Tortuga, 1936 Classic Wooden Powerboat, is Sold.

I sold Tortuga on April 13, 2022 and the boat departed for her new home in Beaufort, SC on April 15, 2022.

Cruise in classic style aboard Tortuga. Tortuga is a west coast (San Francisco) boat built in the style of Lake Union Dreamboats and Blanchard yachts of the 20s and early 30s. She is a head turner having a style that is very nearly unique in Maine.

Tortuga was built by Nunes Brothers Boat and Ways Company in Sausalito, California on San Francisco Bay. The boat stayed in the Bay until the early 2000s when the fellow I bought her from bought the boat and trucked her to Maine. I bought Tortuga in 2007 and undertook a four year refit that included repowering with a new diesel engine.

Tortuga was last surveyed (condition and value for insurance) in May 2021. Survey available.

Tortuga is in the water for 2021 and in active use (last underway August 6, 2021).

Tortuga’s specifications are as follows:

LOA – 32’8″

Beam – 9-5″

Draft – 2’10”

Construction – Carvel planked with 7/8″ Douglas Fir, oak frames, oak stern post and stem, Douglas fir keel. Bronze fastened from the keel to 10″ above the waterline and stainless fastened above that. Varnished mahogany cabin house (new in 2014). Decks and cabin top are marine plywood epoxied to tongue and groove Douglas Fir planking sheathed with 10 oz fiberglass cloth set in epoxy.

Power – Volvo-Penta D2-40F diesel engine (new in 2011) that currently has approximately 304 hours. The boat cruises comfortably at 2,000 rpm making approximately seven knots on 3/4 gallon per hour of diesel. Top speed is approximately 9 knots at 3,100 rpm (wide open throttle).

Tankage – Fuel – 40 gallons in two 20 gallon Moeller Polyethylene tanks (new in 2011); Water 26 gallon bladder tank (new in 2011); Holding – 9 gallon Todd Poly tank (new in 2011).

Upper cabin – Varnished mahogany with 19 windows (9 opening), varnished Douglas Fir tongue and groove sole, mahogany settee with green cushions, two fold down mahogany tables (one each side). Helm is to port with bronze/teak wheel, single lever engine control, Volvo-Penta instruments, windlass control and Fireboy override for automatic fire extinguisher in Engine Compartment.

Lower cabin – The lower cabin is finished Herreshoff style with white painted bulkheads, varnished mahogany trim and painted cabin sole. The galley is aft (Origo 2 burner alcohol stove, bronze sink with hot and cold pressure water, Dometic 40 quart 12 V refrigerated cooler, dish cabinets and a separate prep area to starboard with several drawers). Forward of the galley there are two 6’10” settee berths with Sunbrella cushions. The port settee has the water tank and pump under it and there is storage under the starboard settee. Forward of the settees there are lockers with shelves to port and a hanging locker to starboard. At the forward end of the cabin is the head with a Wilcox Crittenden Skipper II manual head and a porcelain sink. Day/night solar vent in head (new 2021)

Anchor gear – Lewmar 1000 horizontal electric windlass with controls at the helm. 120 ‘ of 1/4″ HT chain and 200’ of three strand nylon rode connected to a Delta 22 galvanized anchor on a stainless steel anchor roller. The anchor is self launching. All anchor tackle new in 2011 and has been lightly used.

Running lights – Bronze side lights on mahogany name board mounts on the cabin top. All around white light on varnished Douglas Fir mast. All original to the boat.

Electrical system – 1000 cranking amp start battery and two 105 amp-hr grp 27 house batteries. Batteries new in 2020. House and starting batteries are interconnected with a Blue Sea automatic charging relay. 115 amp alternator on the Volvo-Penta diesel. Two 50 watt solar panels connected to a Victron 75/15 MPPT charge controller keep the batteries charged. Circuit breaker panel with a separate circuit breaker for the windlass. All LED lights in both cabins.

Electronics – Standard Horizon VHF radio with new (2021) antenna, Apelco depth sounder. Raspberry Pi based 7″ touch screen chart plotter running Open CPN with current USCG charts for Maine (all US charts available free for download from NOAA). Electronics have been kept to a minimum intentionally to keep the vintage appearance of the boat. There is also a gimballed compass in a mahogany box at the helm.

Bilge pumps – Three electric pumps on individual float switches. Two pumps are Rule 1100 GPH mounted at the lowest point in the bilge on either side of the keel and the third pump is a Rule 4000 GPH pump mounted on top of the keel as a backup. There is a spare (new) 1100 GPH pump on board.

Fuel system – Two 20 gallon Moeller polyethylene tanks. Tanks have separate deck fills. Valving allows the engine to run of either tank and the return can be set to either tank. Two Racor 500MA fuel filters with change over valve allowing change with the engine running. Entire system new in 2011.

Tortuga underwent a major rebuild from 2007 to 2011 that included reframing most of the boat with laminated Oak frames, new floors, new engine beds, repowering, all new systems and replacing many planks. The lower cabin interior was also completely rebuilt during that refit. All systems were replaced during the refit including water heater, tankage (fuel, water, waste), all seacocks and thru hull fittings, bronze raw water strainer, fresh water plumbing, windlass and anchor tackle, most wiring, etc. The 20×13.3 three blade bronze propeller was also reconditioned and repitched to match the new engine. Since 2011 the aft and side decks have been rebuilt and the cabin house was completely rebuilt in 2014. A Webasto diesel fired heater was also installed in 2014. Annual maintenance includes replacing ALL suspect wood and completely repainting/varnishing the exterior of the boat. Work on the boat continues. For example I replaced part of the foredeck toe rail this week and will repaint the aft and side decks this summer.

Pictures (all taken in 2021).

Hanging on the mooring
Port side at the dock
Bow on
Looking aft in the upper cabin (7/1/21)
Looking forward in the upper cabin (7/1/21)
Volvo-Penta D2-40F diesel
Lower Cabin looking forward
lower cabin looking aft port
Origo alcohol stove
Lower cabin aft starboard
Head sink
Completely rebuilt engine compartment with fiberglass pan under engine prior to new engine installation in 2011.

How CLL Can Mess Your Summer Up

The Summer season here on the coast of Maine is drawing to a close. My 1936 powerboat,Tortuga, will be hauled out around the end of this month and my sailboat Seaquestor, which I am sitting on now, will be out of the water for the Winter by the end of October. So far, this has been a disappointing season for me. For the first time sine we bought Seaquestor in 1996, we have not taken either boat for an overnight outside the Great Harbor of Mount Desert Island. That circumstance is a consequence of my health. Basically I have been experiencing significant fatigue, which is a common symptom of Chronic Lymphocytic Leukemia (CLL).

I have been to doctors four times this Summer. The last two visits were the most consequential. As far as the CLL itself goes, on August 24th my hematologist/oncologist said my disease has progressed to Stage 4. That is a consequence of my continuing low platelet count (consistently below 100 for a year now – 150 is the bottom of the normal range) and the fact that my lymphocyte count has increased to 85,000-90,000 per microliter of blood. A normal lymphocyte count is between 1,000 and 4,000 per microliter of blood. During that visit my doctor said that if my platelet count doesn’t rebound by my next blood test (October 5), I will be looking at starting treatment for my CLL late this Fall (November).

