I extrapolate the future. If I am going to tell you what treatments are coming next, I think it's important to start with the ROOT CAUSE of aging - all the treatments above are treatments for first order effects - symptoms if you will - how do you better fix things after something has gone wrong. I want to talk about how we will be able to prevent things from going wrong in the first place inside your cells. It turns out that there might be a few things that cause aging, but far and away the most important of them is cellular disregulation. Think about this... We have a system that regulates what genes are on, and which ones are off, and how much of each gene is expressed. It's called the epigenetic system. I'll describe how it works in slightly more detail a bit later. For now, imagine that over time, the epigenetic system "degrades". And we have about 20,000 genes that do different things, and the DNA for each of those is in every cell in the body. Think about what might happen if a cell that makes light receiver in your eye gets turned on in a cell in your heart. Having to make those extra proteins will take some of the ATP that it takes to beat that heart cell - and having that protein present in the cell might interfere with other things in the cell - and this is one singular example. At the point that enough cells in your skin degrade, it will get saggy, at the point that enough muscle cells stop working right your muscles degrade, etc, etc, etc. In short aging. Now, I am not the first person to say that cellular disregulation is the most important thing, a number of people think that this is THE biggest problem we need to solve, and the entire field is slowly shifting to this point of view.Ok, if thats the biggest problem... what causes the epigenome to "degrade"? Again, there are a number of causes, but right now the evidence points to "double stranded DNA breaks" being far and away the most important cause. Thats right double stranded DNA breaks. What? We have proteins that repair those right? Yes. But... There are side effects. It turns out that Dr. David Sinclair did an experiment with mice that doubled the double standed DNA break rate in very specific places on the genome of a mouse. He performed this experiment over the span of a year, and at the end, compared it to a litter mate, and yes, the DNA break mouse looked very elderly compared to it's one year old bretherin that was in the prime of it's life (mice live about 2 years, so testing aging in mice this way is fair game.) The takeaway of that experiment is that double stranded DNA breaks mess with the epigenome and that... causes aging.OK, I've mentioned the epigenome a few times now, I'd better give a little bit more depth on it. Let me start with a statistic: We think we maybe understand the function of %90 of the DNA we have (I can justify this if needed) - but we maybe only understand %50 of what there is to be learned from the DNA we have. Compared to this, we understand only about %5 of the big picture of what there is to be learned about the epigenome. Let me give you a big picture overview of the basics: What we do know is that there are two main mechanisms at play. The way that genes are turned on or off (or regulated up and down like a volume control knob) is by that DNA being accessable to the proteins that make RNA copies of it. The first mechanism: On the outside of your DNA, almost as an annotation system we get "methylation", and in most cases, if you methylate something that gene turns off - think about it, the protein that wants to make a copy comes along and oops, it's blocked from getting to the DNA it wants by a methyl group, so... no copy is made. This is kind of the on off switch. The second mechanism is way way way more complicated (it's more the volume control knob). We have 2 meters of dna if you stretch it out. Thats a lot. Imagine it being a ball of yarn stuffed into the neucleus of a cell, how do you find anything? Well... in that scenario, you can't... but we have evolved "histones", and the dna wraps around them, and gets all coiled up. Lots of histones which allow everything to be wrapped up neatly and predictably. Now, histones have certain tails of amino acids hanging off the side that things can bind to. DNA has a very slight positive charge. And methyl groups have a very slight positive charge... and acetyl groups have a very slight negative charge. So... imagine adding a methyl group, and the two positives charges push each other away, meaning the dna wraps less tightly around the histone, meaning it's slightly MORE available to be transcribed, and acetyl groups help to wrap the DNA more tightly and turn down transcription. And now, let me blow your mind... there are about 200 different epigenetic markers that have been discovered, and people are working feverishly to decipher and understand and map them all. It's my understanding that DNA methylation has the largest "control authority" over gene expression so lets talk only about that.It's clear that if the epigenome gets messed up by double standed DNA breaks that the implication is that the proteins that go to the break and repair it also knock some methyl groups off, or add some extra ones as they do their job - it appears that in certain areas of the genome it's more "add" and in other areas it's more "remove", but with age, gene expression TENDS to drop (meaning more methylation). Now the damage (extra methylation) appears to be somewhat random. Today noone knows the exact mechanism that causes this damage - so if you are looking for a PHD project? This is a really solid one to take on.But what we DO know, is that there is a specific profile of DNA methylation that seems to be present at varying ages - certain important points on the genome either have it or don't. And as you age, other IMPORTANT points get methylated. This work was done by Horvath and Hanuum in about 2013 when they published separate papers on the "DNA methylation clock". There are 400ish sites that get methylated, and which of those sites is currently methylated can be used to determine your age (barring