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Making Life More Affordable for Families
It's been another busy week on the campaign trail. In between canvasses, I've attended a number of meetings, including one with parents and teachers from...April 29, 2018
Five Priorities, 47 Days To Go
The weather is warming up and so is our campaign here in Eglinton-Lawrence. I've just come back from door-knocking with a group of PC...April 25, 2018
The campaign is underway
Despite the horrible weather on the weekend, our campaign office opening was a resounding success. At 3:00 PM yesterday, our campaign office was full...April 21, 2018
Spring Greetings
This weekend, as we experience the first few days of spring, Jews and Christians will mark important days in their respective faiths.April 02, 2018


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Categories: Fruit Tree
It originated in the orchard of S. Lyman, Manchester, Connecticut, and was recorded in 1834. Large in size, and rectangular to truncate-conic in shape, with distinct ribs, the yellow skin is marbled with a greenish-yellow, and usually has a brown flush. There is scarfskin over much of the surface.
The yellow flesh is firm and crisp with a sweet flavor. Suitable for baking, frying, preserving or dessert. Often used for apple butter making. Sometimes, this variety was also stewed with quince. It is highly productive, but bears biennially, and the fruit ripens unevenly and tends to watercore. It ripens in September.
We do NOT SHIP plants. ALL Sales are in person at our garden center.

subset: commoncrawl


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Hewlett-Packard Co., the world's largest personal-computer maker, confirmed its decision to spin off its PC business and even more shocking: it is going to "discontinue operations for webOS devices". In other words, this is the end of the line for its just-launched tablet, the HP TouchPad as well as for its smartphones that challenged Apple Inc.'s iPad and iPhone. This is a drastic change from past strategies and it will undo the famous HP-Compaq merger that was engineered by then-CEO Carly Fiorina a decade ago.
At the same time HP announced its spinoff plan, it agreed to buy U.K. software firm Autonomy Corp. for about $10.25 billion, seeking to move further into the higher-profit business of analyzing data for corporations. This plan also marks the second time the company has looked to divest a core business to keep up with the changing tech industry. Just to remind that in 1999 HP spun off its measurement-device unit-which included technologies that were the genesis of the company and core to its success-into a firm known as Agilent Technologies Inc.
The main reason for Leo Apotheker, HP Chief Executive since November, to consider the decision of getting out of the computer business the best possible choice, are the low margins and low growth in PC business the company is facing. Mr. Apotheker strongly believes that the company can invest its capital in better places in order to improve its overall profit margins, even though it may cut the company's revenue by roughly a third. His goal is to reposition HP into an enterprise business and move away from consumer products. Over the past few month it became clear that the only way Mr. Apotheker to achieve this goal is to add software products for business and to find a way to get rid of the company's PC arm and use the cash to buy into these new areas.
Website design and development| London
Tags: business, E-commerce Development, hp, Web Design and Development Company, Web Design and Development London, web design london, web development london


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by: Sonic
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- This event has passed.
Messages from Heaven with Medium Hope Taylor
April 13 @ 6:30 pm - 8:00 pm
Location: Hilton Garden Inn, Allentown Bethlehem Airport, 1787-B Allentown, PA 18109
Date: 4/13/20
Time: 6:30pm-8pm
Cost: $45 online or $55 cash only at the door
Group events are healing for all who are present. If you have been missing a passed loved one please join Evidential Medium Hope Taylor as she validates your loved ones with evidence, personality, memories and messages of love.
Hope will provide as many connections and messages as possible. Although all attendees are not guaranteed a personal reading during this event, there is so much comfort in knowing that all of our passed loved ones are present as Hope delivers evidence and messages to those read.
Must be 16 to Attend.
Are you kidding me… Hope is incredible and so are her abilities as a medium. Most recently, she was able to connect with a family member that I actually never met but gave me so much info/validation that I was able to in fact validate that it was him. She has such a calming & positive energy and what a gift—can't say it enough. Thank you Hope 🙌🏼🤟🏼🙏🏼💪🏼 -Ashley Kissinger
Hope shared her wisdom, along with messages from lost loved ones, giving me comfort, knowing they are with me; confidence I will get through difficult times; and courage to trust my intuition. The concrete, specific images she shared dispelled any cynicism I held, and her authenticity was evident. A more than worthwhile experience. Thank you, Hope! -Ruthanne Herzing
Five Stars. Hope is a tremendously gifted medium and a lovely and loving human being. She quickly connected me to my lost loved one and gave me information and messages that no one could ever know without a direct connection to him. After my private session with her, I was able to connect with him directly myself. And I was also able to re-tap into my own spiritual and psychic gifts, that I have been allowing to stay dormant for too long. Her name describes her perfectly…Hope. Thank you for everything you do, and everything you are…a precious gift to so many of us. Much love to you, dear Hope. -Kara Suzanne
Find more about Hope WWW.HOPETAYLORMEDIUM.COM
For legal reasons we must inform you that this demonstration is for entertainment purposes only, and is at no time a substitution for professional services. Should you receive a reading, Hope Taylor assumes no responsibility for what you chose to do with the information provided, as the information is subject to personal interpretation. At no point should the information provided be a substitution for medical, financial, legal, or psychological services.


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Beginners and experts alike should always be learning the latest information related to buying real estate to stay on top of their game. If so, then you have come to the right place. The following tips will help you buy a great property without getting ripped off.
Be moderate in your real estate negotiations. Some people feel as though they should be aggressive in order to get the best price; this can backfire on them. You can have a firm idea of what you want to pay, but let the Realtor and lawyers have some leeway.
If you have or are planning on having kids, you should look at homes that will have enough room for your family. Not only is space important, but so is safety. Things like bad wiring, steps, a pool, and other potential hazards need to be looked at. If you buy a house from a family who has raised their children in it, it should ensure that the house is relatively safe.
Generally, properties that are in need of multiple upgrades or repairs carry a lower price tag. This will let you save some money in the beginning, and fix up the house as you see fit. You can not only redesign the home over time, but the modifications you are making build equity you can trade on later. It is important to look at the positive potential in the home rather than the drawbacks. Your perfect new home could be hidden behind superficial drawbacks like bad paint or cracked paneling.
When you decide to purchase a new house, look at the long term potential. While you might not have kids currently, for instance, it's a good idea to check into the local schools near a potential house if you are planning to have children down the road.
See if your real estate agent has a home-buying checklist. Many Realtors have checkoff lists available that include all steps of home-buying, including finding the perfect house and mortgage procedures. Having a list like this can be invaluable in coordinating everything to coincide with closing day.
Prior to purchasing any real estate, you first need to have a firm understanding of what a mortgage loan is and its many terms and conditions. It is essential that you know exactly how much you will be paying every month and what the total cost of the loan over the entire length of the mortgage will amount to.
You are already aware of an asking price on a potential home, but you should also have your offer firmly in mind. Your real estate agent can help you negotiate a good deal that satisfies everyone's needs.
Ask the seller of the home to help with the closing costs before making an offer. You can often "buy down" an interest rate, in which the seller pays to lower your interest rate for some time in the beginning. Adding financial incentives to your offer will make the seller more likely to stick to the selling price.
As you can see from the above list of tips, buying real estate can be a bit daunting when you first start, but applying a bit of common sense and doing your research can put you ahead of the game. Using the tips in this article can help you become a smart property purchaser.


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Company Details
Jiangsu QiSheng Cable Co., Ltd.
Weak cables refer to cables used for security communications, electrical equipment, and related weak current transmission applications.
Wire and cable refers to materials used for power, communications, and related transmission purposes. "Wire" and "cable" do not have strict boundaries. Usually, the product with a small number of cores, a small product diameter, and a simple structure is called a wire. A wire without insulation is called a bare wire. Others are called cables. A conductor with a larger cross-sectional area (greater than 6 mm2) is called a large wire. Small (less than or equal to 6 mm2) is called a small wire, and an insulated wire is also called a cloth wire.
Wire and cable include bare wires, electromagnetic wires and insulated wires for electrical appliances, power cables, communication cables and optical cables.