On August 30 my GP, after looking at my blood results for the summer (four tests) came to the conclusion that I have Hashimoto’s hypothyroidism. That is an autoimmune disease in which your lymophocytes produce antibodies against your thyroid. Those antibodies damage the thyroid which reduces its capability to produce T4 thyroid enzyme which essentially controls your metabolism. Low T4 results in fatigue and weight gain among other things. Consequently, since August 30th I have been taking the generic version of synthroid (levothyroxin). Since Hashimoto’s is an autoimmune disease involving lymphocytes, it appears that my condition is likely related to my CLL. In addition the damage to the thyroid is not reversible, so even if my CLL is effectively treated reducing or eliminating future thyroid damage I will be taking synthroid for the rest of my life. I see my GP again on September 20 to adjust the synthroid dosage if needed.

I have also been experiencing significant sinus congestion since last Spring. That congestion is primarily in my ears and it has been effecting my balance for much of the summer. My GP told me to start taking an over the counter anti-histamine called Centirizine HCL (Zyrtec). After a week of it my sinus congestion is decreased but not gone.

Over the last 18 months I have gone from taking an occasional ibuprofen to taking four pills a day. I start my day with 300 mg of allopurinol (to reduce my blood’s uric acid content) and 50 micrograms of synthroid (for the thyroid condition). I take those pills before breakfast. After I eat I take a 10 mg centirizine pill (for the sinus issues). In the afternoon I take a 150 mg ranitidine pill to control acid reflux disease. Basically I have become one of those old people with a pill box loaded with my daily drugs. If I go into treatment for my CLL this Fall it will get a lot worse.

Despite my misgivings about all the pills I now take, I have to say that they have improved my quality of life. The allopurinol has greatly reduced my uric acid level and has also effectively controlled my gout. So far I seem to have more energy after starting the synthroid. The centirizine has decreased my sinus conjestion to the point that I no longer feel dizzy although I can still feel the conjestion. Finally the ranitidine is very effective at eliminating my chronic acid reflux. I am hoping that all these drugs will let me get out for a couple of overnights on the boats before it is time for haulout.

Why Is Chronic Lymphocytic Leukemia Incurable?

In this blog I will be putting forward my thoughts on just why Chronic Lymphocytic Leukemia (CLL) remains essentially incurable.  The points expressed here are based on my reading over the last fourteen months on the topic of CLL and its treatment.  I want to stress that the conclusions put forward in this blog are my own opinions based on that reading.  I am wholly responsible for any errors of fact or logic in this discussion.  Bear in mind that I am not a medical doctor and my Ph.D. is in geochemistry/physical-inorganic chemistry not molecular biology or biochemistry.

Hematopoesis and Proliferation of CLL B-Lymphocytes

I will start this discussion by looking as the hematopoesis and proliferation of CLL monoclonal B-Cells.  Monoclonal CLL B-Cells initially arise as a consequence of
a mutated precursor cell. The initial mutation can be in a hematopoetic stem cell (HSC), multi-potential progenitor cell (mppc) or lymphoid progenitor cell (LPC), all henceforth referred to progenitor cells.  Once a stable mutation occurs the mutated progenitor cell can undergo cell proliferation leading to a monoclonal
population of mutant progenitor cells that in turn produce monoclonal mutated B-lymphocytes.

Growth of the Monoclonal B-Cell Population

The rate of mutant progenitor cell proliferation is a controlling factor in the growth of the CLL monoclonal B-Lymphocyte population during early stages of the disease (i.e., Monoclonal B-Cell Lymphocytosis (MBL)). However, the generally quiescent nature of HSC and more specialized progenitor cell populations mitigates against progenitor cell proliferation being a major contributor to the accumulation of monoclonal CLL B-Cells.

Since monoclonal CLL B-Cells are generally long lived (typical lifetime of CLL B-cells averages 100 days) compared to normal B-Cells (lifetime is typically 5-7 days), monoclonal B-Cell proliferation (i.e., cell division) appears to be a primary driver in the growth of the monoclonal cell population relative to the normal B-Cell population.

The expression of B-Cell receptor proteins (BCR) on the surface of B-Cells is known
to play a critical role in B-Cell proliferation. Furthermore CLL monoclonal B-Cells
have been found to generally under express BCR, which is consistent with the generally indolent nature of CLL.  The differences in the progression rates of the various genetic variants of CLL (17p, 11q, trisomy 12, “normal” and 13q) my reflect differences in the expression of BCR on monoclonal CLL B-Cells.

CLL Treatments and Their Targets

With the exception of allogenic stem cell transplantation, the treatment of CLL has historically concentrated on killing B-cells either by direct mechanisms (chemotherapy) or by marking cells for attack with antibodies (anti-CD20 monoclonal antibodies). More recently, targeted therapies have been developed that interrupt the BCR signalling pathway by disrupting either the BTK or PI3K kinases which are critical components in that pathway (i.e., ibrutinib and idelalisib, respectively). Similarly apoptosis stimulating drugs (venetoclax) work by blocking the anti-apoptotic BCL-2 protein, thus allowing apoptosis.  All of these treatments are based on B-Cell proliferation being the primary mechanism of accumulation of monoclonal CLL B-Cells. Despite producing long remissions for some patients (primarily those that are 13q deleted and have mutated IgVH genes), none of these therapies has produced a cure for CLL.

Allogenic stem cell transplantation is the only therapeutic approach that has been shown to cure CLL. The procedure works by eradicating the B-Cell population in the periferal blood, lymphatic system and the bone marrow via intense chemotherapy. The chemotherapy also eliminates the stem cell population, which is then replaced by donor stem cells.  Unfortunately only a small subset of patients are candidates for transplant and the mortality among suitable patients is very high (> 30%). Thus stem cell transplantation is only suitable as a therapy of last resort after other therapies have failed.  In addition, not all stem cell transplants actually produce a cure since a significant percentage of patients (35-40%) relapse after transplant. That result strongly suggests that the pre-transplant chemotherapy did not completely eradicate either the entire population of monoclonal CLL B-Cells or the population of HSCs and other progenitor cells in the bone marrow.  This takes me to the question posed in the title of this presentation:

Why is CLL currently incurable?

I would like to suggest that the answer is that current treatments, with the exception of stem cell transplantation, target monoclonal B-Cells and not HSCs
and other progenitor cells. Consequently, even when a patient achieves Minimal
Residual Disease negativity (MRD- status) after treatment, a population of mutated HSCs or other progenitor cells persists in the marrow. That population of cells provides the mechanism for future development of a new population of monoclonal CLL B-Cells.

Because of the quiescent nature of HSCs and other progenitor cells in the marrow, the progenitor cell population is small. Thus, for patients with particularly indolent disease (13q deleted with mutated IgVH gene), the patients may be effectively taken back to the very early MBL stage of the disease and may not progress to formal CLL during their lifetime.  In other words, the patient may appear to be cured although in fact there are still mutated precursor cells or a small number of monoclonal CLL B-Cells in the peripheral blood or lymphatic system.  This appears to be the case for some 13q deleted, IgVH mutated patients after FCR therapy.  The arbitrary boundary between MBL and CLL is 5,000 monoclonal B-Cells per microliter of peripheral blood.  Furthermore only about 1% of MBL patients progress to CLL per year. However, patients with a more aggressive form of the disease (17p or 11q deleted) may relapse more quickly after achieving MRD negativity.   Thus it appears that the current treatment paradigm, which targets B-Cells , will not produce a cure for CLL although as I just noted it may produce an apparent cure for some patients.