radiation, obesity, or smoking exposure) to within a few years. In fact, this clock is accurate enough that one european government is using it to determine the age of refugees who have no documentation (to determine if they are over or under 18 years old as the law has different rules for the two groups.) The method gives you an answer at the age of 18 thats within 2 years, and previously they called in dentists to look at wisdom teeth and got answers that were within 5 years. Even though this is a new technology, and it has so much room for improvement, it is already better than the old methods of determining age. (scary right?)So, now you know what causes aging! Double stranded DNA breaks cause DNA methylation to increase messing up gene regulation. it's SO SIMPLE, RIGHT? Here is a paper with a bit more depth to it that explains what I just did again with diagrams and definitions, and way more detail: http://www.longlonglife.org/en/transhumanism-longevity/aging/epigenetic-aging-longevity/epigenetic-alterations-as-a-cause-of-aging/So whats coming? Here is where I make my specualtive prediction: We will take every cell in your body and RESET the epigenome.WHAT? How the hell is that possible?!? Well... if we look to biology for answers, how does the methylation on your DNA get there in the first place? We have an enzyme called DNA methyltransferase (actually there are alot of them that do this kind of thing), and there are other mechanisms that remove methylation.You have all heard of CRISPR right? CRISPR is a combination of two things. First is the Cas9 gene that likes to cut DNA, and second is a peice of RNA that guides the Cas9 gene to the place it's needed to do that cutting. WAIT!!! Cutting DNA? Thats bad, right? Yes, but...As of 2016 some scientists in China (Shawn Liu and Xuebing Wu, and others) developed a version of CRISPR where they took off the part that cuts DNA, and added on a part that demethylates DNA, and you can buy this off the shelf now.So, all you need to do (hahaha, as if this really is easy, right?) All you need to do is to identify all the places that need to be demethylated, build the correct guide RNA, and deliver a cas9-dna-demethyltransferase along with the guide RNA into every cell in your body, and voila! No more cellular disregulation. And at that point the cell will behave normally, and it won't become senescent, or die, or misbehave in any way.As part of identifying those genes that need to be reset? Lets talk for a moment about how we might do that. Remember the Hanuum clock? %10 of the methylation marks are in a gene called KLF14 which is a master regulator of metabolism and obesity. (I'll also note that one of the stem cell creation factors - Klf4 - is a brother protein to this). It strikes me that a lot of the drugs mentioned earlier focus on metabolism related things, so pointing at this gene seems to pass the smell test.My bet is thats it's not a bad gene to start with, and resetting it might show some mild improvement in lifespan. But more likely, doing this will backfire as the gene regulation system is ridiculously complicated, and so I think that to get ANY effect we may need to reset a dozen or so genes, and to get the DESIRED true longevity effect, we may need to reset somewhere between 200 and 500 genes. and all I've talked about is the methylation. Remember there are 200 or more epigenetic marks to take into account and decipher.And then there is the issue of delivering this drug to every cell in the body. We use viral vectors to do this today in gene therapy, and so some of this delivery part is available, but... it's expensive today, and as a technology, it too is in it's infancy.And now, just to make sure that you understand the hieghts of the smooth granite mountain peaks you are about to free climb... there are 240 or so tissue types that are tracked today, thats clearly not all of them, and each tissue type is likely to have it's own set of genes that need specific "settings", and since the viruses used to deliver gene therapy products are usually attracted to very specific tissue types, we will need at least that many viral variants to deliver these specialized cocktails to those cells... Trivial, right?So, I think we CAN fix our gene regulation, and our first attempt, with limited understanding and maybe a dozen genes, we can make some headway, and herald it as a major breakthru, but 10 or 20 years later when we REALLY understand what we are doing? These postulated first efforts will seem like the dark ages where we drilled holes in the skull to "let the demons out".When will this happen? All the tools are there, heck, I've even identified an initial gene as a possible target. All it takes is someone to fund the study in a lab. Are we at the point where most funders see this as the next logical step? From what I know today? No they do not. This means we will need at least 5 more years of epigenetic mapping and research and refinements to the clock and understanding gene regulation pathways, and more importantly progress into the second and third epohs listed above to show that logevity is actually achievable, and and and... and then we can see some early results for a version 1 that mitigates aging in elderly folks who have gene disregulation, and once reset they get healthier. (the fact that they will live longer, thats not what the FDA will focus on - they will want to see folks with a better metabolism, with more muscle tone, etc, etc, etc, things they can measure NOW.)So, when will this happen? I think we may see the first scientific paper that addresses this root cause of aging within the next 10 years (unless you count THIS as the first paper, in which case... I'd be honored), and that... that will be the beginning of the 4th epoch of longevity.So, this is my take on the treatments, pills, therapies, processes, procedures, research and so on that will lead to a revolution in longevity.The short version to wrap this all up is: Given the roadmap I've laid out here and the progress we have already made - I THINK that we can get there.. Title by: John_Schlick Posted By: www.eurekaking.com