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6 Day Chimps in Kibale, Gorillas in Bwindi and Wildlife Game viewing
Trek Gorilla Safaris connects discerning travelers with top best travel agents who compete to customize your luxury trips. You get:
- Quality service at best value
- Authentic travel experiences
- Expert destination advice
6 Day Chimps in Kibale, Gorillas in Bwindi and Wildlife Game viewing
Tour Route: Kampala – Kibale – Queen – Bwindi – Kampala
On the 6 Days Chimps in Kibale & Wildlife Safari, you get to hang out with habituated chimpanzees in Kibale Forest National Park then later follow this Uganda Safaris route to Queen Elizabeth National Park to explore the savannah wildlife safari action in the grasslands. Chimpanzee tracking is a good alternative to the pricy mountain gorilla trekking in Bwindi.
The Chimps in Kibale Safari route can be customised to fit your trip plans and budget. Also, this Uganda safari trip can leave anytime with any number of people. The chimps tracking permit, accommodation and transport are included in the quoted price of the package.
Safari Highlights
- The thrill of tracking the wild but habituated chimps in Kibale and other primates in their natural environment
- A guided nature walk in the Bigodi Wetland Sanctuary for birding and primate viewing
- An opportunity to explore the beautiful crater lakes surrounded by gentle hills and stunning views
- Sightings of the carpets of green tea plantations and long horned cattle
- Enjoying game drives in Queen Elizabeth National Park and a boat cruise on the Kazinga Channel.
- The thrill of a game-walking safari and canoe ride at Lake Mburo National Park
- An opportunity to stand in two hemispheres at the Equator for memorable photos.
Day 1: Travel to Kibale Forest National Park, Bigodi swamp walk
You will depart from Kampala after breakfast and head westwards to Fort Portal town. The drive will take about 4 -5 hours. You will have lunch in Fort Portal and continue to Kibale. In the afternoon we visit a nearby forest swamp that is excellent for viewing primates and other forest animals. At the Eastern edge of Kibale forest is Bigodi Wetland sanctuary which is maintained by the local community. You will expect birds like the great Blue turaco, blue monkeys, baboons, otters, mongoose, bush bucks, bush pigs and among others. Dinner and overnight will be at your reserved lodge.
Day 2: Chimp tracking and transfer to Queen Elizabeth
After breakfast, you will report to at the Kanyanchu Tourist Centre at 08.00 am for a briefing before tracking the chimpanzees. The forest is only accessible on foot and the walk will provide you with the opportunity to see a variety of other primates and animals as well as birds, and a variety of butterflies and other insects. You will return to the lodge for lunch and in the afternoon you will transfer to Queen Elizabeth National Park. You will have dinner and overnight at your lodge.
Day 3: Game drive and boat cruise in Queen Elizabeth National Park
After your morning breakfast, you will have an early morning Wildlife safari Game drive where you will see the lion, leopard, giant forest hog, Cape buffalo, elephant, defassa waterbuck, Uganda Kob, topi and bushbuck among others. You will return to your lodge for lunch and in the afternoon go for a 2-hour boat cruise on the Kazinga Channel. It is a 42km channel that joins Lake Edward and Lake George. This trip passes through possibly the highest concentration of hippos and offers an excellent platform for photography, bird watching and game viewing. The prolific bird life is colorful, with well over 550 resident species.
Dinner and overnight will be spent at your reserved lodge.
Day 4: Game drive in Ishasha and transfer to Bwindi
After breakfast, you will be transferred to Bwindi via the Ishasha sector with a 2-3 hour game drive in Ishasha sector in search for the tree climbing lions. Expect to see other animal species such as the warthogs, leopard, spotted hyena and birds. After, then you will transfer to Bwindi Impenetrable forest. Dinner and overnight will be at your lodge of booking.
Day 5: Gorilla Trekking (Bwindi Impenetrable NP), and Batwa Experience
Today enjoy surely. After breakfast, proceed for the morning briefing before enjoying the highlight of the trip- Gorilla trekking, which may last the entire day. We trek through the rainforest and bamboo covered slopes, accompanied by a guide and trackers, in search of a mountain gorilla family. The walking can sometimes be tough and long, but when you catch a glimpse of the magnificent silverback, any discomforts will be quickly forgotten. When sighted, visitors will be guided to within 6 metres from the gorillas, sit around them for a whole hour while gazing into their big round eyes. Gorilla trekking is unpredictable. It's difficult to foresee how many hours you will hike. The gorilla excursion can take from 2 up to 8 hours. Expect to walk along distance in steep and muddy conditions, sometimes with rain overhead, before you encounter any gorillas. A good physical condition is recommended. For conservation purposes, time spent with the gorillas is limited to one hour. A ranger will brief you on how to behave with the gorillas. Time allowing you will go for a guided community walk to experience the livelihoods of the local communities. As planned, you take on the gorilla trekking Bwindi route to visit a traditional herbalist to see how he prepares native medicine to treat a wide array of human ailments, see a black smith manufacturing local tools used in everyday life and see how local beer is brewed using local methods. You will also be entertained by the traditional dances offered by the community. Dinner and overnight will be at your lodge of booking.
Day 6: Travel to Kampala with stopover at the Equator
You will after breakfast go for another game drive before setting off your last chimps in Kibale safari last hours on your return journey to Kampala. You will have a stopover at the Equator where you will have the remarkable opportunity of standing in two hemispheres at the same time and take some photos. You will also make another stopover at the Mpigi Royal Drum Makers centre where you will be able to watch the ceremonial drums being crafted using traditional methods passed down through the generations.
You will arrive in Kampala in the late afternoon and either be transferred to the airport for your departure flight or to the hotel of your booking for dinner and overnight.
The safari package includes:
- Transportation by a 4 x 4 station wagon
- Full board accommodation as per the above itinerary
- Park entrance fees
- Chimp tracking permit
- English speaking driver/guide
- En-route Meals
The safari package excludes air ticket, personal travel insurance, visa fees, drinks, cigarettes, tips, souvenirs and any other items of a personal nature.
Gorilla Viewing: Gorilla trekking can take place at any time of year with April/May and November being wetter. However, be aware that rain occurs all year round. For general game viewing safaris, the best time to go is during the dry season (between June and September).


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Autism and Neurodiversity
JKP is the leading publisher in autism and related conditions, publishing authoritative and practical books for professionals, parents, children, and anyone whose life is touched by autism. Our books cover a range of topics including communication and development, relationships and social skills, teaching and assessment, parenting strategies and overcoming depression and anxiety.
Bestselling authors include Tony Attwood, Jennifer Cook O'Toole, Carol Gray, Luke Jackson and Donna Williams.
Children, Youth and Adults with Asperger Syndrome
Integrating Multiple Perspectives
Kevin Stoddart, Rosina G. Schnurr, M. Mary Konstantareas, Barbara Muskat, Trina Epstein, Jennifer Sa... - 2004
This book offers a comprehensive overview of clinical, research and pe...$36.95
Autism, Brain, and Environment
Richard Lathe - 2006
In this controversial new book, Lathe contends that the recent rise in...$34.95
All Cats Have Asperger Syndrome
Kathy Hoopmann - 2006
This book takes a playful look at Asperger Syndrome, drawing inspirati...$14.95
The Imprinted Brain
How Genes Set the Balance Between Autism and Psychosis
Christopher Badcock - 2009
Badcock sets out a radical new theory of the mind based on the recent ...$29.95
An A-Z of Genetic Factors in Autism
A Handbook for Professionals
Kenneth Aitken - 2010
This volume explains the biology and genetics of ASD, and provides cli...$125.00
Inside Asperger's Looking Out
Kathy Hoopmann - 2012
Following in the best-selling footsteps of Kathy Hoopmann's All Cats H...$14.95
Autism Spectrum Disorders Through the Life Span
Digby Tantam - 2012
This book contains the latest research on assessment, diagnosis, treat...$49.95
The Obsessive Joy of Autism
Julia Bascom - 2015
Julia Bascom offers a rare and powerful insight into the joys of autis...$15.95
All Cats Are on the Autism Spectrum
Kathy Hoopmann - Oct 2020
Brand new update to the bestselling All Cats Have Asperger Syndrome, w...$15.95


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New Delhi, Jan 18 (PTI) Handset maker Tecno today said it aims to double its pace of growth in the hyper-competitive Indian smartphone market, bringing in devices with features like full-view display and enhanced camera capabilities.
Tecno -- which is a part of Transsion Holdings -- had entered the Indian market last year and introduced a slew of smartphones in the offline market.
"Last year was more of a testing phase for us and now we are geared up for the Indian market. In 2017, we will bring to customers devices packed with features including full-view display (18:9 display) and camera functionalities," Transsion Holdings Vice President Lin Qin told PTI.
He added that the company is looking at cornering a spot in the top five smartphone tally for handsets sold in the Rs 7,000-15,000 category in the Indian offline retail market.
"India is a big and important market for us. We are looking at doubling our growth this year," he said.
Tecno today launched a new handset, Camon i, which will start selling in the first week of February, priced at Rs 8,990.
It features 5.6-inch display, 1.3GHz quad core processor, 3GB RAM, 32GB inbuilt-memory, 13MP rear and front camera, and 3050 mAh battery.
The Indian handset market is one of the fastest growing markets globally and is dominated by players including Samsung, Xiaomi, Lenovo, Oppo and Vivo. PTI SR SBT


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Ego is identification with form. Form includes not just the body and physical forms, but also thought forms and mind constructs. This extends to your 'story' which is a thought form about your past which you may take to be who you are. Who you actually are is formless. Who you actually are is the observer behind the thought form. Think for a minute about the fact that you can observe your thoughts. If you are your thoughts, how would you be able to step outside of them and observe them? The one who is doing that observation is you. The thoughts are not you. Elizabeth Gilbert in her book "eat, pray, love" mentions at one point that after she underwent her spiritual transformation, she began to think of her thoughts as 'noisy neighbors.' These neighbors are not you. They are forms which are temporary, they come into form and out of form and they only linger when you allow them to. When you can get to a point where you are able to observe your thought forms, rather than be caught up in the endless stream of the babble inside your head, that is where you begin to let go of Ego and find your true self and your true source of power.
Related articles
- Ego-Tripping (namasteallday.com)


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Arlington rapper and hip-hop artist Hovey Benjamin released his most recent video, Sweet Sixteen, on March 7th. In less than 24 hours, the video was trending in Brazil and Germany and had racked up almost 900,000 views. The next day it topped 1 million views.
4,000 comments later, many of which are in different languages, the video is still going strong and is closing in on 1.2 million views less than three days after it had been released.
Buoyed by a faux press release that claimed the video was a clip from a reboot of MTV's My Sweet Sixteen, outlets ran with the story. Apparently, outlets missed the part of the press release that said the release was intended as a parody.
The song, which is definitely NSFW, chronicles a drug dealer that is struggling to learn the metric system.
The video, which is definitely very NSFW, shows a girl celebrating her sweet sixteen that starts out as a tame family affair and quickly turns into a drug and alcohol-filled family affair.
Hovey Benjamin lives in Los Angeles and was recently signed to a record deal. Hovey grew up in Arlington and went to Yorktown High School.