Thus, it appears to me that the current treatment paradigm and associated research, which focuses on eliminating CLL B-Cells will not succeed in producing a cure for CLL.  I would suggest that in addition to developing more effective and less toxic therapies specifically targeting monoclonal B-Cells, that research should focus on characterizing mutated HSCs and other progenitor cells that generate monoclonal CLL cells in the marrow. A successful characterization of CLL B-cell progenitors could lead to therapies that target those specific HSCs and progenitor cells while leaving those cells producing normal blood components unharmed.  Unfortunately because of the relatively small numbers of progenitor cells such research will be difficult.  Such therapies would have to be coupled with therapies that target monoclonal B-Cells because their elimination from the peripheral blood, lymphatic system and the bone marrow is a necessary condition for a cure.  Thus there is still a role for current therapeutic research.

Sizing Wires for a Solar Panel Installation

When installing solar power on a boat or RV the wires that connect the components are often overlooked.  This short blog post is a companion piece for my YouTube video of choosing and sizing wires for a solar power system.

The post consists of a number of images of the results of calculations of wire size for a solar panel installation.  I have calculated wire sizes for specific solar panels and combinations of panels.  Watch the video to get a more thorough explanation.

Here is a link to the best prices for marine tinned stranded wires

Note that the calculations below are done for all common solar panel sizes individually, wired in parallel, wired in series and wired in series parallel.


The CLL Treatment Paradigm

Chronic Lymphocytic Leukemia (CLL) treatments have changed greatly over the past 25 years.  In order to more completely understand the magnitude of that change a bit of historical perspective is needed.  This blog is my attempt to describe the CLL treatment paradigm and how it has changed through the years.

Early Treatments and the Advent of Chemotherapy

Leukemia was formally defined in 1845 as a blood disorder characterized by an over abundance of white blood cells. Early treatment for leukemia was arsenic trioxide.  That persisted until about the 1920s when radiation was recognized to reduce tumor size and decrease white blood cell counts.  Early radiation therapy was administered both externally using X-rays and internally by intravenous administration of Phosphorus-32, a short half life (14.29 days) beta emitter.

CLL was first defined as a variant of leukemia in 1913.  Prior to that date leukemia included all blood diseases characterized by an over abundance of white blood cells.  It was not until after world war II that chemotherapy was developed and applied to the treatment of CLL.  The early chemotherapy agents were derived from mustard gas after it was discovered that soldiers exposed to mustard gas developed low white blood cell counts.  The sulfur mustards in mustard gas were too toxic for clinical use so nitrogen mustards were developed.  The early aliphatic nitrogen mustards (i.e., they had straight carbon chains) included drugs like mechlorethamine hydrochloride (mustine hydrochloride).  In the 1950s less toxic aromatic mustards (with 6 carbon rings rather than straight carbon chains) including chlorambucil (Leukeran).  Chlorambucil was approved for medical use in 1957 and became the primary treatment for CLL.  Chlorambucil is an oral therapy administered as pills.  Chlorambucil was used as a single agent treatment or combined with cortico-steroids.  Now, 60 years later, chlorambucil is still occasionally used in treatment of CLL, particularly of frail elderly patients due to its low toxicity compared to modern chemotherapy agents.  Chlorambucil is also frequently used in clinical trials as a reference treatment although that practice is decreasing since it is widely thought that virtually all modern treatments are more effective than chlorambucil.  Chlorambucil is in the class of chemotherapy drugs known as alkylating agents.

Cyclophosphamide was developed in the early 1950s and was FDA approved as an anti-cancer drug in the USA in 1959.  Like chlorambucil, the drug is a nitrogen mustard derived alkylating agent.  Cyclophosphamide was used extensively in CLL treatment as a single agent and combined with cortico-steroids.  The drug can be administered both orally and intravenously, but is generally administered intravenously in CLL therapy.  Although no longer used as a single agent, the drug is still commonly used in multi-agent chemotherapy regimens.

Bendamustine (Treanda) is was developed in 1963 in East Germany.  It was not available outside East Germany until 1990.  Bendamustine is also a nitogen mustard based drug and is classed as an alkylating agent.  Bendamustine was approved by the US FDA in 2008 for the treatment of all patients with CLL.

Fludarabine (Fludara) is a purine analog chemotherapy agent first synthesized in 1968.  Early clinical trials showed that fludarabine was more effective than chlorambucil.  Later trials looked at the combination of fludarabine with cyclophosphamide (FC therapy) as well as the chemo-immuno therapy combinations FR and FCR where R refers to the monoclonal antibody rituximab.  Fludaranine single agent therapy was approved by the FDA in 1991 for patients who had not responded to or relapsed after previous therapy.  FCR therapy was approved for all CLL patients in 2010.  Fludarabine is normally administered intravenously although an oral version of the drug (approved in 2008) is available.

There are a number of other chemotherapy agents used in some treatment protocols for CLL  As far as I can tell the following drugs are used off label  In some protocols pentostatin is substituted for fludarabine in the FCR protocol.  Pentostatin is approved for tratment of hariy cell leukemia, but not CLL.  Similarly cladribine is sometimes substituted for fludarabine.  Like pentostatin, cladribine is approved for hairy cell leukemia.  Lenalidomide, a thalidomide derivative, is approved for multiple myeloma and myelodysplastic syndrome, but has shown some efficacy in CLL.  Vincristine, which is approved for acute lymphoblastic leukemia, is also sometimes used off label to treat CLL.

Monoclonal Antibodies

Rituximab (Rituxan) is a chimeric monoclonal antibody which targets the CD20 protein expressed on healthy, mature B-cells and to a lesser extent on CLL B-cells but not on immature or developing B-cells. A chimeric monoclonal antibody is a drug that contains murine (mouse) and human components.  Rituximab works by binding to the CD20 protein on the surface of B-cells causing cell apoptosis (cell death).  Rituximab was developed in the late 1980s/early 1990s and was approved for the treatment of non-Hodgkins Lymphoma in 1997.  In the late 1990s clinical trials of rituximab (R) combined with fludarabine (F) and cyclophosphamide (C) began.  Those trials showed superior results to F monotherapy and FC combination therapy.  However it was not until 2010 that FCR therapy was approved in the USA by the FDA for for treatment of CLL in previously untreated and treated CLL.

Since the development of rituximab there have been two newer C20 monoclonal antibodies developed.  They are obinutuzumab and Ofatumumab.  Both drugs work by the same mechanism as rituximab, but the newer dugs are fully humanized and do not contain any murine components to reduce allergic reactions.

Obinutuzumab (Gazyva) is a fully humanized CD20 monoclonal antibody. Obinutuzumab was given FDA approval in 2013 for use in combination with chlorambucil for treatment of all CLL patients.

Ofatumumab (Azerra) is a fully human monoclonal antibody that targets CD20 on the surface o B-cells.  Ofatumumab was FDA approved for treatment of relapsed, refractory CLL in 2009.  It received a further approval for treatment in combination with chlorambucil of previously untreated patients in 2014.  In early 2016 the drug was also approved as a maintenance therapy for patients after at least two prior lines of therapy.  Later in 2016 Ofatumumab was also approved in combination with fludarabine and cyclophosphamide  (FCOf therapy)for treatment of relapsed CLL following prior treatment.