[dailytechnologynews]

The 4 Epochs of longevity

I have been studying Genomics for the last year, with a focus on longevity. I have come to the conclusion that there will be 4 distinct (although somewhat overlapping) epochs in the goal of living longer and healthier lives. I'd like to lay them out for you.

This is a long article, and the last epoch has the most to read because it's about research that hasn't even started yet, and I have to talk about the science we know today that will lead to that research. let me also be clear, that while this is based on letitimate research I have read, some of this is SPECULATION. Although in a conversation with the guy that runs the lab I am in the other day, he endorsed my speculation has having solid logical roots.

Epoch 1: Health Consciousness. This is the era that began as far back as we can imagine, and we are deeply into this today. This is the notion that (using the best current knowledge that) avoiding sugar, not smoking, eating well (more greens, more rawish foods, less processed stuff, less preservatives), not getting fat, and exercizing can all lead to longer healthier lives. This is undoubtably true. My local PBS station has shows that basically advertize programs (books, videos, you name it) detailing all the things you should do. This is at the rate of about one of these shows a week. I guess, as a species, we got serious about this when the surgeon general banned advertizing of cigarettes in 1970, and as time has passed, we have gotten more serious about it. Lets note, no matter how far forward we go with this process, these fundamental understandings of how NOT to abuse our bodies will always be good advice.

Now, an argument can be made that Mary-Claire King is singularly personally responsible for raising the average lifespan age by about 2 years worldwide based on her discovery of the BRCA1 gene - the breast cancer gene - allowing women to get screened and being able to largely avoid dying from breast cancer by knowing that they should get screened more often if they are at risk, and then getting treated early if something is detected. I believe this is true, and I mention it as a proxy for a whole host of life saving interventions (Seatbelts and airbags are two other technologies that are examples), but I don't see those as being DIRECTLY aimed at the issue of longevity, so... Even though that sort of thing is going on in the background, and they are all working in concert to increase the average lifespan, I am going to choose to not count them here. What DO I count then? Well...

Epoch 2. Longevity drugs. Starting as far back as 1999 (the earliest paper >I< have seen, though there are certainly earlier ones that I don't know about), specific drugs are mentioned as increasing healthspan, and that implies not dying from age related diseases, and that implies living longer.

A few people realize that we are in this epoch right now, and the awareness that we are in it is slowly dawning on the general public. I have 5 treatments that are the hallmarks of this age. 2 are diets and three are drugs. Buckle up, if you haven't heard about these they are becomming mainstream fairly quickly.

Lets start with the diets. It's long been known that Dietary Restriction leads to an increase in lifespan. If you knock off about %15 of the calories that you "need" on a daily basis, you tend to live about %20 longer. This, to a person living in the west, means living like a supermodel, and avoiding all those yummy calories - forever. And it turns out that very very very few people are willing to do that. So, a guy named Valter Longo said something genius: What is the minimum thing we can do to get the same effect as Dietary Restriction? He found that for a large number of reasons, fasting sporadically could accomplish that. There are some rules, During the fast, you can eat some things every day for minimum nutrition, but intake of calories is limited to 700 calories per day. Secondly, the fast has to be 5 days long, as you need your body to go into ketogenesis (where weak cells die and break apart and get flushed out of your body). Thirdly, you need to do this at least 7 times in a year for the longer term effects to show up. (These effects also include weight loss, and if you have pre-diabetic readings on some levels, those go back into the normal range). In fact, he was able to get FDA approval for this diet based on these pre-diabetic symptoms disapearing. An FDA approved diet. In this world of fad diets, this is a rarity.

Based on Valters work, I was told by a nutrition researcher at the Fred Hutch Cancer Research Center that someone said: Oh, this diet also has anti cancer benefits... What can we do thats the minimum possible that gives >those< benefits.... and based on that the 8/16 diet was born. Basically you eat normally for 8 hours a day, then you don't eat the rest of the time. Think about it... whats the job of a cancer cell? To grab nurients and replicate. But you have antibodies that go find cancer cells and tear them apart allowing those bits to get flushed from your body. (In fact it has been said that everyone has had cancer multiple times, it's just that the antibodies got rid of those cells before they could replicate. So? In that kind of war, if you don't eat for 16 hours a day, thats time for the antibodies to wipe these cells out when they aren't gathering nutrients and making more of themselves. It's about leveling the playing field. Seems legit to me. and if you don't die of cancer? That will certainly lead to a longer lifespan... right?

Moving on to the drugs: Rapamycin: This trug targets a gene called mTOR (want to know something funny? the TOR stands for Target Of Rapamycin). Now mTOr regulates a pretty well known metabolic pathway, so it turns out that rapamycin provides benefits in sort of the same way as Dietary Restriction. Lets note that there is a healthspan study in dogs at the University of Washington right now run by Dr. Matt Kaeberlein, but it's not in any clinical FDA trials for longevity even though it's FDA approved for transplant patients, but a number of scientists swear by it.