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When it comes to his offensive contributions, Stephen Curry's impact extends far beyond the numbers that show up in the box score at the end of a game.
Although he finished Game 1 of the 2017 NBA Finals second to only Kevin Durant in scoring for the Warriors, there were several possessions in the first half in which his 3-point shooting created easy baskets for others. Curry wasn't credited for assists in those situations because he didn't actually touch the ball or make the pass, but the threat of his jump shot alone was enough to draw multiple defenders in his direction and create openings for his teammates to attack.
MORE: SN's look at Game 1 as it happened
Sometimes the tactic of shading more toward Curry more than anyone else on the Warriors works for the defense. Curry converted 41.1 percent of his 3-point attempts in the regular season and led the NBA in 3-pointers made for the fifth consecutive season. It's no surprise that trying to limit his open looks from the perimeter is a priority for the Cavaliers since his ability to make 3-pointers in volume can change any game in a hurry.
Just look at what happened in the second half of Game 2, when Curry's four 3-pointers in the third quarter helped the Warriors outscore the Cavaliers by 13 points. However, when the Warriors have an advantage in transition with Durant pushing the pace, the decision can be the difference between the Cavaliers giving up a shot they make 40 percent of the time and one they make basically 100 percent of the time.
For example, watch how LeBron James and Kyrie Irving defend the following possession from the first quarter. Durant pushes the ball following a missed shot from Kyle Korver and Curry, who averaged 1.20 points per possession in transition during the season, beats him up the court and immediately makes himself available on the wing. A simple look in Curry's direction when Durant crosses half court is enough to make James and Irving jump towards Curry out of fear, and Durant makes them pay with a dunk nobody can stop when he has that much momentum.
The Cavaliers should've been able to make the possession more difficult for the Warriors. Better communication would've helped them decide which one of them would pick up Curry and which one would pick up Durant. Then again, the Cavaliers were the NBA's worst team in transition defense in terms of points per possession (1.18) during the regular season, so maybe that play shouldn't be too surprising.
Even so, Curry's willingness to make himself a target early in the possession without the ball in his hands forces the Cavaliers to account for him sooner than they normally would, and it sets Durant up perfectly for a scoring opportunity.
MORE: Durant vs. Rihanna becomes juicy undercard for Game 1
There was an even more blatant example of Curry's gravity as a shooter a couple of minutes later, this time following a turnover by James. The Warriors had a four-on-three advantage with J.R. Smith and Iman Shumpert acting as the last line of defense for the Cavaliers, and the result was incredibly similar. Not only did the defender you'd expect to stop the ball decide to close out on Curry, Durant sauntered into the lane for another uncontested dunk.
The problem? The Cavaliers learned from their mistakes in the second half and it resulted in this…
When Smith slides over to get in front of Durant, it leaves Irving having to decide between closing out on Curry or Klay Thompson. Either way, someone who makes around 44.0 percent of their catch-and-shoot 3-pointers is going to be left wide open, which puts Irving in a lose-lose situation. The Cavaliers would probably prefer Irving to close out on Curry, but the risk of Thompson getting an open 3-pointer and potentially breaking out of his postseason shooting slump is equally terrifying.
MORE: NBA Finals 2017: After Game 1 loss, Cavs face scary reality — Warriors have room to improve
That's why defending the Warriors can sometimes feel like an impossible task. Do what is fundamentally correct, and it can lead to an open 3-pointer from the scariest shooter in NBA history. But take that option away, and one of the scariest all-around scorers in NBA history will end up with the types of shots a player of his caliber should never get on a stage as bright as the NBA Finals.
Considering the Warriors scored a league-high 2,025 points in transition this season and ranked in the 96.6 percentile with 1.21 points per possession, the Cavaliers certainly aren't the first team to not have an answer for Durant and Curry in transition.


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Farmgal Rant..
I am sorry to have this rant, I might not even post this.. I most likely will and I am sure I will lose a reader or two.. but I have to write this.. If you live in an apartment or a tiny condo in the city, you can be many things.. You can be […]
I Yield I Yield LOL
Ok, its just going on record that we are going to be "in just in time mode" on most things this year. Let me give a example.. we have pulled at least a hundred or two wild parsnips but then we needed to focus on this or that.. and suddenly this week, we are like.. […]
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Tag Archives: duck breast in cream sauce recipe
Duck Breast in Cream Sauce
This is a lovely way to serve Skin-less duck breast and is a true delightful treat for those it would be served to.. Its got its fine ducky flavour, with a built in cream gravy and if served of loaded … Continue reading


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Looking for Quick Facial Rejuvenation? Consider BOTOX® Cosmetic
Posted February 02, 2016
Need a quick and effective solution for fine lines and deep wrinkles before your next business event? Want to look more youthful and refreshed for that upcoming wedding or graduation? Board-certified Pasadena plastic surgeon Dr. Martin O'Toole can help. With a BOTOX® Cosmetic treatment, Dr. O'Toole can help eliminate visible signs of aging from nearly any area of the face, creating a youthful, photo-ready appearance with little to no downtime.…Read More


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Tuesday, we went up to my Mom's work so she could show everyone how big Jocelyn is now.
Jocelyn played in a couple of ball pits
went on a swing, which she wasn't a fan of
and bounced on the air mattress with Nana
more please Nana
worn out
The pictures are adorable. So glad you could come to Atlanta. I had a fabulous time.