Alemtuzumab (Campath) is an anti CD52 monoclonal antibody that was initially approved in 2001 for CLL patients who had prior alkylating agent therapy and failed fludarabine therapy.  The approval was expanded in 2007 to all CLL patients.  However, in 2012 the drug was withdrawn from the US and european markets and reintroduced as Lemtrada in 2014, which is only approved for treatment of multiple sclerosis.  The drug is still available for clinical studies and, with some difficulty, off label use for CLL.

Chemo-Immuno Therapy

Chemo-Immuno therapy is the combination of chemotherapy drugs with monoclono antibodies.  This combination has been found to provide better responses and progression free survival results than chemotherapy alone.

FCR therapy (Fludaraine+Cyclophosphamide+Rituximab) was approved for treatment of all CLL patients in 2010.  The initial clinical trials for FCR therapy began in the late 1990s.  The therapy has been found to be particularly effective for patients with mutated IgVH gene and the 13q chromosome deletion.  For those patients FCR therapy generally produces long remissions.  As many of 30% of that group of patients from the initial clinical trials are still in remission 17 years later.  However, FCR therapy was not found to produce durable remissions for many 17p deleted patients with both the response rate and progression free survival of 17p deleted patients being poor compared to other patients.  As a consequence, many doctors no longer advise FCR therapy for 17p deleted patients.  Of the current chemotherapy based treatments FCR is the most harsh and restricted to younger, fit patients without decreased kidney or liver function.  Currently (2017) FCR is the preferred frontline therapy for younger fit CLL patients without the 17p chromosome deletion or mutated p53 gene.  In 2016 and additional FC chemoimmuno therapy combination was approved in which ofatumumab replaced rituximab.

BR (Bendamustine-Rituximab) therapy is a chemo-immuno combination therapy that, in the US, is an on-label use of bendamustine combined with an off-label use of rituximab.  BR is an approved therapy for CLL in Germany.  BR is generally a less intense therapy than FCR.  Consequently it is often used for patients without a 17p deletion or mutated p53 gene who would not be considered eligible for FCR therapy.

Two chlorambucil-monoclonal antibody combinations have also been approved which combine chlorambucil with obiutuzumab and with ofatumumab.

Targeted Therapies

As of 2017 there are three targeted therapies.  These drugs target specific signalling pathways within CLL B-cells.  They are Ibrutinib which targets the BTK pathway, Idelalisib which tarkets the Pi3K pathway and Venetoclax which targets BCL2.  All of these drugs are oral therapies rather than intravenous infusion therapies.  At present treatment with these drugs is open ended.  In other words, treatment continues until disease progression or intolerable side effects occur.  The side effect profiles of these drugs are significantly less than chemotherapy or chemoimmuno therapy treatments.  In addition all of these drugs produce response rates more or less independent of cytogenetics (chromosome mutations).

Ibrutinib (Imbruvica), which irreversibly binds to the Brutons Tyrosine Kinase pathway and triggers cell death, was the first of these drugs to get FDA approval for treating CLL.  Ibrutinib was approved in February 2014 for CLL patients who had received one prior herapy and had a 17p chromosome deletion.  In May 2016 the approval was expanded to all CLL patients.  Ibrutinib has a very high response rate (~95%) and patients respond more or less independent of their cytogenetics.  Consequently ibrutinib therapy has become the front line therapy of choice for those with a 17p deletion.

Idelalisib (Zydelig), which targets the Pi3K communication pathway, was approved in combination with rituximab for relapsed Cll patients in July of 2014.   While the idelalisib part of the therapy is open ended, the rituximab treatment only continues for approximately 5 months.

Venetoclax (Venclexta) is a BCL-2 inhibitor.  BCL2, which is over expressed on CLL B cells, promotes extended cell life.  Bonding of venetoclax to BCL-2 on CLL B cells triggers apoptosis (cell death).  Venetoclax was approved in May 2016 for relapsed refractory CLL patients with 17p chromosome deletion.

Timeline of Treatment Approvals

Prior to the 50s there was only radiation therapy and a few drug therapies I didn’t mention.  None of those therapies was particularly effective in that they only slowed progression of CLL.  In the 50s the development of comparatively effective chemotherapy drugs (chlorambucil and cyclophosphamide) improved the life of CLL patients in that those drugs did generate remissions in some patients.  However those remissions were not particularly durable and the lack of alternate therapies meant that while quality of life was improved, overall survival was not.  The approval of fludarabine in 1991 for CLL treatment brought with it much higher response rates and deeper and more durable remissions.  However, patients with negative prognostic indicators (17p and p53 mutation) still had a very poor prognosis since those patients were often resistant to fludarabine treatment.  The real break through in survival came with the development and approval of FCR therapy.  That was particularly true for some 13q deleted patients with IgVH mutations where FCR therapy might even be a cure.  Again the 17p deleted patients were largely left out of the break through.  In 2014, the approval of the targeted therapies marked another break through that this time included the 17p deleted patients.  Furthermore, while some patients still fail therapy with one of the targeted therapies, the other therapies still appear to work for them.

2017 Treatment Paradigm

In 2017 the approval of the targeted therapy drugs ibrutinib, idelalaysib and venetoclax has completely changed the CLL treatment paradigm.  Prior to the approval of these drugs treatment options were chemotherapy and chemoimmuno therapy.  Since people with 17p chromosome deletions tended to respond poorly to those therapies, and also relapsed relatively quickly if they did respond, the prognosis for 17p and to a lesser extent 11q deleted patients was poor.  Survival often depended on receiving multiple rounds of treatment.  The approval of the small molecule targeted therapies changed that completely because responses were more or less independent of cytogenetics.  As a consequence, cytogenetics has become more of a guide to treatment choice than a prognostic factor.  Despite that statement having an 11q or 17p chromosome deletion still is worse than any other genetic anomaly, but the difference is considerably less than it was before the targeted therapies were developed.

2017 treatment options.

As of 2017 treatment options fall into two categories – chemoimmuno therapy and targeted therapy.  Cytogenetics and other prognostic factors are used more now to guide therapy than they are for prognosis.

Chemoimmuno therapy is still a valid option for some patients, although some doctors are suggesting that chemo is now a thing of the past.  The reasons chemo remains viable are two fold.  First for the subset of patients with 13q deletion and mutated IgVH genes, FCR therapy holds out the possibility of a very long deep remission that might even be a cure.  Unfortunately, only relatively young and medically fit patients are candidates for FCR, so the population it is viable for is small.  The other argument for chemo is that it is a relatively short term treatment – 6 months and done.  That prospect makes it preferable to some patients particularly given the very high cost of the targeted therapies.  Cost is often a significant consideration for older patients on Medicare since the oral targeted therapies can cost as much as $10K per year even with Medicare Part D drug coverage.  Many people simply can’t afford that.  For those that prefer the shorter term treatments of chemo, but are not as fit, the options are BR therapy, which still requires a reasonable level of fitness, or chlorambucil with either obinutuzumab or ofatumumab.  The two chlorambucil regimens are less physically demanding than either FCR or BR, but the responses are not as deep or durable.