Metformin: This is an FDA approved drug used by diabetics. It works to lower the amount of sugar in the blood. It's milder in terms of effect than rapamycin, and it IS in human trials for healthspan improvement by the FDA at present. These trials are called TAME - Targeting Aging with Metformin. Again, a number of people swear by it.

NMN or NR. If you look at a cells energy cycle, cells burn ATP. The make ATP by breaking up sugar that enters the cell, and using some of the parts to make ATP. But they also make NAD+ out of other parts of the sugar - and later on the NAD+ also gets turned into ATP. Now, NMN and NR are chemicals that are along the pathway that cells use to make NAD+ so it's very easy for cells to use this same pathway to make extra NAD+ from a supplement that you take and that NAD+ is then later used to make more ATP. It's well known that NAD+ levels go down as people age... so it makes sense to try to boost those levels right? There have been a few human trials although none were FDA sponsored. There is really solid laboratory evidence in mice these two molecules work AMAZINGLY well, there are ongoing human trials right now, and there is loads of anecdotal evidence. There are also shenanigans about how it's made (enzymatically is FAR preferred to the solvent based manufaturing process), and there are a few lawsuits between some of the companies that sell one or the other as a supplement. But it's the big stick of the current crop of Epoch 2, and it looks like keeping energy levels in cells up helps them function well for a LOT longer.

Thats where we are today. There are a few drugs being tested, and in use by early adopters, and it looks very very promising. Where are we headed?

Epoch 3: Stem cells and senescent cell removal.

There are two breakthrus that will dramatically increase lifespan that are in the "actively being researched" but farther out than the drugs above which are already on the market.

Lets tackle stem cells first. These are basically skin cells turned into stem cells that get injected into problem areas, but since they can multiply and become any kind of cell, they can be used to repair damage from any number of age related maladies. Also stem cells tend to decrease with age, so this forced replacement of them can be a good thing if done right. There are stem cell therapies today (things like repairing severed neurons, restoring heart muscle after a stroke, and maybe helping to repair joint function, and on and on and on), none of them were specifically engineered with aging in mind, adn so like above, I won't dwell on them. But... you ask... why did I mention stem cells? Well, there are folks working on aging specific stem cell therapies. These longevity related stem cell therapies tend to be in the realm that uses genetically engineered stem cells. Repairing macular degeneration, and tissue regeneration are two that are on the radar. Lets talk about the first: It turns out that in the eye, there is a specific protein that builds up, that our bodies can't get rid of, but with a 1 base pair change to our dna, there is a protein that CAN get rid of it. So, we take a sample, make a few stem cells, then edit the dna of those stem cells so that they can clear this protein out of the eye, and grow a large number of them, and inject THOSE stem cells back into the eye. This is the macular degeneration fix. It is NOT here today, but there are labs that have done this in mice. This is the exact same approach that is being talked about for arterial plaque buildup. This first use is really indicative of a larger "category" of age related diseases where the body has built up some gunk outside of the cells over time, and it needs to get removed, but it never gets built up too much until after we have kids, so evolution doesn't see it as a problem. (Since evolution only cares about the genes we pass on, adn thats already done by the time this issue crops up.) We who want to live longer, clearly DO think that this is an issue. Since I mentioned them, for muscle regenation or nerve regeration, it's basically a genetically edited stem cell where the appropriate growth factor is somewhat overexpressed, injected into the correct tissue to stimulate faster or more growth thats wanted.

The first one of these stem cell therapies, if I have to guess is 5 to 7 years out since it is a new approach that the FDA has to approve. Thankfully they have approved stem cell therapies in the past, and they have approved genetic editing of single cells that get grown to a large number of cells in the past (the car-t lukemia treatment that got approved as of december 2017), so with the fundamental approaches being known it probably won't take them a full decade for us to start to see these uses for stem cells.

Senescent cells. Also on the "getting rid of what we don't want vein". It turns out that all cells start as a stem cell then divide into a stem cell and a differentiated cell - one that has a specific function. Senescent cells are those that are doing their differntiated job but getting old (and probably starting to be bad at their job), and refusing to die.. They are just a hangin around. Now, the body knows how to handle small scale damage (As a single example - there is a signal called PDGF Platelet Derived Growth Factor) that some cells excrete as they die telling stem cells in the area that someone is gone, and maybe another cell is needed...) So, IF we can get weak differentiated senescent cells to die we can force nearby stem cells to divide and get a fresh cell thats new and NOT bad at it's job to take the place of the senescent cell. Turns out that Hydrogen sulfide (present in garlic) is a good chemical to trigger weak sensecent cells to die. But there are issues getting it to the right cells, not having it be toxic, and any number of other issues. There are folks that have done work in mice that shows DRAMATIC improvement of healthspan, and restoration of many weakened body functions due to "age" when senescent cells are removed. There are no human trials yet, but be sure that once there is a senescent cell removal therapy, you will want to go get it.