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The Marshall Protocol Study Site > PROF. MARSHALL'S PERSPECTIVE > Prof. Marshall's Perspective > Borrelia burgdorferi reduces VDR expression
|Moderated by: Prof Trevor Marshall
Prof Trevor Marshall
Foundation Staff
|A new study has just been published, where a micro-array was used to see which human genes were affected by infection with Borrelia burgdorferi. This adds to the data we have on HIV and M.tuberculosis down-regulating VDR expression.
(here is the relevant data table with VDR in it)
Live Borrelia burgdorferi reduced VDR expression in monocytes by 50 times, and lysates ('dead' Borrelia) reduced it by 8 times (these ratios are not directly comparable with the HIV and TB studies Amy and I cite in our presentations).
So now we can understand the contribution which Borrelia burgdorferi adds to the metagenome...
ps: I would note that M.tb and Borrelia reduce the number of VDRs, rather than block the binding pocket with a ligand, such as capnine. It is believed that VDR is expressed by Estrogen-receptor-beta, but this is still tentative... The bugs know their target better than we do
|Dr Trevor Marshall wrote:
ps: I would note that M.tb and Borrelia reduce the number of VDRs, rather than block the binding pocket with a ligand, such as capnine. It is believed that VDR is expressed by Estrogen-receptor-beta, but this is still tentative... The bugs know their target better than we do
I was wondering about this. This week, you already mentioned that M.Tb's effect wasn't through blocking the VDR itself.
Yet, Wang's table 1 does mention that the VDR transcribes itself, which would make it extremely vulnerable: knock the VDR out and it is gone. It would make sense that other receptors transcribe it, since we know how important it is. I guess that is called functional redundancy in the genome?
Forever learning, Frans
inactive member
Not sure, but this article seems relevant.
inactive member
|Does this now suggest that bacteria not only compromise our Vitamin D Receptors but also make some receptors permanently redundant?
What is the consequence of this if indeed we have a permanent net loss of our VDR quota and diminished antibacterial peptides?
|rick wrote:
-1: Does this now suggest that bacteria not only compromise our Vitamin D Receptors but also make some receptors permanently redundant?
-1: not redundant, but ineffective: remember that rising levels of 25D and 1,25D start knocking out other receptors as well as the VDR and as we can tentatively conclude, the bacterial load shuts down other receptors as well as the VDR (in the case of Bb perhaps the Estrogen beta receptor, as shown above)
-2: you get a chronic disease ... However: the MP is designed to turn this around: the actual DNA for the VDR, the other receptors and the antimicrobial peptides does not disappear, it is not being transcribed, so once things normalize again, transcription starts again, leading you to health
Hope this helps,
Research Team
|Dr Trevor Marshall wrote:
I would note that M.tb and Borrelia reduce the number of VDRs, rather than block the binding pocket with a ligand, such as capnine.
This study says that M.tb downregulates expression:
Is there another study you're thinking of or did I misread this? I wouldn't ask were it not for the KB.
Foundation Staff
|@Paul: Are you looking for the reference Dr. Marshall provided in the first post of the thread maybe?
Research Team
|Maybe the problem is that the implications of the paper Trevor references is too subtle for me to get.
The impetus for the question came from the fact that there is other research that shows Bb downregulates expression of the VDR. In the PLoS Pathogens paper Trevor refers to there is (at least according to Trevor) a different mode of action.
I was just wondering if:
1. Bb really cleaves the VDR in particular. There is no indication in the paper I can see beyond generic talk of cleaving and references to caspase-1, which belongs to a family known for cleaving receptors.
2. If yes, I was wondering if this action compliments/contradicts the research referred to here in which Bb downregulates VDR expression (downregulating and cleaving are different!):
I'm trying to make a habit of not including anything in the KB that I don't get. Therefore, I would rather not include this paper until I see how it fits into its proper context.
Prof Trevor Marshall
Foundation Staff
If you look at the differential expression of the VDR on the second to last entry in Table S2 of the paper I cite you can see that expression of the VDR is downregulated by 50 times (0.02) and 8 times (.12) by the Borrelia infection
Expression by the VDR may also be affected (eg by capnine etc) but that isn't clear by looking at the data they collected.
I just found this paper, the latest on VDR. VDR also seems to be downregulated by EBV.
Expression profile of nuclear receptors upon Epstein - Barr virus induced B cell transformation. PMID: 19550398
I cannot access the full-text to see how manyfold it is downregulated, or by what mechanism, perhaps someone can look at it?
Last edited on Sat Jun 27th, 2009 03:52 by Frans
Research Team
|Great find, Frans!
Here's the full text:
Last edited on Sat Jun 27th, 2009 06:33 by paulalbert
|Thanks Paul,
Patrick was even faster in sending a link to the full-text
I am trying to figure out how manyfold the VDR was downregulated, but concentration is lacking.
There are, however, some things that occurred to me.
1: it seems as if bacteria and viruses that have been implicated in a lot of autoimmune (chronic TH1) diseases, like EBV and borrelia ALL act through downregulating the VDR; of course, this makes sense, considering the role the VDR plays in innate immunity ... This might in fact be WHY they are always implicated ... and now we understand why
2: this might also give an indication of why infection by these critters pushes people over the brink, right into th1 disease
3: this particular paper might also give an insight as to why EBV infection (I am thinking of Pfeiffer's disease as we call it (you guys call it the Kissing disease?) is so hard to conquer; innate immunity is severely compromised, so healing takes a long time
Something else just occurred to me: I have seen in pubmed that MicroRNA's play a role in VDR transcription. Wiki tells me EBV encodes several microRNA's, for what it is worth .. Perhaps those microRNA's are involved in the machanism by which EBV downregulates the VDR. Of course, this a reaching a little ...
Edit: EBV does NOT cause cold sores. EBV is a Human herpes virus (number 4), but not all Herpes viruses are EBV's ... If I am not mistaken, cold sores are caused by Herpes simplex. Not EBV. concentration on MP remains an issue...
Last edited on Sat Jun 27th, 2009 12:54 by Frans
Prof Trevor Marshall
Foundation Staff
The 3D-graph is plotted as Log(concentration ratio) and I estimate about 5 times for VDR.You might like to cross-check my numbers.
As for micro-RNAs, note that the Estrogen-beta receptor is not down-regulated. Since VDR is believed to be expressed primarily by Er-beta, that implies (for me) that the mechanism of downregulation is a ligand targeting Er-beta. Micro-RNAs are an unlikely ligand, although I admit I haven't tried to dock them...
Somehow transcription of VDR and transcription by VDR keeps confusing/eluding me. PMID: 19437538 shows miRNA influencing transcription by VDR, not of VDR. My mistake.
But if I am not mistaken, ER beta is also downregulated by EBV ? It is mentioned in table 1 under receptors being downregulated.
In graph 2a VDR and ER beta show a similar slope, going up a little, until about 48 hours, but ending lower. ER-beta is the green one
5 times downregulation is a serious impact btw.
As for checking your numbers: I don't think I have the capability or knowledge at this time, to say the least Ah well, MP is not endless Life after it might very well be, hehe
inactive member
|Reading this thread makes it clear to me that VDR blockage (from bacterial ligands and from ingested Vitamin D) is not the only way in which the immune system of a patient with TH1 disease is compromised. The pathogens mentioned in this thread downregulate the expression of the VDR itself (by targeting receptors responsible for VDR expression) and there are probably other pathogens that have evolved even more creative ways for disrupting the immune system.
The main part of the MP, activating the VDR with Benicar and avoidance of ingested Vitamin D, will counteract blockage of the VDR with bacterial ligands, but my understanding is that it would not have a direct affect in combating downregulation of the VDR or other mechanisms the bacteria might employ. This brings a number of questions into my mind...
Is the expectation that though there are other ways in which the immune system is weakened, that VDR blockage is the main one, and that once this blockage is removed, even if the number of VDRs is reduced thru downregulated expression, that this will restore immune function enough that it can start to go to work on all pathogens, regardless of the mechanisms they are employing?
Is it fair to say that the degree to which all the various immune system weakening mechanisms are employed by a particular patient's bacterial soup (how much is bacteria that block the VDR with ligands, how much is bacteria that downregulate expression of the VDR, etc.) would be a key factor in how they respond to the MP?
Might a patient with a bacterial soup that has a high degree of down-regulation of the VDR require more help from antibiotics than a patient who has a bacterial soup that is mainly just blocking the VDR with ligands?
- Russ
p.s. I only partially take for granted the fact that we have a scientist "working for us", who is completely on top of all the new studies that come out and can explain them to us.
Research Team
|Russ wrote:
Might a patient with a bacterial soup that has a high degree of down-regulation of the VDR require more help from antibiotics than a patient who has a bacterial soup that is mainly just blocking the VDR with ligands?
Unless I misunderstand your question, Russ, I think they're the same thing. Excepting the effects of viruses such as EBV, how else does a VDR get downregulated??? Certainly not by itself.
inactive member
|Hi Paul. I probably didn't word that well. These are the two mechanisms I was trying to differentiate between:
1. Bacteria that produce a ligand (e.g. capnine) that blocks the VDR. Benicar is effective at displacing this ligand from the VDR and re-activating it.
2. Bacteria that produce a ligand that blocks, for example, the Estrogen-beta receptor which Dr. Marshall has said is likely responsible for VDR expression. The result here would not be a blocked VDR but a VDR that is not expressed. I don't think Benicar would be directly effective in combating this down-regulation...I would think you'd need an agonist of the Estrogen-beta receptor to displace the ligand that is blocking that.
I may be missing something, but this is how I was understanding the difference between blocking a receptor and down-regulating it's expression.
- Russ
Prof Trevor Marshall
Foundation Staff
The two things will both be happening at once. Some species doing one thing, some species the other. Benicar will always be useful in trying to start the process of disease reversal.
The extreme case, of course, is the chronic phase of HIV/AIDS. Murdoch University has one of the world's leading research teams in HIV/AIDS, and I spent some time working through these issues in my mind while I was visiting Murdoch last week
Ruth Goold
Health Professional
|Hi Frans,
I think you are not off-base by suspecting that RNA interference and related RNA mechanisms are likely involved in the processes by which the human microbiota exert their profound influence on its host. Micro-RNAs are single-stranded RNAs that primarily downregulate protein production by inhibition of protein translation from messenger RNAs (mRNAs). Thus, production of microRNAs that target either or both of the the estrogen receptor or the VDR could reduce VDR production and activity. Researchers are beginning to document the production of micro and siRNA (small interfering) double-stranded RNA molecules in pathogenic bacteria, their operation in host cells and their association with disease (cancer, in particular).
The mechanisms by which the small RNA classes can affect gene expression are amazing and still being discovered; they can disrupt both protein translation and transcription, and even affect protein function and longevity post-transcriptionally. They are involved in alternate forms of host protein splicing - different 'splice variants' of the same protein can function very differently in the host. I am not aware of small RNAs that act as ligands for host receptors, but anything is possible.
The researchers at West China hospital have the molecular expertise and equipment to help sort things out at the intracellular level in the human host. I am also hopeful that Amy will be pursuing these matters in her graduate work. There are exciting things to come in the next few years,
|I am having a follow-up appt with my Endo who is also a bone specialist (Ha!) on Mon Dec 7th..(I am 44 rys old and have osteopenia, so she is monitoring me.)
She is going to "freak" when she sees how low my 25-D levels are now this year..So I would like to take just 1-2 mins of her time to explain in point forms, why I am avoiding Vit D and why my 25-D levels need to stay low at this time...etc.
Can someone please help me with this...This is my understanding of it all, but I may have my facts mixed up.
1. The VDR controls the innate immune system.
2. People who have Th1 diseases have CWD bacteria (in their phagocytes) which block some enzyme? This is turn causes a rise in the levels of 1-25D in the body.
3. Elevated levels of 1-25 D (above what level?), cause the innate immune system to shut down, so it can no longer fight the intracellular bacteria.
4. When the 1-25 D goes up the 25-D tends to go down.
5. We need to keep the 25-D below 12 ng/ml because taking in any Vit D will cause a conversion into 25-D which in turn will cause 1-25 to rise, which if goes too high (above what number?) will cause the innate immune system to shut down again.
6.We take Benicar b/c it unblocks the VDR from 1-25D? and it allows the innate immune system to wake up and see and attack the CWD once again.
How did I do..yes? no?
I will also be leaving her some research papers etc...for her to read...Ha..like that's going to happen?
Aunt Diana
inactive member
|Good luck with your doc. Be sure to print out the article on Amy Proal's website http://www.bacteriality.com re: Vitamin D. She explains it in simple terms.
Research Team
|Everything you say is pretty much right except re: #5, we are also concerned that 25-D will bind and inactivate the VDR. Also, re: #6, when Benicar binds the VDR it turns it on transcribing enzymes which reduce high levels of 1,25-D, which reduces the chances that high 1,25-D interferes with other receptors - many of which also play key roles in immune function.
If you want to know what Marshall says about what is happening to cause your vitamin D metabolites to be out of whack, check out this article:
That said, I wouldn't go too deep into the molecular biology or the bacteria. You could say that it has been our experience that people simply do not get better when they have high levels of 25-D. You could also point out that MP patients take a medication that binds to and activates the Vitamin D Receptor, so you are in a completely different boat than most other people with an inflammatory disease. And then say, if you have any questions, have a look at this peer-reviewed paper.
Cynthia S
Foundation Staff
|3,4, and 5 seem to leave out the suppression of the immune system by the VDR itself being blocked. Here is a summary I put together for Bill-K in the TH1 questions forum:
"A) The VDR is responsible for a great deal including
1) part of innate immunity
2) a feedback system controlling the level of 1,25D
B) Several other nuclear receptors are responsible for many things including
1 )part of innate immunity
C) 25D (and D2 & D3 also) blocks the VDR and shuts it down resulting in, among other things
1) From A1, suppression of the immune system to a degree
2) From A2, disregulation of 1,25D allowing 1,25D to go too HIGH resulting in
a)1,25D docking in other nuclear receptors where it does not belong shutting them down resulting in
1) From B1, further suppression of the immune system
So you see, high 1,25D does suppress the immune system and is accounted for in the MP. And unfortunately, as you can see, 25D has a double whammy effect on the immune system."
|Okay I am getting my notes together and constructing a document I can read to my Endo at my next appt.
Is it the 1-25 being too high that causes the innate immune system to shut down?
If so, at what level does it start to do this...or what level is considered acceptable and by whose standards? I remember reading something in the past about the Merck Manual...Is this where we are getting our numbers from or is this the standard book in medicine?
I ask b/c when I first mentioned the MP to her in 2005 (on the recommendation of my G.P. at the time)...As he felt of all the info, I have ever brought to him on treatments for chronic Lyme /CFS.....he said this (MP) makes the most sense to me as it is scientifically based..
Anyways back in 2005, I had my first 1-25 D levels checked and they were 173 pmol/L (or 72.08 pg/ML) which is HI as the range here in Canada at that time was 30 - 120 pmol/L
At that time my Endo said my levels weren't really that high as labs were now changing the acceptable levels of 1-25 D to be up to 150 pmol/L.
As of Sept 2008 (8 months of being on Olmesartan & NO Minocin) my 1-25 levels dropped to 73 pmol/L , which is 30.41 pg/ML and my 25-D is now 14 nmol/L or 5.6 ng/ML
Is my 1-25D level too low now?
health professional
|Both a high 1,25-D and a high 25-D can contribute to suppression of innate immune function according to the MP perspective.
I discuss this in the NY Annals paper (Waterhouse et al, see http://mpkb.org ).
Your 1,25D is fine now and so is your 25D. Yes, we use the Merck manual limit. I think others raise the limit because they don't understand what a high 1,25D means. You might also show your doctor the paper by Blaney et al (also in the KB).
Joyce Waterhouse
PS The MP perspective is that it is not necessary to measure 1,25-D once one has started the protocol. One might review the KB with regard to measuring D metabolites and related documents for more on this.
Last edited on Sun Nov 22nd, 2009 12:10 by jcwat101
Foundation Staff
|Lisa, this article, " Test: 1,25-dihydroxvitamin D (1,25-D)", in the MP KB gives some information on the lab ranges also.
Foundation Staff
Thanks so much for mentioning your article here. I had printed out the "six key papers" and have been working through reading them all but hadn't finished yours yet. Now I have and....wow--what a great explanation of the impact of VDR dysregulation all in one place. I've been flipping around between 4-5 different links to information and trying to piece it all together. Each link covered part of it, and some were more detailed than I could fully grasp.
You and your "et al partners" (Tom Perez and Paul Albert) did a great job explaining it all in a very readable format. For anyone who hasn't read it yet, here is a direct link to the full 11-page preprint:
Reversing Bacteria-Induced Vitamin D Receptor Dysfunction is Key to Autoimmune Disease
Pages 5-7 in particular cover the impact of high vitamin D levels on innate immunity and using serum levels for diagnostic purposes.
Thanks again for all your hard work.
|When you see so many reports in the news about how Vit D is good for your immune system and that it can help reduce cancers etc...
Is there actual research proving this? OR....Are the researchers just making a conclusion (without any proof) that low levels of 25- D contribute to/cause cancer....because they find that so many people who get cancer, have these low levels of 25-D and thus are making an assumption.
Just wanting to get my facts accurate...As I know the Endo is probably going to say to me, that everything I am telling her is wrong and incorrect about our high 1-25D & low 25-D's and that we need Vit D to prevent cancers etc....
Research Team
|Here's the ol' KB article on cancer and vitamin D:
This article may also be helpful:
|Tanks Paul..will take a look!!
Foundation Staff
Paul has written some other good articles in the MP knowledge base too...
See especially:
Mistaking correlation for causation in vitamin D studiesAlso:
Assessing the published literature
Foundation Staff
|Joyful, thanks for those extra links.
In the "Assessing the published literature" section, #5 states,
The concept of the "blood-brain barrier" has lost meaning in today's world of molecular genomics.2
And, there is a link to this pubmed article/abstract:
Could someone (maybe Paul) explain this article to me. I get that it has something to do with contradicting current thinking about the blood-brain barrier since you referenced it, but I don't understand what the article is saying enough to make the connection.
Research Team
Well, according to Trevor and co., the blood-brain barrier is this idea that all types of stuff - chemicals, drugs, bacteria - are incapable of passing the barrier, but this study and various others suggest the opposite.
Here's the Wikipedia article repeating some of the folklore:
Foundation Staff
|Thanks Paul.
The descriptions of the various diseases associated with the blood-brain barrier listed there (in Wikipedia) are interesting. Hmmmm....more examples of "bacterial involvement" regardless of whether the blood-brain barrier actually exists as stated or not.
health professional
|My recollection is that the point is that the barrier is not totally absent but that it is just not as effective as previously thought. Some things don't get through very well, but others do. And how much of a barrier it is may also vary according to the individual and the circumstances and what substance or cell type is at issue.
Joyce Waterhouse
Research Team
|Good point, Joyce. I didn't mean to imply that everything gets through.
|Thanks Joyful for the additional links to articles
|UPDATE with BONE SPECIALIST :
Okay folks, here's how my appt went with the Bone Specialist.
She actually took the time to listen to me explain some of the info behind the MP and she did take a quick look at some of the research papers I brought her…(this is a step forward from when I saw her last year).
While she may still not quite understand all the workings of the VDR & innate immune system etc..She still disagrees with me keeping my 25-D (Vitamin D stores so low).
She acknowledges that 1-25 is what build bones/density…But she said I will develop SOFT BONES without enough D stores, which is what the body needs to assist in absorbing Calcium….This is different than having less dense bones, which is where the 1-25 D comes in.
She has had patients who have had normal 1-25 D levels, yet still had 'fractures and when they went in and did a bone biopsy their bones were all MUSHY (Soft Bones) So she said just because you have a normal 1-25 D, doesn't mean you are not a risk for developing Osteomalacia…soft bones….
She also said you can't rely on the Merck Manual for 1-25 D levels, as each lab uses a different assay for their test, they are not all the same…
She also made some rude comment that b/c Dr. Marshall is not an M.D., he really doesn't understand how all the physiology works (or something to that affect, can't remember the word she used right now)..So then I said well the Dr. who is overseeing my care while on the MP, is very knowledgeable of the protocol and "IS" an M.D….She then said, Yes, but he isn't a bone specialist…..I think no matter what I say, she would have an answer for everything.
While I respect Dr. Marshall's discoveries & research very much, I feel I also need to respect and be open to where she is coming from ie - her education, knowledge and first hand experience dealing with patients, as a Bone specialist/calcium disorders clinician…
When I looked up info on the Knowledge Base site under "Concerns for Physicians" I see concern #4 is re: "Avoiding consumption of Vit D leads to Osteoporosis" when I explored the link further, there are only 3 studies quoted, that dispute Vitamin D supplementation can prevent Osteoporosis etc…But there is no mention of Vitamin D preventing SOFT BONES…which I would suspect is an entirely different thing…
My concern is: Does my Bone Specialist have a valid point about keeping my Vitamin D stores up, to assist with calcium absorption so as to prevent developing SOFT BONES?
If not, then why?
Is it possible we are overlooking something important here?
Prof Trevor Marshall
Foundation Staff
|Bone matrix is dependent on estrogen homeostasis, not on Vitamin D. The estrogen receptor is expressed by the VDR. If your bone specialist did not stress the importance of estrogen to bone matrix then she is way out of her depth.
We have already been there, done that, years ago.
Get another bone specialist
|I wonder if bone marrow is too?
We now know that the brain controls the formation of bone (12/22/2009)
Just plucked this off of Ray Kurzweil's RSS feed.
"The brain acts as a profound regulatory centre, controlling myriad processes throughout the body in ways we are only just beginning to understand. In new findings, Australian scientists have shown surprising connections between the brain and regulation of bone mass."
This quote struck me as being interesting:
"It is now clear that the neural network which controls appetite and energy also alters bone density. When we are starving, our brains don't allow us to waste energy by reproducing, making fat or creating new bone. When we are eating too much, on the other hand, our brains make it easier to reproduce, store fat and create bone."
It seems to me that the body downregulates a lot of bodily processes in response to stress, however defined. Inflammatory cytokines like TNF alpha for example can lead to cachexia (weight loss/wasting), bone loss and other sick behaviours including depressive disorders, etc.
So to me the real question (in the context of this article) is what signalling pathways are involved in the modulation of NPY measured by the researchers? It doesn't just happen on its own. TNF aplha, IL-6, IL-1b, AT2? The reseachers indicate that NPY is modulated in response to stress, presumably infections are part of that equation.
Last edited on Thu Dec 24th, 2009 07:14 by Phillyguy
|Thank-you for your reply and the links to the following papers...I will check them out when I have a moment.
I take it when you mention bone matrix, that this includes soft bones...
Yes, she has mentioned once before, that keeping estrogen levels up is important too, but never mentioned it in the context of 'soft bones'....She measures my estrogen yearly and it is just fine, so no peri-menopause for me..
I suspect she is on a bit of an EGO trip here (being affiliated with two hospitals and one University) and not use to patients questioning or challenging her...and perhaps she doesn't want to see (via my treatment results down the road) that her beliefs about Vitamin D stores are incorrect or outdated...
|Dr.Marshall perhaps you could speak to this:
I just remembered the other day..that during my childhood whenever I got ill, the Dr.'s never really knew quite what I had...It was like I never got a full blown case of anything.
For Example: They thought I had the measles but weren't 100% sure..same with the mumps I believe...and they thought I might have Scarletina, but didn't know for sure.
Then when I was 18 yrs old, I got this severe flu-like illness, w/alot of dizziness, weakness, fatigue, excessive sleep, nausea, weight loss, light sensitivity, (possibly the start of Lyme disease) and again they didn't know for sure what I had...I was told it was "probably" a virus and that I would slowly recover over time...(which I did) but was never really the same after this episode....
Is this not presenting with full blown sxs (thus Drs' not knowing what I had) a good indication of a poorly functioning immune system (VDR) right from a very young age/perhaps birth? (Oh, and I was born 2 wks premature)
If so, would that be from inherited bacteria from the mother?
Does this only come from the mother or can it come from the father (via sperm) as well?
I say this b/c my mother is fairly healthy except for some osteoarthritis in her knees..Where as my father has had alot of health problems for many many years now...Heart disease (with a triple by-pass 9 years ago), now the start of Macular Degeneration (which I heard Dr B. say is a Th1 disease), 3 hernia operations, polyps in the colon, prostate cancer a few years ago, gall bladder removed...
Both he and I are very much a like immune system wise...we are both very sensitive and react to alot of medications, herbs etc..
Your thoughts would be greatly appreciated!
Prof Trevor Marshall
Foundation Staff
(slide #27)
Mothers with low Vit D status (and Th1 disease) typically deliver pre-term
|CMV downregulates VDR 2.2 Fold
Take a look at the data supplement for the full transcriptome:
CMV dramatically increases the expression of inflammatory cytokines. Per the transcriptome, IL-6 is increased 280 fold! The TNF family is also significantly upregulated.
This little nasty also significantly downregulates TLR1 and TLR6.
The primary known ligand for TLR1 are bacterial triacyl lipopeptides while the primary known ligand for TLR6 are diacyl lipopeptides from mycobacteria.
Most TLR's function as homodimers, however, TLR2 forms heterodimers with TLR1 or TLR6, each dimer having a different ligand specificity. CMV directly hits TLR1 & 6 and indirectly hits TLR2 via VDR.
inactive member
|Dr Trevor Marshall wrote:
Live Borrelia burgdorferi reduced VDR expression in monocytes by 50 times, and lysates ('dead' Borrelia) reduced it by 8 times (these ratios are not directly comparable with the HIV and TB studies Amy and I cite in our presentations).
Finally dug up this discussion thread that you initiated back on 6/14/09 regarding Bb and VDR suppression, as you can imagine it had caught my attention. The 50:1 VDR suppression rate, in the presence of live Bb, might account for the level of co-infection I was burdened with when I began the MP March '08. With that in mind would you please, on a scale of 1-5, rank this statement's merit:
"If HIV (Human Immunedeficiency Virus) suppresses VDR 200:1 then is it not plausible that Borrelia.burgdorferi, at a 50:1 suppression rate, be viewed as a form of Human Immunedeficiency Bacteria, or HIB."
Look forward to your most serious thoughts on that comment/observation....
Last edited on Tue Jun 7th, 2011 19:51 by TikBitten
Prof Trevor Marshall
Foundation Staff
|Borrelia does not persist as the complete organism, unlike HIV, they are not comparable.
There is no need to focus on Borrelia. Some of our most seriously ill members have never had a Borrelia infection. It is part of the mix, not a causal factor.
The size of the 50X factor was due to the assay method this study used. There is no reason to suspect there is any major difference in suppression effectiveness between Mycobacterium tuberculosis and Borrelia burgdorferi.
That said, I have long pointed out that HIV profoundly downregulates VDR, but new knowledge is suggesting that it also has a key action on MAF, also called DBP, which the other primary pathogens do not exhibit. So the situation re HIV's virulence is becoming clearer as the years go by.
A lot has changed in our scientific understanding since I started this thread Sometimes it is tough to understand the pace of progress. Change it is, but it is also progress.
Last edited on Wed Jun 8th, 2011 01:28 by Prof Trevor Marshall
|Dr Marshall, if one organism affects VDR in a stronger degree and other organism affects it in lesser degree... Will standard olmesartan dosing work for all these organisms ?
Could there be a pathogen that affects VDR so strongly, that olmesartan won't be able to reverse this process ?
|Yes good point...What about Babesia?
Prof Trevor Marshall
Foundation Staff
|Indeed, what about Babesia? What harm does it do? I am not interested in what ILADS says it does, I want to know what harm, and by what pathways...
Babesia survives in weakened immune systems. The organism is impressive under a microscope, but it lives within red blood cells, and therefore does not significantly affect proteome interference. Easy to see, easy to diagnose, and exaggerated as a pathogen, IMO
inactive member
|wrotek wrote:
Dr Marshall, if one organism affects VDR in a stronger degree and other organism affects it in lesser degree... Will standard olmesartan dosing work for all these organisms ?
Actually, Borrelia doesn't directly block the VDR like other organisms. Instead it downregulates it's expression which is a different way of interfering with the immune system and one which Olmesartan does not directly counteract.
In order for the VDR to be "working", the receptor has to be expressed and there needs to be an agonist that binds to it and turns it on. The way I think of it, a receptor is expressed when it is present in the cell and available for something to bind to it. It is then turned on when something binds to it and that something is an agonist that turns it on (1,25D, Olmesartan) and not an antagonist that turns it off (25D, bacterial substances).
Some organisms produce substances that bind to the VDR and block 1,25D from turning it on. The VDR is still present in the cell, it is still "expressed", but it is not turned on. Olmesartan, with it's high affinity for the VDR, is able to displace the bacterial substance and turn the VDR on.
Other organisms - like borrelia, m. tuberculosis, and EBV - prevent the VDR from even being expressed in the first place. So there is no receptor present for Olmesartan to bind to and therefore Olmesartan does not directly counteract this bacterial survival mechanism. But I guess the idea is that though borrelia reduces the number of VDRs that are expressed, it does not prevent *all* VDRs from being expressed, so there are still some VDRs out there and by taking Olmesartan you are ensuring that the remaining VDRs re turned on.
I imagine that in severely infected tissues, borrelia might reduce VDR expression so much that it is very difficult for Olmesartan to work it's magic. This might be where antibiotics are more necessary, since they would likely interfere with whatever mechanism borrelia uses to prevent VDR expression. Also, I suspect that carbohydrates/glucose are a key part of the ability of borrelia to do whatever it is that it does, and so eating low-carb would also help and this would explain why some people get much higher IP from lower carb intake.
So I would think that the MP treatment, and especially Olmesartan alone, would be most effective for people with a pathogen mix that leans more towards VDR blockage than one that leans more towards VDR downregulation, since Olmesartan directly counteracts the former but not the latter.
That is my layman's understanding of it.
Last edited on Sun Jul 10th, 2011 11:56 by Russ
|Interesting. We would have to know how borrelia reduces vdr expression to reverse this .
Prof Trevor Marshall
Foundation Staff
This might be where antibiotics are more necessary, since they would likely interfere with whatever mechanism borrelia uses to prevent VDR expression
We really don't know that bacteriostatic antibiotics directly act on the intracellular organisms. We do know that Mino and Clindy definitely affect the human immune system directly. So the answer is likely even more complex than 'antibiotics', Russ
Further, it is believed that VDR is expressed by estrogen-receptor-beta, and in turn the VDR expresses the estrogen receptor precursor protein, so we have a ying-yang feedback/feedforward there.
But you have hit upon the reason I don't talk much about Capnine any more - the complete answer is getting a lot more complex than I contemplated just a few years ago...
Last edited on Sun Jul 10th, 2011 12:23 by Prof Trevor Marshall
inactive member
|Wrotek & Trevor wrote:
Dr Marshall, if one organism affects VDR in a stronger degree and other organism affects it in lesser degree... Will standard olmesartan dosing work for all these organisms? Could there be a pathogen that affects VDR so strongly, that olmesartan won't be able to reverse this process?
Further, it is believed that VDR is expressed by estrogen-receptor-beta, and in turn the VDR expresses the estrogen receptor precursor protein, so we have a ying-yang feedback/feedforward there.
Wrotek & Trevor-
IMO, I believe there are two primary levels of concern, at a minimum, in addressing microbacterial persistence:
i. The first, of course, as stated above, pathogenic effect on VDR expression but, also;
ii. Each pathogen's inherent ability (genetic makeup) for biofilm persistence, cyst formation, sequestering and immune system evasion.
Case in point, me....
After three plus years on the MP I am far more comfortable discussing the topic as it appears this is the exact diagnostic scenario that's unfolding in my treatment of Late Stage Lyme Disease, the result of an underlying long standing Borreliosis (Bb) condition. Just as a comparison, much like AIDS is the disease state of HIV, Lyme Disease is the disease state caused by Borreliosis.
As way of some background, the major concern when embarking on the MP was that, although the MP had the potential of clearing much of the micro-bacterial and other pathogenic load, in the end, a Borrelia infection would be far too resilient to roll back entirely. And, unfortunately, at this point in time, my test results indicate just that scenario.
When I started on the MP in March 2008 it was difficult to know, due to a plethora of positive fungal/viral/bacterial test readings, if Lyme Disease was in fact the primary diagnosis. By April of 2010, however, the underlying "pea-soup" condition became far clearer and the only detectable IGenex western blot signature left, kdA bands 31 & 41, was that of Borrelia. Again, the causative agent underlying Lyme Disease. Please know that when only those two bands are present (31 & 41) the likelihood of a positive Borreliosis diagnosis (Specificity & Sensitivity) reaches a 97% confidence level -- and additionally confirmed as positive with further 31 kDa epitope Igenex testing.