Targeted therapies are now available to all patients.  For those with the 17p deletion the first line treatment of choice is now ibrutinib.  This option is also open to all CLL patients.  Should a patient relapse or have to stop ibrutinib therapy, idelalisib and venatoclax are available.  Those options appear to work well after failure of one of the other targeted therapies. With the exception of cost, these therapies have significantly lower side effect profiles than the chemo regimens and are thus possible for older, more frail patients.  All of these therapies also hold out the prospect of minimal residual disease negativity, which may be a cure for some, although that determination is pretty far away at present.

Finally, there are currently a number of other targeted therapies in the pipeline.  They include several newer BTK therapies with apparently even fewer side affects than ibrutinib as well as other drugs targeting different signalling pathways.  In addition there is a lot of clinical research on combinations of targeted therapies (i.e. venetoclax and ibrutinib) and combinations of targeted therapies with monoclonal antibodies.  Those studies hold out the possibility of even deeper and more durable remissions and the possibility of stopping targeted therapy after achieving minimal residual disease negativity.

There is also work going on with CarT-cell therapy in which the patients own T cells are removed, modified to attack their CLL B cells and reinjected.  Finally, there is always the possibility of a stem cell transplant.  However, I am of the opinion that transplant is declining in importance because of the success of targeted therapies, not to mention the risks of stem cell transplant.

I hope this discussion has been useful to you.  Please comment if you have any questions.

Why I Haven’ty Been Posting Much Lately

It has been nearly a month since my last post.  Why?  Well it comes down to one thing.

I discovered creating YouTube videos.

I have been watching YouTube videos for a couple of years and I finally decided to learn ho to make videos and post them.  Making videos (shooting, editing and posting) is time consuming and has kept me away from blogging.

So far I am making three series of videos:  Videos in which I talk about CLL, travel videos that focus on Mount Desert Island, ME and Acadia National Park, and videos about my cat – GrayC Grayfur.  As of today I have made twelve videos of greatly varying quality.  As soon as the weather warms up a bit I will be making additional videos on the subject of boating in which I will show maintenance, boat tours and boating around Mount Desert Island.

Here is a list be series.

Videos About Chronic Lymphocytic Leukemia (CLL)


Travel Videos Centered on Mount Desert Island, Maine and Acadia National Park.


An the obligatory CAT videos (only one so far)


Let me know what you think about my new endeavor.  If you feel so inclined, I invite you to visit my YouTube page and subscribe  to see how far I push this foolishness.



My One Year Anniversary of Having Cancer

It has been a year since I was diagnosed with blood cancer – Specifically Chronic Lymphocytic Leukemia (CLL).  In previous blogs I have looked at the medical and financial impacts of being diagnosed with cancer.  Today I want to talk a bit about the emotional impact that being a “Cancer Patient” has had on my life.

Let me preface my thoughts by saying a bit about the physical nature of my cancer.  My diagnosis was incidental in that it came from a routine blood test.  I had no physical symptoms that I was aware of.  What potential symptoms I had I put down to getting older.  In other words I didn’t have any inkling that I had the big “C”.  Now after a year of knowing that I have cancer I have to admit that physically nothing has changed.  In other words, if I didn’t know I that I have cancer I wouldn’t know it.  I have no symptoms other than one slightly enlarged lymph node in my neck and you have to know exactly where that node is to feel it.  My new oncologist missed it until I pointed it out to him.  Furthermore, my blood tests are within error of where they were when I was diagnosed.  So my leukemia is stable and there really has been no physical impact.

Despite the lack of physical manifestations, my CLL has had a rather significant and ongoing mental/emotional impact.  While it may seem trite to say that being told you have cancer is not the high point of your life, I will say it anyway.  When I got the call on my 64th birthday and was given the news that I have Chronic Lymphocytic Leukemia, I was less than thrilled with my “birthday present” despite it being the most expensive birthday gift I had ever received.  Unfortunately a cancer diagnosis is not the type of birthday gift you can return because you don’t like it.  When I was diagnosed I had never heard of CLL.  My initial mental picture of leukemia was of very sick bald kids waiting to die in the hospital.  That was not an encouraging image.  Although I was more than a bit stunned by the diagnosis, I didn’t feel despair or depression.  Instead I was motivated to find out everything I could about CLL in advance of my first appointment with an oncologist the next week.

My initial research was both encouraging and discouraging.  The discovery that there were different “flavors” of CLL with prognoses ranging from death within as little as two years to living a normal life left me hopeful that I might be in the latter category.  The day of my first appointment with MY oncologist started with blood draws for more blood tests.  The results were ready by the time I met the doctor in the late afternoon.  The physical examination suggested that I was in the early stages of the disease, but my blood tests didn’t agree.  As I had read, one of the markers of rapidly progressing CLL is a doubling of the lymphocyte count in the blood in a year or less.  Well despite my positive physical exam, my lymphocyte count had increased from about 50,000 per microliter to 90,000 in THIRTEEN DAYS!  That was NOT a relaxing finding.  My doctor told me that if the increase was sustained I could be looking at treatment sooner, much sooner, rather than later.  He scheduled me for a slew of additional tests and then apologized for the fact that he wouldn’t be able to see me again for four weeks.  So I left my first appointment with rather conflicting results.  Physically it appeared that I had little to worry about, but my blood analyses gave me a lot to worry about.  My blood results were quite effective in dashing my hopes for a normal life and I left the office feeling quite apprehensive. The tests I was scheduled for the following week, but wouldn’t see the results of for a month became critical.

The forty minute drive home was not a pleasant one as my mind kept coming back to the possibility that my life might be over in as little as two years.  Upon arriving home and explaining the results to my wife I did what any self respecting scientist would do.  I immersed myself in the scientific literature on CLL and did a few calculations.  While I was doing that I was not unaware that I was avoiding thinking about my situation by making it into a scientific problem.  Fittingly, I took my solace in doing a least squares fit of the appropriate cell growth equation to my blood data and then projecting that equation to the date of my next blood test (including an appropriate 95% confidence error envelope, of course).  As the four weeks between appointments with my oncologist ever so slowly crept by I became increasingly apprehensive, as I waited to find out just when my expiration date would be.  I unsuccessfully tried to lose that apprehension by analyzing the CLL literature.  Nevertheless, by the time my next appointment finally rolled around and I nervously sat in the waiting room after my latest round of blood tests fingering through my notes, spread sheets and graphs, I was strangely conflicted.  At one level I was worried about what the doctor would tell me – would I live or would I die.  While on another level I was thinking about where my new blood results would fall relative to my mathematical models.  I had derived explanations for every eventuality from my reading of more than 100 scientific papers on the subject of CLL.  I just needed to know which explanation was appropriate for my situation so I could select the appropriate sheet of questions from my compiled options.

I guess my scientific curiosity was winning the battle because when the nurse took my blood pressure, after heralding me into the examining room, it came out as something like 105/62 – hardly an indicator of extreme anxiety.  Nevertheless, the worry was there at a deeper level as results would demonstrate.

I spent the time while I waited for the doctor reading a paper on B-cell signalling pathways.  The first thing I noticed when the doctor arrived was that he looked cheerful which suggested that what he had to tell me would not include the words “untimely death”.  Things got better from there as he told me that not only did I have the “best” cytogenetic markers (13q-, CD38- and Zap70-), my lymphocyte count was also back to 50,000, where it had been at diagnosis.  That my anxiety about the results had not been completely subsumed within my scientific curiosity became evident when I completely forgot to pull out my prepared list of questions.  I left that appointment feeling almost euphoric since my reading had shown that median life expectancy at diagnosis for a CLL patient with my genetic markers was 17 years, which was only 11 months less than the actuarial life expectancy for men my age in the US population as a whole.  Just how much stress and anxiety I had been operating under for the last four weeks hit home when I realized that I actually felt joyful during the drive home.  In retrospect it became obvious that I had been pretty much an emotional wreck since my diagnosis.