I espect this to come about (given the state of research and published papers) within the next decade. These two technologies will make for a HUGE leap forward in both quality of life and longevity.

And if this is going to make things so much better, what could possible be epoch 4?

Epoch 4, Epigentic resetting.

This is where I extrapolate the future. If I am going to tell you what treatments are coming next, I think it's important to start with the ROOT CAUSE of aging - all the treatments above are treatments for first order effects - symptoms if you will - how do you better fix things after something has gone wrong. I want to talk about how we will be able to prevent things from going wrong in the first place inside your cells. It turns out that there might be a few things that cause aging, but far and away the most important of them is cellular disregulation. Think about this... We have a system that regulates what genes are on, and which ones are off, and how much of each gene is expressed. It's called the epigenetic system. I'll describe how it works in slightly more detail a bit later. For now, imagine that over time, the epigenetic system "degrades". And we have about 20,000 genes that do different things, and the DNA for each of those is in every cell in the body. Think about what might happen if a cell that makes light receiver in your eye gets turned on in a cell in your heart. Having to make those extra proteins will take some of the ATP that it takes to beat that heart cell - and having that protein present in the cell might interfere with other things in the cell - and this is one singular example. At the point that enough cells in your skin degrade, it will get saggy, at the point that enough muscle cells stop working right your muscles degrade, etc, etc, etc. In short aging. Now, I am not the first person to say that cellular disregulation is the most important thing, a number of people think that this is THE biggest problem we need to solve, and the entire field is slowly shifting to this point of view.

Ok, if thats the biggest problem... what causes the epigenome to "degrade"? Again, there are a number of causes, but right now the evidence points to "double stranded DNA breaks" being far and away the most important cause. Thats right double stranded DNA breaks. What? We have proteins that repair those right? Yes. But... There are side effects. It turns out that Dr. David Sinclair did an experiment with mice that doubled the double standed DNA break rate in very specific places on the genome of a mouse. He performed this experiment over the span of a year, and at the end, compared it to a litter mate, and yes, the DNA break mouse looked very elderly compared to it's one year old bretherin that was in the prime of it's life (mice live about 2 years, so testing aging in mice this way is fair game.) The takeaway of that experiment is that double stranded DNA breaks mess with the epigenome and that... causes aging.

OK, I've mentioned the epigenome a few times now, I'd better give a little bit more depth on it. Let me start with a statistic: We think we maybe understand the function of %90 of the DNA we have (I can justify this if needed) - but we maybe only understand %50 of what there is to be learned from the DNA we have. Compared to this, we understand only about %5 of the big picture of what there is to be learned about the epigenome. Let me give you a big picture overview of the basics: What we do know is that there are two main mechanisms at play. The way that genes are turned on or off (or regulated up and down like a volume control knob) is by that DNA being accessable to the proteins that make RNA copies of it. The first mechanism: On the outside of your DNA, almost as an annotation system we get "methylation", and in most cases, if you methylate something that gene turns off - think about it, the protein that wants to make a copy comes along and oops, it's blocked from getting to the DNA it wants by a methyl group, so... no copy is made. This is kind of the on off switch. The second mechanism is way way way more complicated (it's more the volume control knob). We have 2 meters of dna if you stretch it out. Thats a lot. Imagine it being a ball of yarn stuffed into the neucleus of a cell, how do you find anything? Well... in that scenario, you can't... but we have evolved "histones", and the dna wraps around them, and gets all coiled up. Lots of histones which allow everything to be wrapped up neatly and predictably. Now, histones have certain tails of amino acids hanging off the side that things can bind to. DNA has a very slight positive charge. And methyl groups have a very slight positive charge... and acetyl groups have a very slight negative charge. So... imagine adding a methyl group, and the two positives charges push each other away, meaning the dna wraps less tightly around the histone, meaning it's slightly MORE available to be transcribed, and acetyl groups help to wrap the DNA more tightly and turn down transcription. And now, let me blow your mind... there are about 200 different epigenetic markers that have been discovered, and people are working feverishly to decipher and understand and map them all. It's my understanding that DNA methylation has the largest "control authority" over gene expression so lets talk only about that.

It's clear that if the epigenome gets messed up by double standed DNA breaks that the implication is that the proteins that go to the break and repair it also knock some methyl groups off, or add some extra ones as they do their job - it appears that in certain areas of the genome it's more "add" and in other areas it's more "remove", but with age, gene expression TENDS to drop (meaning more methylation). Now the damage (extra methylation) appears to be somewhat random. Today noone knows the exact mechanism that causes this damage - so if you are looking for a PHD project? This is a really solid one to take on.