To make matters worse, as another confirmation, I recently performed a new, more comprehensive test panel from NeuroSciences Labs, Inc. that scanned not only western blot bands but also looked for key markers of Bb biofilm formation. So as of March 23rd 2011, my results remain weakly positive for kDa bands 31 & 41 but, more alarmingly, a key marker (DbpA) for Bb extracellular matrix binding (i.e. biofilm formation) was identified and off the scale. Thus leading my physician to believe that, although the MP was likely successful at clearing out much of the pathogenic pea-soup, much work is still needed to fully address the in-vivo biofilm life cycle of Bb.
While I have surely improved greatly from 2008, at this point in time, the underlying causative pathogen, Bb, is proving to be very, very resilient. At present I am working with my physician to develop additional layers of therapy, come December, that will compatibly overlay the MP and breakdown or interfere with ongoing Bb biofilm formation.
So net, net, in contrast to Dr. Marshall's beliefs, I am definitely not of the opinion all bacteria are created equal and, hence, evenly susceptible in-vivo to the MP – at least not yet!!JJ
My 2 Cents,
Last edited on Sun Jul 10th, 2011 13:42 by TikBitten
Prof Trevor Marshall
Foundation Staff
a new, more comprehensive test panel from NeuroSciences Labs, Inc. that scanned not only western blot bands but also looked for key markers of Bb biofilm formation
Is that an FDA-approved test, or are you placing your fate in the hands of pseudo-science, TB?
|Dr Trevor Marshall wrote:
"We do know that Mino and Clindy definitely affect the human immune system directly".
What exactly do we know about Clindy in that respect ? Quite a bit of info on Mino has been posted (Bane, Phillyguy), but Clindy ??? Nil specific in the MPKB either.
Thx, Leo.
|This is off topic(I dont want to start new thread), but perhaps it could be possible to clone a conference countdown timer to http://marshallprotocol.com and mpkb.org websites ?
I have just realized that i missed 3 conferences and tomorrow i have 3 hours to catch up
Last edited on Sun Jul 10th, 2011 21:44 by wrotek
Prof Trevor Marshall
Foundation Staff
|My response was a bit terse TB. Sorry about that. I get very upset over the way that the"Lyme" industry drains every penny from members by convincing them they have "Lyme" and then coming up with bogus test after bogus test until both the patients, and their families, have been bankrupted.
The new test you mentioned has (at least) the following flaws:
Firstly, it is based on antibodies which have not been demonstrated to be specific for Borrelia, with a real risk of false-positive against other components of the microbiota. If you watch Amy's presentation at the Intl Congress on Antibodies:
you will hear her explain how useless the average 'antibody' is, as they are non-specific, and hit hundreds of targets. None of the experts in the audience challenged this. Another paradigm shift for clinical medicine to leap, I am afraid
Second, biofilms are not what are making you ill. If you have any Borrelia in your bloodstream it is because of the combined load of all the intra-phagocytic pathogens weakening your immune system, thereby allowing "cysts" and whatever, to persist in the blood and tissues. The concept of "Borrelia cysts" in-live- Homo-sapiens is junk science anyway, for a host of other reasons which I have enumerated over the last decade.
While you have any immune system at all, it will deal with blood-borne flotsam and jetsam. If your immune system is too weak to do this you will die because of the accumulating apoptotic cells, quite apart from any pathogenic issues.
I hope that helps.
IMO it is always best to ask before spending money on what the Lyme-financial-ecosystem is pushing at you
Last edited on Sun Jul 10th, 2011 16:05 by Prof Trevor Marshall
Prof Trevor Marshall
Foundation Staff
Clindy has been reported as a CYP3A4 enhancer, and it was reported that this was achieved via the PXR.
Although I did confirm (in-silico) the PXR activity of mino, I was unable to confirm that clindy was a PXR agonist, and so there is a question in my mind about the pathway, but I will accept the researcher's observations that clindy enhanced the expression of CYP3A4, which, among other things, breaks down 1,25-D into inactive metabolites
inactive member
|TikBitten, I think Dr. Marshall is right about antibody tests being non-specific and not a good marker of the level of infection. I had a bunch of blood work done shortly after starting the MP and all sorts of antibody tests that had been negative prior to the MP were now positive because my immune system was working and killing pathogens.
As far as your main point about whether the MP alone will allow recovery in all cases, regardless of severity of disease and pathogen mix, I have wondered the same thing. It's hard to think that it would, given the infinite number of pathogen combinations and ways in which the pathogens affect the body. I guess only time will tell.
And I also think that biofilms play a role. Or at least some mechanism in which they are able to go into "hiding" when the environment is not right.
Last edited on Mon Jul 11th, 2011 01:15 by Russ
Prof Trevor Marshall
Foundation Staff
The key thing to understand is that a pathogen living in a biofilm outside a cell (for example, a biofilm on a hip-joint) can evoke an immune reaction, while a pathogen living inside a nucleated cell can change the way the body works. In particular, an intra-phagocytic pathogen can change the way that the immune system works.
So a pathogen in tissue or the bloodstream has to survive by evading the immune system, while a pathogen inside a cell can modify the immune system itself to survive - eg by dysregulating the VDR.
It is the second function - changing the way the body works - which causes chronic illness.
I did write a paper in 2003 explaining the importance of pathogens getting inside a cell, but it is such an old paper now, with so many poorly developed ideas (heck, that was nearly a decade ago) that I don't cite it much
Proteomic interference, genomic interference, the actual chronic disease mechanisms, can only occur when a pathogen survives phagocytosis and persists within the nucleated cell.
I hope that helps,
|That is a nice, concise description of chronic disease and the fundamental differences between the effects of microbiota persisting inside a nucleated cell and those gathered in colonies outside.
Many times I read or hear about biofilms in general being the big issue in chronic disease,never much about intraphagocytic microbiota.
That being said....can we assume biofilms that exist in outside these nucleated cells are probably persisting because of the changes that the intracellular bacteria have made to the immune system?
I wish there was a better way to limit the exaggerated immune responses to extracellular bacteria and proteins while the innate immune system clears.
|Hi Dr. Marshall......that was a great explanation! Helped me a lot! Graduated college without ever having to take a biology course so this is a hard learning experience for me, but between you and Google I'm doing O.K. Have decided to be an immunologist in my next life. Never really knew in this life!!!!!!!!!!!!
|Reading this thread about Borrelia burgdoferi is interesting. Since I watched Lida Mattman's presentation from the 2005 Chicago Conference about ALS being basically a late-stage Lyme disease I have wondered if I have borrelia causing my ALS. While I had tests two years ago from the recognized leader in Lyme testing, and those tests came back negative for borrelia, I wonder if that pathogen is what ultimately tips the scales to ALS as Dr Mattman surmised.
If, as described on this thread, borrelia downregulates the VDR and does not BLOCK it .. and that olmesartan may not be effective for pathogens that work by down-regulating the VDR ... then I wonder how effective my current regimen of just Benicar is going to be? I have been on the MP now for almost two years and have not seen any neurological improvement yet. Also Scott K was on the MP for over two years with ALS and did not get much improvement. Given these facts, I wonder if a Benicar only approach is the correct path for ALS that possible could have borrelia as a main component of the microbiota that ultimately causes ALS!
Prof Trevor Marshall
Foundation Staff
|Lida Mattman was using (her own) antibodies to determine if a species was Borrelia. The poor selectivity of antibodies probably explains why everything she saw identified itself to be Borrelia
As for the scare mongering about people being too-ill to recover on the MP there is NOTHING, nothing at all, which would indicate that is true. Stop worrying, stress will definitely make the disease worse...
It is important to recognize the way that the disease, and IP, can change the way you think..
|Thanks Dr Marshall.. it is always reassuring to hear your positive attitude! I am TRYING very hard to stay positive and not get under too much stress ... trust me on that. But I must admit it is difficult to remain stress free given how much motor function I am losing and how close to be totally bed ridden I am coming! I want to believe all this is just IP and part of the healing process. But it is hard not to wonder and worry about the terrible consequences if it is NOT IP but just the normal progression of ALS. Hopefully the pure olmesartan study can get underway SOON as I think that may help me considerably.
As always I do really appreciate your reassuring advice!!
Prof Trevor Marshall
Foundation Staff
|It is almost certainly not the normal progression of ALS. Mean survival is 18 months after diagnosis Your cardiac and pulmonary status has not deteriorated at that rate...
I know it is tough losing so much neurological function, and it is also tough waiting for the body to regenerate. I thought your chess had been improving recently?
|Well now that you mentioned my chess ... that remains the lone bright spot in my life! I just won my 15th game in a row last night! And this is from a group of expert chess players that in the past I would have been lucky to break even with! That is another thing I wonder about.. how is it that I have avoided the "brain fog" that so many others report as part of the IP.
But it is known that ALS does not really affect the logical thinking processes much if at all. It for whatever reason goes after primarily the motor CNS of the brain and spinal column. And while it is true the mean time for ALS to mortality is startlingly short.. for some it can take years and years. The neurologist that was my doctor's predecessor as head of the UCSF ALS center, Dr Olney, has had ALS now for 8 years and is just now reaching the fatal end stages.
You are correct that my pulmonary and cardiac function remain strong and healthy at this point.. exactly two years to the day from my ALS diagnosis! So that is very encouraging indeed and something my neurologist stresses when I meet with her.
I guess the only way of knowing the outcome of this long difficult journey is ... one foot in front of the other ... step by step ... til the end! But be assured I AM willing to take this ALL THE WAY though to the end. You will NOT see me giving up on the MP as others have done! I intend to either prove it works for ALS.. or vice versa. At least I have that to reassure me that my efforts will not be in vain and will help others in the future no matter my ultimate outcome.
|What exactly is the difference between the VDR being blocked and being downregulated?
|Hi Chris,
I guess you are in good smart company with Stephen Hawking! I know it is hard to wait around for progress but I am seeing some good results too after almost 2 years. My lungs feel so clear this summer in the middle of allergy season, so I am hanging onto that. It sounds like you have some excellent signs from what the experts have said.
|seanlane wrote:
What exactly is the difference between the VDR being blocked and being downregulated?
Blocked: a ligand, like 25D, binds to VDR itself and shuts it off (number of VDR's stays the same)
Downregulated: upstream of VDR, Estrogen Receptor transcribes VDR, if a microbe blocks the Estrogen receptor, VDR will not be transcribed, ergo: downregulated (number of VDR's goes down)
Hope this helps,
Best Frans
|Frans wrote:
And if the Estrogen Receptor is blocked, Osteoporosis may be the consequence, isn´t it ?
Thus the correlation between chronic infections, blocked VDR and Osteoporosis could be explained via ER ?
Last edited on Thu Jul 14th, 2011 12:03 by Alejandro
|Thanks for the encouragement Deb ... I appreciate it!
And Frans, thanks for the nice example of how upstream from the VDR the estrogen receptor can affect the expression of the VDR. This makes me wonder about some studies I read recently that show some benefit for traumatic brain injuries by giving massive doses of progesterone. Could it be that this helps the immune system clean up not only infected cells.. but also damaged cells?
I guess I can only hope that IF borrelia does play a key role in ALS, and Dr Marshall has said it probably does NOT ... and if borrelia does downregulate the VDR somehow, that olmesartan will impact the proper receptors enough to eventually turn the tide against this terrible disease.
But it is interesting to speculate and wonder if this difference of blockade of a receptor versus downregulation of a receptor might account for the different rates of recovery for different chronic illnesses that we see on the MP. Maybe there are pathogens that can still evade olmesartan's reactivation of the VDR ... by downregulating the VDR so that there are not many VDR expressed in those infected cells.
Prof Trevor Marshall
Foundation Staff
Maybe there are pathogens that can still evade olmesartan's reactivation of the VDR ... by downregulating the VDR so that there are not many VDR expressed in those infected cells
But Olmesartan hits many receptors, at least a half-dozen strong-hits that I know of It apparently has just the right profile to do the job
Progesterone reduces inflammation, because it is immunosuppressive. Hence, the patient would feel better, and there would be less swelling (in the short-term)
|Thanks Dr Marshall! Good to have it reinforced that olmesartan hits those other receptors also.
Could this difference of VDR blockade vs VDR down regulation be the reason why the recovery rate for some chronic illnesses, i.e. neurological, take longer than others on the MP? It would seem like a plausible reason why the recovery takes a lot longer in some illnesses.
Prof Trevor Marshall
Foundation Staff
|Indeed, variation from patient to patient, from microbiota to microbiota, is what causes the variable length of recovery (IMO). But I have seen no evidence to date that recovery does not come incrementally for all those who manage to stick with the IP for long enough...
|Music to my ears Dr Marshall!!
Aunt Diana
inactive member
If it is any consolation to you, I did not have any neurological improvements until I was well into my 4th year of the MP. Many times I felt much worse than I had before starting the MP....I believe it is IP you are dealing with.
Even knowing this does not make it any easier to go through.
It certainly seems to me that with your chess game improving things are looking up.
|Thanks Aunt Diana for your encouragement!
I guess I just have to be patient and wait for that turning point where I realize some neurological improvement. But I do know if I continue on this trajectory for another two years ... it is going to get VERY difficult on me and my loved ones! I was hoping that due to being relatively healthy back when I started in Aug 2009, that I'd have a faster recovery time. Now that does not look like it is the case.
But as I said in an earlier post on this thread... I am in this til the end! ... whatever the ultimate outcome! I intend to help prove that the MP either works or doesn't work for ALS! You will NOT see me giving up on the MP to try some other crazy cure out there. I have spent two years now studying and learning the science behind the MP. The science is too strong to give up on. And I feel strongly the MP gives me the BEST chance at defeating this terrible disease called ALS!!
If I am fortunate enough to defeat this normally terminal disease with the MP ... you'll see me working as hard as I can to assist Dr Marshall's efforts to spread that victory as far and wide as possible! That is a goal that helps me keep my sanity and focus when I am feeling down and tempted to doubt things.
|Now Armin Alaedini at Weill Cornell Medical College in New York and his colleagues have found that patients diagnosed with post-Lyme disease syndrome have antibodies that suggest they carried the infection for an unusually long time. The finding, published in Clinical Immunology1, might help the syndrome to be better understood, diagnosed and treated.
Alaedini's team looked at antibodies made in response to a protein called VlsE, which is found on the surface of Borrelia burgdorferi, the tick-borne bacterium that causes Lyme disease.
The antibodies recognize a snippet of the protein called an epitope, and recruit the immune system to attack the bacterium. The researchers found that post-Lyme sufferers have a greater variety of antibodies to this epitope than patients whose infection cleared up quickly.
This finding suggests that patients with chronic symptoms have experienced a prolonged infection, caused by microbes that have evaded the immune system by varying the epitopes they carry. As a result of these variations, the body makes new antibodies targeting the modified protein. The longer the microbe manages to keep changing, the more diverse its host's antibodies become.
Prof Trevor Marshall
Foundation Staff
|The group at Weill Cornell did not consider the possibility that their testing procedures might be confused by the thousands of other species present along with the Borrelia. I read this report, and although not junk science, it is of little practical use until their procedures become more precise, IMO. They really don't have much of a clue.
Rule #1 - whenever you see the word "antibodies" the research is most probably suspect.
|Interesting Frenchie..thanks for posting this..
|Dr Marshall, I saw in Your patent, that on page 3 there is information olmesartan docks into borrelia GPCR receptor.
Is this knowledge current ?
Do we know what this receptor does for borrelia ?
patent link
Last edited on Fri Sep 16th, 2011 01:41 by wrotek
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Coming in January: Parent Workshop regarding Social Media
by Karen McGrath, Technology Department Head – Sandwich High School
On January 6, 2015 at 6pm the Sandwich High School Technology Team, along with School Resource Office Christa Cabral and Social Worker Susan Coutinho, will be hosting a parent workshop titled: "Empowering Parents with Social Media".
All parents of students in grades 7-12 are invited to attend this evening. The event will take place in the high school library media center and will include sessions on current popular social media sites, legal issues surrounding social media use and tips for parents on how to monitor students' technology use in the digital age.
We hope you will join us as we partner to cultivate an awareness of the role social media plays in the life of students in grades 7-12. Participants will feel empowered with tools and resources to help guide them as they navigate this area with their children.
You can get your free ticket to this event at: http://tinyurl.com/nhvmeuh
Please fill out our Survey at: http://tinyurl.com/kxjllbu
We look forward to working with you on January 6th!