Unfortunately, the joy I felt right after my appointment didn’t last.  My growing knowledge of my disease made it all to obvious that although my prognosis was good, every patient is different and averages mean nothing to the individual.  So I had traded anxiety about imminent death for worry about the results of my periodic blood tests.  I found myself becoming increasingly anxious as the date for my June blood test approached.  At my June appointment my lymphocyte count remained unchanged, but my platelets were low and my doctor uttered the words autoimmune thrombocytopenia (medicalese for your immune system attacking your own platelets causing them to be low) for the first time and changed my appointment schedule from three months to two months.  That appointment gave me something new to research and worry about.  I was discovering why many CLL patients called my “Watch and Wait” status Watch and Worry.

My next appointment was at the end of August.  I was quite concerned about where my platelet count would be.  That concern was not decreased when my platelets came in at 85,000 per microliter, well below the 100,000 point at which hematologists took notice.  My anxiety was not helped when my doctor opened the conversation by talking about possible treatment for my low platelets.  I left that appointment with my blood test frequency changed to every four weeks and the knowledge that although my next appointment wasn’t formally until late December, a further decrease in my platelet count could trigger a bone marrow biopsy followed by an immediate appointment and the initiation of treatment.  In other words anxiety about my CLL progressing was replaced by anxiety about my platelet count and I started living from blood test to blood test.  My monthly cycle became increasing anxiety as the date of my blood test approached followed by a period of relief as each successive test put off the immediacy of treatment for another month.

Now, after a year of knowing that I have CLL, I remain on a monthly blood test cycle with the associated anxiety.  However, after six months on that cycle with no significant change in my platelet count coupled with an increased understanding of the precision of automated platelet analyses data made it clear to me that my platelet count hasn’t changed significantly since diagnosis. That realization reduced the level of my monthly anxiety, but it is still there.  I am learning to live with it and am even starting to plan more than a month ahead.  Another sign that I am becoming more relaxed about my situation is that I more or less stopped reading papers about thrombocytopenia after my December appointment.

Overall I have to say that the month between diagnosis and getting my cytogenetic results was the toughest.  Things leveled off emotionally until late August when the possibility of treatment for thrombocytopenia pushed my anxiety level up again.  Over the last six months my anxiety level has dropped again and I feel pretty much normal except for the last couple of days before each blood test despite still being on a four week test cycle.  However, at the back of my mind there is still some anxiety about what will come next. Will my platelets start dropping again?  Will I become anemic?  Will my lymphocyte count start increasing?  Will my neutrophils drop?  I am gradually becoming used to those nagging worries being with me, which is good because those concerns will be there for the rest of my life since the only cure for CLL at this time is death.

After a year with CLL I am getting used to the anxiety and manage to live almost worry free for three and a half out of each four weeks.  I can only hope that at some point my doctor will switch me to less frequent blood tests so that I can live normally for say twelve and a half out of every thirteen weeks.  Having cancer is certainly not fun, but I have to admit it isn’t as bad as I thought it would be a year ago.

Life in Trumpmerica – Chapter III – Betters

Geoffrey Adkin-Trump-Fitzhugh, hereditary Secretary of the Interior, dismounted after his morning fox hunt in the Virginia countryside and passed the reigns of his horse to a waiting groom.  Turning he nearly bumped into a waiter who held a golden tray with an iced drink on it.  Somewhat nonplussed by the close proximity of the waiter he snatched the glass from the tray and raised it to drink.  He had taken a deep drink of the mint julep before he noticed that the glass was beaded with moisture, which was soaking into his albino fawn-skin glove. Outraged he threw the glass onto the neatly raked white gravel at the waiter’s feet.  Before the shocked waiter could speak, Geoffrey slashed the fool across the face with his riding crop.

“You fool.” he shouted, shaking his water stained glove in the waiter’s now bloodied face.  “Do you know what this glove is worth?”  Geoffrey took a deep breath.  “Of course not.” he said with exasperation.  “Fetch your manager at once.”  he ordered.

The waiter ran off, his hand pressed to his bleeding cheek.  While he waited for the manager to arrive, Geoffrey noted that in addition to his wetted glove, the fawn-skin tip on his riding crop was stained with the waiter’s blood.  His riding boots and white jodphurs were also blood spotted.  His outrage built until the club manager arrived a few minutes later.

“I want to express my apolo…” the manager began before Geoffrey cut him off.

“Do you see this.” he waved the wet glove in the manager’s face, “and this”, he held up the bloodied riding crop, “and this.” he gestured at his blood stained clothing.

“Yes sir.” the manager replied, “The club will, of course, pay for the cleaning.”

“Cleaning!” Geoffrey shouted.  “Are you implying that I would wear used clothing?”  Before the manager could reply Geoffrey continued, “The Club will replace my boots and jodphurs, but this and this,” he gestured with the riding crop at the wet glove, “are irreplaceable.  Both are made from albino fawn skin from a deer I shot myself while on safari in Yellowstone last year.  Do you have any idea how rare albino fawns are?”  Before the manager could answer Geoffrey continued, “Of course you don’t.  The Club shall hear from my solicitors about this matter.”  Geoffrey turned and stalked away from the manager.

Later, while riding back to Washington DC in his limousine, Geoffrey thought about the hunting trip to Yellowstone during which he had bagged the albino fawn.  “The national parks really are a national treasure.”  he reflected, “particularly now that they are closed to the rifraf.  The hunting there was excellent.  The game was abundant and after over a century of the parks being closed to hunting, not at all timid of man.  I will have to head to Maine for some bird hunting in Acadia National Park as soon as my new shotguns are ready.  Peregrine falcon hunting is supposed to be quite a challenge.” he thought, then settled into the soft leather cushions and began dictating the letter to his solicitor about the matter of the club’s incompetence.

Two weeks later Thomas Smith, manager of the Virginia Sporting Club, looked up from the letter he held at the man who stood apprehensively in front of his desk.

“How long have you been at the Club, Mike?” he asked.

“Twenty nine years sir.”  the waiter replied.

Waving the letter Thomas continued, “I assume you know what this is about.”

“Yes sir, the Secretary.” Mike answered, absently fingering the partly healed scar on his cheek.

“Normally I would simply demote you back to grounds keeper over something like this, particularly now that your appearance,” Thomas gestured at the waiter’s scarred face, “is no longer appropriate for a service position.”  he paused and piked the letter up again.  “Unfortunately, they are demanding restitution for the gloves and riding crop.  They set that at twenty thousand DOLLARS.”

“Twenty thousand.” Mike spluttered.  “I can’t pay that.  The medical bills from this,” he fingered the scar again, “nearly cleaned out my savings.

“I know.  That is why you are leaving us.  You will be taking up a position in the Secretary’s service.”

“What?  I figured he would never want to see me again.”  Mike spluttered.

“Well I doubt he will see you again.  You will be going into indentured servitude until the twenty thousand is paid off.  The letter says twenty years and you lose your seniority.”  Thomas paraphrased as he read from the letter.

“He can’t do that over a glove?  Mike argued.