But what we DO know, is that there is a specific profile of DNA methylation that seems to be present at varying ages - certain important points on the genome either have it or don't. And as you age, other IMPORTANT points get methylated. This work was done by Horvath and Hanuum in about 2013 when they published separate papers on the "DNA methylation clock". There are 400ish sites that get methylated, and which of those sites is currently methylated can be used to determine your age (barring radiation, obesity, or smoking exposure) to within a few years. In fact, this clock is accurate enough that one european government is using it to determine the age of refugees who have no documentation (to determine if they are over or under 18 years old as the law has different rules for the two groups.) The method gives you an answer at the age of 18 thats within 2 years, and previously they called in dentists to look at wisdom teeth and got answers that were within 5 years. Even though this is a new technology, and it has so much room for improvement, it is already better than the old methods of determining age. (scary right?)

So, now you know what causes aging! Double stranded DNA breaks cause DNA methylation to increase messing up gene regulation. it's SO SIMPLE, RIGHT? Here is a paper with a bit more depth to it that explains what I just did again with diagrams and definitions, and way more detail: http://www.longlonglife.org/en/transhumanism-longevity/aging/epigenetic-aging-longevity/epigenetic-alterations-as-a-cause-of-aging/

So whats coming? Here is where I make my specualtive prediction: We will take every cell in your body and RESET the epigenome.

WHAT? How the hell is that possible?!? Well... if we look to biology for answers, how does the methylation on your DNA get there in the first place? We have an enzyme called DNA methyltransferase (actually there are alot of them that do this kind of thing), and there are other mechanisms that remove methylation.

You have all heard of CRISPR right? CRISPR is a combination of two things. First is the Cas9 gene that likes to cut DNA, and second is a peice of RNA that guides the Cas9 gene to the place it's needed to do that cutting. WAIT!!! Cutting DNA? Thats bad, right? Yes, but...

As of 2016 some scientists in China (Shawn Liu and Xuebing Wu, and others) developed a version of CRISPR where they took off the part that cuts DNA, and added on a part that demethylates DNA, and you can buy this off the shelf now.

So, all you need to do (hahaha, as if this really is easy, right?) All you need to do is to identify all the places that need to be demethylated, build the correct guide RNA, and deliver a cas9-dna-demethyltransferase along with the guide RNA into every cell in your body, and voila! No more cellular disregulation. And at that point the cell will behave normally, and it won't become senescent, or die, or misbehave in any way.

As part of identifying those genes that need to be reset? Lets talk for a moment about how we might do that. Remember the Hanuum clock? %10 of the methylation marks are in a gene called KLF14 which is a master regulator of metabolism and obesity. (I'll also note that one of the stem cell creation factors - Klf4 - is a brother protein to this). It strikes me that a lot of the drugs mentioned earlier focus on metabolism related things, so pointing at this gene seems to pass the smell test.

My bet is thats it's not a bad gene to start with, and resetting it might show some mild improvement in lifespan. But more likely, doing this will backfire as the gene regulation system is ridiculously complicated, and so I think that to get ANY effect we may need to reset a dozen or so genes, and to get the DESIRED true longevity effect, we may need to reset somewhere between 200 and 500 genes. and all I've talked about is the methylation. Remember there are 200 or more epigenetic marks to take into account and decipher.

And then there is the issue of delivering this drug to every cell in the body. We use viral vectors to do this today in gene therapy, and so some of this delivery part is available, but... it's expensive today, and as a technology, it too is in it's infancy.

And now, just to make sure that you understand the hieghts of the smooth granite mountain peaks you are about to free climb... there are 240 or so tissue types that are tracked today, thats clearly not all of them, and each tissue type is likely to have it's own set of genes that need specific "settings", and since the viruses used to deliver gene therapy products are usually attracted to very specific tissue types, we will need at least that many viral variants to deliver these specialized cocktails to those cells... Trivial, right?

So, I think we CAN fix our gene regulation, and our first attempt, with limited understanding and maybe a dozen genes, we can make some headway, and herald it as a major breakthru, but 10 or 20 years later when we REALLY understand what we are doing? These postulated first efforts will seem like the dark ages where we drilled holes in the skull to "let the demons out".

When will this happen? All the tools are there, heck, I've even identified an initial gene as a possible target. All it takes is someone to fund the study in a lab. Are we at the point where most funders see this as the next logical step? From what I know today? No they do not. This means we will need at least 5 more years of epigenetic mapping and research and refinements to the clock and understanding gene regulation pathways, and more importantly progress into the second and third epohs listed above to show that logevity is actually achievable, and and and... and then we can see some early results for a version 1 that mitigates aging in elderly folks who have gene disregulation, and once reset they get healthier. (the fact that they will live longer, thats not what the FDA will focus on - they will want to see folks with a better metabolism, with more muscle tone, etc, etc, etc, things they can measure NOW.)