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(CIDRAP Business Source Osterholm Briefing) – It's my job to stay current—even anticipate—what the world of pandemic influenza will look like over the next months. But you will never hear me predict severity. Never. You deserve better than that! The severity of past pandemics predicts nothing about the current pandemic. Worse, it distracts our attention from what we must do right now.
If anyone could accurately forecast the onset and severity of pandemic H1N1 cases in your community, business locations, and international supply chains, then preparing for a next wave of H1N1 would surely be made easier. Isn't going to happen—despite some of my professional colleagues' recent attempts to predict that future.
Now it's one thing to overlay (for purposes of illustration) the morbidity and mortality statistics from previous pandemics on today's population to fathom the scope of a pandemic's power, to understand the range of ensuing problems. And in many years of making presentations, I've used such examples; they wake people up, get them thinking, and maybe encourage them to act. But that's as far as we can go. And that's a far cry from forecasting the severity of a completely unpredictable new virus based on the history of others.
Don't get me wrong, influenza experts do need to lay out as clearly as possible evidence of where we see this H1N1 pandemic going so that we can all execute responsible pandemic preparedness plans that are grounded in flexibility. Your guiding principle must remain the following: Expect the unexpected.
Severity is only one part of the equation that determines a pandemic's impact. How widespread the transmission is is another. If you're feeling like a ping-pong ball with all the new reports and predictions about severity coming out, let me help you stop the senseless distraction so you can focus on your priority tasks.
Blundering into the past
To be blunt, any attempt to use past pandemics to predict severity of the current one is pure puffery. Let me explain why.
Just this week, two of my colleagues (and friends) from the National Institutes of Health (NIH) wrote a piece in the Journal of the American Medical Association (JAMA) suggesting that there are assumptions about the course of the 1918 influenza pandemic (also caused by an H1N1 influenza strain) that may be leading to misperceptions of what the current H1N1 has in store for the world.
Researchers, including noted influenza historian John Barry—another friend and colleague—have compelling data showing that soldiers in US military training camps in April and May of 1918 who experienced a relatively mild outbreak of "flu-like illness" were largely protected against the much more serious illness that occurred later in the fall and early winter. We didn't have the capability to isolate viruses back then, so no one will know with absolute certainty that Barry and his co-researchers are right. Furthermore, because illness was mild, finding genetic material from anyone whose deaths were caused by the pandemic virus is virtually impossible.
But based on epidemiologic data, I, for one, think Barry is correct, that there was a mild wave spring in 1918 that preceded the much more serious wave later that year. My colleagues from the NIH disagree with that conclusion and believe that today's planners are assuming that the current H1N1 pandemic will worsen in terms of disease severity this fall, based on what they believe are the faulty conclusions of what happened in 1918.
That's not the end of the story. Two days ago, Helen Branswell, one for the world's leading influenza journalists, wrote a story about the JAMA piece and interviewed other infectious disease experts for their opinion. It's worth a read.
As you might expect, every expert had an answer but no more data to support their cases than my NIH colleagues. One of the experts interviewed for Branswell's piece is convinced that what we'll see during the next wave of H1N1 will look much more like what happened in 1957 with the H2N2 pandemic. In that pandemic, there was no evidence that the virus got more virulent (able to cause more severe disease) during the second wave of illness.
So why do I even mention this JAMA article and get into the nuances of what influenza experts are predicting? Because both the JAMA and Branswell pieces are circulating in the preparedness world, leading many to believe that we are capable of predicting what will happen in the upcoming weeks. Nothing could be further from the truth. I see two reasons why you should interpret with great caution the JAMA report and the comments of the experts in Branswell's piece.
Reason 1: The virus itself is unpredictable
Nobody really knows what is going to happen when this next wave of H1N1 is overlaid on the traditional "enhanced influenza transmission period" of our northern hemisphere winter season.
Yes, the current pandemic strain of H1N1 could either mutate or reassort (ie, mix genes with an existing influenza virus) and change in its ability to cause serious disease. But remember that means it could become either more severe or less severe. We just don't know.
Please—view with skepticism anyone who tells you that he or she knows what this virus will do when it comes to severity. And if someone tries to sell you a previous pandemic occurrence as the model for what will happen this year, say "thank you" and move on. We can view pandemic history with interest. I sure do. But would I use that history to predict whether or not today's pandemic will be a model that differs from or resembles what we saw in 1889, 1918, 1957, or 1968? No. I know I can't give you a definitive answer. What I can tell you is that not one of the pandemics I just mentioned was similar to any of the others.
Reason 2: It's the economy, my friends
The current pandemic is the first to occur in a world with a global just-in-time economy. We have precious little to no surge capacity for many of the critical products and services we count on every day, including many life-saving medical supplies and drugs. What's more, as part of the global nature of our new economy, most of the products or their key components originate in Asia. And their supply chains are long and fragile.
Remember: We do know that pandemic H1N1 is disproportionately hitting people younger than 50 years old, regardless of where they live. Unfortunately, neither China nor India will have much H1N1 vaccine to administer to citizens, including their workforces. Even if the current H1N1 influenza virus changes little over the next months, just consider the sheer numbers of people who'll be affected by this easily transmitted virus. We do know we're going to see greater transmission. The very real possibility of substantial illness among workers and their family members and resulting absenteeism for several months is staggering.
Bear in mind I'm not even talking about severity.
Bottom line for your organization
Don't get caught up in the esoteric debate of some academic flu experts about what is going to happen over the next 6 months. Trust me, they don't know. I promise to alert you as soon as information that does merit your attention becomes known.
So here's our imperative: We must plan as if things could be worse, even if no more than 30% of our population under age 55 will get sick with H1N1 and limit our workforce for weeks. Such a scenario doesn't turn on the virus's changing. Also, don't forget the backdrop against which this pandemic is unfolding—the global just-in-time economy. None of us have any idea how this factor will change what happens with H1N1 infection in our communities.
In the end, this fact may be the wild card my virologist friends know little about. But you must consider it in your organization's preparedness plans.