“The Secretary is a Trump.”  Thomas said.

Mike’s face fell as the reality of his situation hit home.  “When?” he asked weakly.

“Now, I am afraid.  The letter was delivered by Department of the Interior police.  They are waiting outside.”  Thomas said apologetically.

“My family?”

“They won’t be going with you, but two of your sons work here.  Your wife and younger children will move in with them.  I will look at your boys for promotion to fill your job.”  Thomas explained then pushed a button on his desk.  Seconds later two large uniformed police entered the office and took the sobbing waiter away.

The End of My First Calendar With Chronic Lymphocytic Leukemia – Medical Costs

I was diagnosed with Chronic Lymphocytic Leukemia (CLL) in late February 2016.  I will be writing a future blog about the emotional impact of finding out that you have an incurable cancer.  This blog looks at the magnitude of my medical bills for 2016.  I will preface the discussion by saying that my total exposure to the medical world was minimal before 2016.  My total lifetime medical bills were under $1,000.  Other than as a visitor I had only been in a hospital twice.  The first time was in 1952 when I was born and the second time was in 1957 for a tonsillectomy.  Like most people I have heard that medical costs have gotten very high, but never having experienced those costs first hand I didn’t know just how high they could be.  Well after ten months with CLL I have a better feel for just how expensive modern medicine can be.  The following is a summary of my medical costs from February 17 through the end of December, 2016.  I now have a much better understanding of how medical costs can impact a person’s life.  The costs can be substantial even with health insurance.

What I am going to do here is give my total medical costs for 2016 and then break those costs down into the major categories.  I will also discuss the impact of having health insurance versus not having insurance.  Before I get to the money details I want to state that I was not admitted to a hospital during 2016 and never spent  more than about three hours at any time receiving treatment.  In addition, one aspect of my cancer (CLL) is that the initial treatment is simply monitoring.  In other words my medical costs did not include any treatment for my CLL.  All the costs below were for outpatient procedures incidental to CLL.

I will start with the overall costs for the year.  Since I have insurance I am going to give both the cost billed by the various medical providers as well as what my insurance actually allowed.  My total medical bills for 2016 came to $30,274.76.  Of that total my insurance allowed $23,057.02.  The total of my health insurance premiums for the year was $8,892.  That brings the total cost for 2016 to $39,166.76 (total billed plus insurance premiums).  Of that total insurance paid $15,809.55 and I paid $16,139.47 (medical bills plus insurance premiums).  The medical providers wrote off the $7,217.74 difference between what was billed and what insurance allowed.  No matter how you look at it, 2016 was an expensive year.  I can only guess at what the costs would have been if I had ended up in the hospital for a few days or had received treatment for my CLL.  If I hadn’t had insurance I would have had to pay the entire $30,274.76 that was billed, so even with my high deductible and out of pocket limits, having health insurance saved me $14,135.29.

Now I will take a look at the big ticket areas in the medical billing.  I am rounding these amounts off to nearest $100.

Blood Tests

Since CLL is a blood cancer, it is not surprising that the various blood tests I had were at the top of the list.  I had more than 40 blood tests during 2016.  The total billed for those tests was $9,200.  Of that amount my insurance allowed $7,400.  Within this category a single test (Fluorescence In-Situ Hybridization -FISH) accounted for the largest part of the cost (billed at $5,000 and allowed at $3,900).


My oncologist, at my first meeting with him, sent me back to my family doctor with a list of tests to arrange.  Those tests included a colonoscopy since CLL patients tend to have higher rates of other cancers than the general population.  The colonoscopy had three parts: consultation with the internist who did the procedure, the procedure itself and pathology studies on polyps (2) removed during the procedure.  The biggest part of the cost was the procedure since the local internist does colonoscopies in the hospital’s out patient surgical center.  Consequently, the procedure was much more expensive than it would have been had it been done in a clinic.  The total billed cost of the colonoscopy was $6,000 of which my insurance allowed $4,500.  That is rather a lot of money for a procedure that took less than half an hour with an additional two hours spent in the hospital waiting.

Skin Cancer

I was also sent to a dermatologist for a skin cancer checkup.  The dermatologist found a lesion that turned out to be a basal cell carcinoma and referred me to a surgical specialist.  The specialist (a Mohs surgeon) lopped a 1-1/4″ by 3″ chunk out of my face then did a plastic surgery procedure to close the wound.  Billing for the surgical procedures came to $5,100 with $2,900 allowed by insurance.  Not bad money for under two hours work.  That procedure was cheaper than the colonoscopy despite being more time consuming and more involved because it was done in the doctor’s office, not in the hospital.

Other tests and pathology

I also had a number of other tests done, including two CT scans, a chest x-ray, an EKG, a cardiac stress test, several biopsies and a variety of pathological analyses and radiological interpretations. All together they came to about $7,000 of which insurance allowed $5,700.  The two CT scans and their interpretation made up the bulk of those charges.

Doctor’s Bills

Surprisingly, the bills for office appointments with the various doctors I saw last year only came to about $2,900 with $2,500 allowed by insurance.   So actual billing for office visits came to less than 10% of my total medical bills.


The numbers above illustrate just how expensive medicine in the USA has become.  In my case charges for things done at the local community hospital made up about 80% of my total bills.  All together I estimate that I spent about twelve hours having things done at the hospital and in clinics and about eight hours in doctor’s offices.  Looking at time only, 40% of my medical “time” generated less than 10% of the charges and the remaining 60% generated more than 90% of the charges.  My doctor’s visits averaged about $365 an hour and my hospital and clinic time cost about $2,280 per hour.  I shudder to think what it costs to actually be admitted to the hospital for any kind of surgery or other treatment.

My cancer, CLL, is both chronic and incurable.  Consequently, barring some sort of medical break through, I can expect to have CLL for the rest of my life. I can use the costs I incurred this year to estimate my future annual medical bills, at least until I need treatment for the CLL.  As of now I get a monthly complete blood count (CBC) blood test.  I see my oncologist every six months and have additional blood tests done for those visits (metabolic panel, uric acid, etc.).  I also see the dermatologist and the opthamologist once a year for checkups.  Finally, I will see my family doctor twice a year for general exams.  Those tests and doctor’s visits make up my “base” medical treatment for a typical year.  Based on what I was billed in 2016, the total billing for those services would be approximately $3,600 per year.  If I continued to have commercial insurance the allowed amount would be about 75% of that or $2,700 per year.  However, I start on Medicare in early 2017, so I expect the allowed amount will be less, so lets say my base expenses will be about $2,400 per year.  That means that I can expect medical expenses of at least $2,400 (2016 dollars) a year for the rest of my life.  In addition, I will always have the specter of treatment for my CLL hanging over me.  The least expensive CLL treatment costs about $75,000 and current “novel” oral therapies cost $150,000 to $180,000 per year indefinitely.  What it comes down to is my future medical costs could be high, even if I don’t end up in the hospital, which is very likely because CLL does nasty things to the immune system.

As far as being insured or uninsured goes, all I can say is that even with poor insurance, having the insurance will save you a lot of money if you end up in a situation similar to mine  I had a bronze insurance policy with a $5,500 deductible, 50% copays after the deductible and an out of pocket limit of $6,850.  I ended up paying more than $6,850 out of pocket because my insurance denied coverage for some of my tests.  They did that retroactively after initially approving them, so I had to pay the full billed price.  That irked me and I did appeal, with support from my doctor, but the appeal was unsuccessful.