So, when will this happen? I think we may see the first scientific paper that addresses this root cause of aging within the next 10 years (unless you count THIS as the first paper, in which case... I'd be honored), and that... that will be the beginning of the 4th epoch of longevity.

So, this is my take on the treatments, pills, therapies, processes, procedures, research and so on that will lead to a revolution in longevity.

The short version to wrap this all up is: Given the roadmap I've laid out here and the progress we have already made - I THINK that we can get there.

[addictionfreedom]

Cocaine Plant For Sale

Contents

Been genetically modified

44 alcohol and drug

Chile and argentina

Sees many who get treatment wind

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The post Cocaine Plant For Sale appeared first on Freedom From Addiction II.

[kansascityhappenings]

Joe’s Weather Blog: We’re going to need a bigger shovel-maybe (WED-2/13)

Happy Wednesday! The good news is that we’ve got a breezy and milder day heading this way with highs into the 50s. Get out…enjoy it…do whatever…but get out of the house because regardless of how much snow we get from these systems that are coming through over the next week…it’s going to get cold. Thursday will be the transition day…and we’re into the cold on Friday with alternating snow chances and sticking snow likely. As I mentioned yesterday we won’t get blasted by the full-on effects of each potential storm but at least one get us…and the one that I’m most concerned about at this point is the one for Friday afternoon>evening.

Forecast:

Today: Lots of high clouds around…turning windy in the afternoon with highs 50-55° or so. Winds possibly gusting to near 30 MPH

Tonight: Milder with fair skies and lows well into the 30s

Thursday: A cold front will move through with variable clouds. The timing of the front appears to be near or after lunch. Highs may reach about 50° (colder north>warmer south) before dropping into the 20s in the evening with teens as wind chills.

Friday: Snow developing with accumulations likely. Highs 20-25°

Discussion:

First of all…as usual thanks for reading the weather blog. Yesterday it was the #1 item on our web page which is always humbling. It still amazes me the comments on FB I get about this “outlet” for me. So many mention that they learn about the weather and like the whys and whatfors about these storms…set-ups…whatever. A darn weather blog. Still amazes me.

Onwards.

Won’t bother with today or tomorrow as that is pretty straight-forward. The issue for Thursday is when the cold air is injected into KC from the north. My thought is sometime around or after lunch with the 50° weather turning into 30° weather by the time evening rush is done with…and colder with the wind chills.  There could be a few sprinkles with this but not much is expected rain-wise.

OK now the elephant in the room. I think by now everybody knows about the snow potential over the next week. 3 storms through next Wednesday. As I mentioned yesterday I’m not in the mindset that ALL three give us crazy amounts of snow. Last night there was a rather significant change, in at least one model, for the weekend system and the one next TUE>WED.

So to try and simplify things…let’s refer to Friday’s system as storm #1…Saturday night’s system as storm #2 and then the TUE>WED AM system as storm #3. I still worry that we may be vulnerable to other “things” beyond that but IF I start talking about that possibility I’ll need security guards in the grocery store (kidding not kidding)

So my confidence level about the 3 storms is “somewhat” strongest for what’s ahead of us…storm #1. Storm #2 and #2 I have less confidence about…especially #3 at this point because…well it’s about a week away. Storm #2 is somewhat problematic as well…I think we’ll get something from that…but I’m not sure if we get the “big one” from that.

Then there is storm #1 (the one due in Friday).

I want to show you some of the data from the newest weather satellite that became “operational” just yesterday. It’s the GOES 17 satellite that is more focused on the western part of the country and the central and eastern Pacific Ocean.

  Pretty shots…but there are issues with the satellite. There are some problems with the equipment up there and in particular with a cooling fan. Remember this satellite is way up there…some 22,000 miles up…the Space Station is 254 miles up…so it’s not as if we can send maintenance up there. They’ve come up with some workarounds, which is still amazing to me for something that is orbiting the Earth and so far away…but for several hours each day during certain times of the year when the sun heats up the satellite too much…pictures won’t be usable. Regardless there is still a LOT of good data coming down the pipeline towards us.

So with that said…Storm #1 is still off the western US…off the coast of CA.

It’s that mass of clouds on the far right hand side…hopefully when daylight comes the US borders will become more evident.

That storm right now at least is in a few pieces (yellow flag in my mind) and when it comes ashore in CA tomorrow afternoon and crosses into the Rockies Friday morning…we’ll see what kind of shape it’s in.

That yellow flag is one of the problems I have with this set-up right now. The storm is going to be a fast mover it appears when it gets into the Plains and I’m still not sure how well put together it’s going to be when it flies through KS on Friday afternoon. Let’s go up to about 18,000 feet and show you the 3 storms. The one is KS is storm #1. The map shows areas of “vorticity”. These areas are where the atmosphere shows cyclonic tendencies and ahead of these features you  get “lift” (good for precipitation) and behind the features you get sinking air (good for clearing). These areas have varying intensity…big storms generate lots of lift…weaker ones…less lift.