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The New Wave of British Heavy Metal (often abbreviated as NWOBHM or N.W.O.B.H.M.) is a movement that began during the late 1970s in Britain. Following early heavy metal groups like Black Sabbath, the era developed the sound into a more hardcore less blues tone, often with a faster tempo and sometimes clear punk influences. Hard rock also seemed to be of similar style too. NWOBHM became an influence to later heavy metal groups like Metallica in developing their own style. The image of NWOBHM bands was characterised as long hair, denim jackets, leather and chains, later becoming the predominate image of heavy metal as a whole.
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By Submitted Story on February 7, 2020
Alba Marie DiFabio DelVacchio, 97, of Kill Devil Hills, NC died Wednesday, February 5, 2020, at Vidant Medical Center, Greenville, NC.
Born in Philadelphia, PA on January 7, 1923, she was the daughter of the late Cecelia Filippone and Pierino DiFabio.
An avid reader, Alba enjoyed playing bridge, working on several jigsaw puzzles at once and completing crossword puzzles in ink. She was often referred to as a force to be reckoned with. A parishioner of Holy Redeemer by The Sea Catholic Church, she found joy in taking care of others.
Alba is survived by a daughter, Karen M. DelVacchio; and a son, Daniel W. DelVacchio.
In addition to her parents, she was preceded in death by her husband, Donato Raymond DelVacchio; a daughter, Eileen R. DelVacchio; and her three younger siblings.
A Mass of the Resurrection will be celebrated Friday, February 21, 2020 at 11:00 am at Holy Redeemer by The Sea Catholic Church by Rev. Dr. William F. Walsh, osfs. Following the Mass, a reception will be held at Basnight's Lone Cedar Café. Bring your best Marie story!
As a breast cancer survivor, in lieu of flowers, donations in Alba's memory may be sent to the Outer Banks Relief Foundation's Breast Cancer Fund, 103 East 8th Street, Nags Head, NC 27959. Funds are used for ancillary expenses during breast cancer treatment.
Twiford Funeral Homes, Outer Banks is assisting the family with arrangements. Condolences and memories can be shared at www.TwifordFH.com.