I want to note that I chose the bronze plan, despite its apparently poor coverage, intentionally over silver and gold plans based on financial considerations.  Those were simply that I added up the total of the premiums and out of pocket limits for each policy and used the total potential cost to compare plans.  The idea behind that comparison was simple.  All the available policies here in Maine for 2016 had substantial deductibles ($2,500 minimum), so routine medical care would be out of pocket for all of the plans.  Consequently, I looked at insurance cost from the perspective of having an expensive medical event and chose the policy that cost least in terms of the sum of premiums and out of pocket limit.  That turned out to be the bronze plan, where the lower premiums more than balanced the higher out of pocket limit.  Had I chosen a gold plan my total costs for 2016 would have been thousands higher than with the bronze plan. Basically, I view medical insurance as just that – insurance.  It is there to cover extraordinary costs, not routine costs.  I find that to be a significant failing of the US “health insurance” model.  Starting in 2017 I will have Medicare, which at a premium cost of $134/mo is much better health insurance than even the best “gold” policy available here in Maine.  Despite,that Medicare still has the disadvantages of deductibles and 20% copays for doctor’s services.  Given that I could be looking at substantial costs for deductibles and copays should I need treatment for my CLL or end up in the hospital as a consequence of my CLL impaired immune system, I felt it was necessary to buy a Medicare supplement policy to cover potential deductibles and copays.  With that supplement my health insurance costs come to $321 per month (or $3,852 per year). That is higher than my projected base expenses, but should I have chemoimmunotherapy treatment for my CLL at a cost of say $75,000, I would be looking at a $15,000 copay which more than makes up for the added cost of the Medicare supplement policy for more than six years.  Furthermore, with the supplement I chose (Medicare type F supplement), my out of pocket costs after premiums will be zero.  I am absolutely certain a 65 year old man can’t buy a commercial policy with zero deductible and zero copays for $3,850 per year, or for any price.

Life in TrumpMerica – Chapter II

Chapter II – New Revelations

Sal had just finished putting the last of the breakfast dishes away when there was a knock at the door.  She took the few steps and opened the door to see Joe Jr.’s wife Kat standing there holding the hand of her 3 year old daughter and holding her 8month old son.  The young woman was just starting to show with her third child.  Sal was glad Joe Jr. had been promoted to miner last year.  That promotion let him earn enough money to support his growing family without help from Joe and Sal.

“Come in dear, I have tea on.  Would you like a cup?”  Sal asked.

Kat herded the children in ahead of her, “That would be wonderful Sal.  I would love to just sit for a few minutes.”

Shutting the door, Kat returned to the stove and poured two cups of steaming tea.  She stepped over to the table where Kat was sitting and set the cups down.  “Here you go.  Sorry the tea is a little weak, but the bag is getting old.”

“it’s wonderful Sal.” Kat said, picking her cup up and breathing in the fragrant steam.  “Its not even 8 Am and I already feel like its late at night.  Tim here”, she patted the baby, had a bad night so I didn’t get much sleep.  I have been up since 5 AM making Joe’s breakfast.  He is sleeping now, so I had to get the kids out of the house.   I will be so glad when he gets his 20 year pin so he has a chance at the day shift and we can have a two room house.”

“Don’t worry dear, it gets better.” Sal consoled the young mother.  “The first years of marriage are the hardest.  At least Joe got promoted to miner.  Having more money makes it a lot easier.”

“There is never enough though.” Kat said, “The hospital charges so much for a delivery.  I was at the bank yesterday making my weekly payment on the baby loans and it took almost half of Joe’s pay for the week.  The interest went up too.  I don’t know how we are going to make it when the new one comes.”

“Don’t worry dear.  We’ll help as much as we can.  You’ll manage.”  Sal replied, thinking that it was harder for the young now than when she was first married.  Back then most births were at home, so the only costs were the birth tax and the name fees.  Now all births were required to be in the hospital, which was expensive.  Well it was safer than home birth and it provided for the mid-wives.  She remembered what it had been like before there were mid-wives.  Back then if a woman was widowed, which happened way too often here in coal country, she was dependent on the charity of her family for her upkeep and that of her children.  Now the widow was made a mid-wife and her children went into the company creche.  The mid-wives lived at the hospital and the balance of their earnings went to the creche to support their children.  “Everyone was better off, thank Trump.” she thought.

Sal finished her tea and set the mug aside.  “Kat I have to go to the bank this morning.  You are welcome to stay here while I am out.”

“Thank you Sal.  I will make sure the children get their schooling.”

Sal walked down the side of the road toward the mine.  She wore her winter coat despite the typical January 90 degree heat only because the law said that it was cold in Winter and required that all residents of West Virginia wear Winter coats.  “Well, at least it’s not 120 like in August.” she thought as she unzipped the coat all but the last inch or so.  She still had half a mile to go when she heard the town bus coming up behind her.  Despite the sweat dripping off the end of her nose she waved the driver past, then held her breath as the black coal smoke from the bus wafted over her.  The choking cloud had cleared by the time the “chg, chug” of the bus’s steam engine faded below the general noise level.  She was glad for the face mask she wore.  Ten minutes later when she was only 100 yards from the mine office she was finally ably to make out the buildings of the town center through the murky air.  She walked past the mine office to the Trump National Bank and pushed through the doors into the interior.

In contrast to its grimy exterior, the interior of the bank building was spotless.  The white marble floor was polished and the varnished wood work and leaded glass windows gleamed in the bright light from the incandescent bulbs in the golden chandeliers.  She felt grubby as she walked across the spotless lobby to an open teller’s window.  When she stepped up to the window, the neatly dressed man behind the partition said  simply, “State your business.”

“I want to make a deposit to my savings account.” Sal replied passing her bank book and a ten script note under the edge of the partition.

The teller opened her bank book and placed it face down on a glass plate.  A light flashed under the bank book and the computer screen next to the teller filled with writing and numbers. The teller typed into the computer for a few seconds then pressed a button, while pressing her bankbook down firmly on the screen.  The light under the bankbook flashed again.  The teller put the script note into a drawer that had popped open when he hit the button and handed her bankbook back. Looking at her book she noticed that the balance had increased less than one dollar.

“Has the exchange rate changed?” she asked.

“No, it is still 10 to 1.” said the teller “But there is now a 5% transaction fee on all deposits.  The interest rate has also gone up from one and a half to two percent.”

“Thank you.” she said feeling a bit stunned as she turned to leave the bank.  Back outside, she began the mile long walk home.  Her thoughts were on the new deposit fee and the increased interest rate.  She had deposited ten script, which after the conversion to dollars and the deposit fee left her with ninety five cents.  Two percent interest was two cents per year for each dollar in the account.  She furrowed her brow as she laboriously went through the calculation to see how much the ten scrip she had just deposited would be worth when Joe retired in 20 years.  It took several minutes to subtract two cents off 20 times, but she finally arrived at a figure of fifty five cents.  Sal knew the number wasn’t quite right, but her math skills were stretched thin just to do adding and subtraction.  She wondered if they would be able to afford to survive on their savings.  Everything cost more each year and despite frequent deposits her savings changed very little, but you had to keep making deposits to keep up with the interest charges or you could end up owing the bank money when you retired.  She knew people that had happened to and the prospect terrified her.