Here is wayyyy more information than you want to know about the above map.

So the rough idea of a “transition zone” between rising air…lift…and sinking air…is the axis location of the “U” dips in the above map. With me so far? Notice as well the size of the “U” dip. For storm #1 it’s not overly “dippy” compared to storm #2…do you see that.

Less “dippy” storms tend to move fast. So the time that we’re in the “favorable” zone of lift is shorter than when the dips are deeper in size. Still with me?

Now that is up there at around 18,000 feet. We have to look at the entire atmosphere though as well. That smaller dip will be bringing some decent moisture with it and tapping into some sub-tropical moisture coming up from western TX…and that moisture will be one of the keys for us to get significant snow. IF that moisture isn’t as impressive or it gets pushed a bit farther east or south of here…we may NOT have a big snowstorm in KC on Friday. Nuisance snows yes…I think that’s unavoidable at this point (nuisance meaning 1-4″ or so) …it could be a sign that the wave is moving too fast or isn’t strong enough and this has to be at least looked at right now and NOT discounted at this point.

Then there is the matter of a building southwards area of high pressure…this is the cold air maker for us…BUT it’s also a dry air maker too. So the feed in the lower part of the atmosphere is of drier air…and that too can chew on what falls for awhile. Too much dry air and decent snowmakers can turn into blah snow makers. I may be making too much of a deal on this BUT it’s in the back of my mind as well.

Right now I think the odds of all this happening and ALL of this just turning into a “nuisance event” is around 55% and 55% should NOT be discounted at this point.

If you want something more significant (meaning in my weather head…4″ or more) you would like to see that moisture source be 1) real and 2) have that wave a bit more focused and “sharper”. That helps maximize the lift a bit more…that lift then works in concert with the moisture coming northbound…and as a result you get more impressive swaths of snow moving through the area.

There are some so-so favorable jet stream dynamics at play with this as well…for conciseness I won’t get into that right now. Not the greatest set-up and I’ve seen better over the years.

The new data slows the onset of sticking snow to the afternoon Friday. That makes sense and I can see how the dry air flow from the north is sort of working against the snow as it tries to come eastbound. However I also see how the snow out west is coming together better later in the morning and that snow would then come along the I-70 corridor in the afternoon…the issue remains how well it holds together as it comes eastbound along I-70.

You can see the conundrum. Dry air…sort of a disjointed broken up wave moving through the Plains…lift in the atmosphere that isn’t exactly super focused and a snow window that may be only around 6-8 hours or so…and some of that may be chewed on by the dry air.

This is the reason why we want to hold off on how much snow will fall from this. I know many are seeing all sorts of numbers on their various apps and with other sources…last night I mentioned that there was potential of over 4″ on Friday. That is still there certainly BUT I’m not sure how much over 4″ we will get at this point and that’s why I don’t want to do any snow maps yet with more precise information.

Trust me I know you want all the answers but for those who DON”T want a ton of snow…consider the early data today a better trend for your side. I don’t want to throw a 4-8″ amount out there at this point because my confidence isn’t there for something like that right now. The dry air scenario chewing at the snow because the wave coming in is sort of a mess needs to be factored into the equation. IF that dry air is “less” dry and IF the wave is better put together then yes over 4″ is VERY doable…again though lets try as we can to keep the horses in the barn for a bit longer.

There is still all sorts of potential with these 3 storms…and I won’t be surprised by some significant snow on the ground in a weeks time but let’s try and deal with them one at a time.

Takeaways from this…

Snow arrives after lunch Friday and sticks right away

The evening rush hour may be a mess

A LOT of schools are NOT in session anyway because of in-service conference days ahead of the 3 day weekend anyway

The dry air seeping southwards may “chew” on the snow as it comes eastbound

The wave needs to be better organized with more focus to tap into the moisture trying to come northwards and also to act as a better “tug” on that moisture

The weekend system bears some watching as well as does the one next week. Still WAYYYY to early to worry about forecast accumulations with that one.

OK that’s it for now. I’ll get an afternoon update out on FB by 3PM or so.

Our feature photo comes from ‎Sharon Griff Holloway‎ outside of Trenton, MO

Michelle and Karli will have more information as the day moves long on FOX 4.

Joe

    from FOX 4 Kansas City WDAF-TV | News, Weather, Sports https://fox4kc.com/2019/02/13/joes-weather-blog-were-going-to-need-a-bigger-shovel-maybe-wed-2-13/

from Kansas City Happenings https://kansascityhappenings.wordpress.com/2019/02/13/joes-weather-blog-were-going-to-need-a-bigger-shovel-maybe-wed-2-13/