Officer Wes' & Daddy Barry’s 2016


The year started off with a strange Windows 10-related computer problem: AVG Web TuneUp tried to cache the entire hard drive, and in doing so filled up 471.9 GB -- til it was full.  It took hours and probing to find the cause and remove the software.

Lots of health stuff for Daddy Barry.  VA electromyography (EMG) nerve tests.  Orthopedics for hip pain and surgery authorization.  Radio frequency ablasion of C5, C6, C7 for neck pain.  Sonogram of heart before surgery due to past smoking.  EKG -- same.  Meanwhile, our neighbor Gary experienced a series of strokes after a long flight and spent over a day unable to move and use the phone to call for help.

We had some nice social things.  Melissa at the Chicken Pie Shop.  Eli’s TGIF Mixer.  Koffee with Karl.  Chinese New Year street fair.  Birch Aquarium.  Boots & Cigars.  San Diego Leathermen’s Potluck.  Lunch with The Kids.  The 3rd Annual Leather Fetish Ball – EROTICA.  Guys Games & Grub.  Painting classes.  Gentle yoga.  Water aerobics.  Game Day with Farrah & Alison.  And Dion got honored at the Bayard Rustin Civil Rights Honors & SD Diversity Awards.

Farrah & Kim again kicked it up for their joint birthday celebration with a party at Wong's Dragon Room featuring singer Laura Jane Wilcock and The Tighten Ups.

We took in a few movies: The Danish Girl (great), Joy (well, uh), The Big Short, Deadpool, and – Daddy Barry with George - The Revenant.  Also enjoyed good TV like Master of None & The Americans.

We did work joining finances through the bank and credit cards, including updating direct deposits.  Taxes.

Meanwhile I attended Phil’s mom’s funeral and did my annual ADAP renewal.  Daddy Barry had HOA meetings, and spent time on replacing the garage doors, gutters, mailboxes, trash removal, and a leak.

We had Dion, Farrah & Kim, Kent, Melissa, Patrick & JT over for my birthday.  Another nice cake & ice cream celebration featuring Cards Against Humanity.  We used the First Expansion Pack for the inaugural time and I learned in real time that it was um, filthy.  Everyone took it in stride.

We also looked for frisking gloves for me, utilizing San Diego Leather, Amazon (Damascus gloves – didn’t fit tight enough in the wrist), Ace Uniforms, and Amazon again (Tough Gloves – sublime fit).

Then all three of us had health things.  Opa, at 10+, had developed some cataracts not long ago.  But suddenly they seemed to bother her.  Walking when the sun was at a low point put the shine right in her eyes – and she would have challenges with curbs and unexpected items at those times.  We tried to walk in front of her to create a shadow to walk in, but she never got in a good rhythm with that.  Meanwhile, I suddenly developed nummular eczema, an incredibly itchy but not contagious phenomenon.  The biggie, though, was Daddy Barry.  He had his right hip replaced April 14 to correct painful osteopenia that was a result of a fracture about six years prior.  This was done at the VA, and he got great service.  Then April 19 he had an episode.  I awoke at 3am and noticed he was up.  I turned on the light.  But I didn’t hear anything.  So I got up to check on him.  I found him sitting on a chair in the dining room:

1.   He was disoriented -- he did not know how he got there

2.   He was confused -- he couldn’t clearly answer when I asked “Are you okay?” instead responding “Uhhh.”

3.   He couldn't stand (due to the hip surgery?)

4.   I patted his head to comfort him, and it was wet.  When I wiped his head with a towel, it turned out he had a sheen of cold sweat all over.

5.   He could not scrunch one side (left?) of his face well.  Right side – easily.

6.   Can you say a full sentence?  Try "Mary had a little lamb" "maary" was all he could get out.

7.   (Additionally, in the hospital on Wednesday he noticed that he has new vision spots, which were not present before.)

I called 911.  The paramedics were here in maybe two minutes.  By that time the episode was already, thankfully, passing.  This would turn out to be a transient ischemic attack (TIA), essentially a short stroke lasting less than 24 hours.  But in the meantime, we rushed him to Sharp, a close hospital with which we’ve previously had good experiences.  The emergency room part went well.  Then he was admitted for observation to the Short Stay / Observation unit.  He had bad experience after bad experience there (things like a nurse pushing on his surgery site when transferring him between beds, despite a very clear warning not to), and was exhausted and spent by the time he was discharged at 3pm the next afternoon.  Later we met with the hospital consumer advocate rep to tell him what had transpired.

The good news was all his tests came back good:

1.   CT - a quick look for gross picture; fine

2.   MRI - stroke would show as shade; didn't

3.   orthostatics - checking blood pressure in three positions (lying, sitting, standing) for dehydration; fine

4.   echocardiogram / EKG / sonogram; fine, no arrhythmia

5.   labs look good; didn't see high cholesterol

6.   carotids - had a sonogram a month ago and were okay

7.   urinalysis - electrolytes low

8.   EEG / electroencephalogram - normal

That left us with two possibilities:  a TIA, or too many meds.  His meds hadn’t been changed, so that was ruled out.

The next three months passed slowly; and quickly:  physical therapy for six weeks, doctors appointments (primary care physician 4/26, 5/25, 7/6; VA 4/29, 5/26, 5/27, 6/24, 7/5; ophthalmologist 5/6; neurologist 5/11, 6/28 with Sharp tests; Weight Loss MD 7/6).

Friends helped in many ways.  Deputy and Chris helped shore up our weak leg – Officer’s cooking during Daddy Barry’s recuperation – by lining up Amazon Prime Now restaurant deliveries; Patrick & JT visited with cupcakes; John & Kent with cake; Mark & Gary brought dinner over; breakfast with RK & Kevin at the Old Mill; matzo ball soup from Robin; Farrah & Kim over for Qwirkle.

Meanwhile Susan and Dan’s Bubbles had surgery after surgery, ultimately coming out okay.

We stayed connected however possible.  Daddy Barry returned to painting class in short order.  We went to the SDCCU Festival of Arts in North Park with Jennifer from art class.  HOA Board meetings in May & June.  My leatherboy hunt continued.  We had time with Patrick & JT.  A Memorial Day BBQ.  Coronado Beach Bonfire in early June.  A video call with Deputy & Chris in Italy.  Leathermen's Potluck.  POZabilities fireworks.  Deep Water workout mid-June.  June Tea with Melissa, Lavon, Anne & Denny.  Officer did delightful viniyoga 6/9 & 7/7.  We shopped baby items for Laura & Jordan.

We also took in movies:  The Hateful 8; The Jungle Book; Alice Through the Looking Glass.

Daddy Barry was particularly satisfied to close our CCCU account.  Their MasterCard service had embarrassingly declined him twice.  In other financial news, Daddy Barry got approved for free classes through Federal financial aid at City College.

Cousin Jo & hubby Steve came to visit for four days on a Western trek.  We hit Boddega Americana, played Qwirkle, ate at Li'l B's, had a scrumptious breakfast at Richard Walker's, took in the Auto Museum, played Settlers of Catan, took a tour of Balboa Park, ate at the Old Mill, toured San Diego Central Library, and ate at Souplantation.  Plus lots of visiting in the meantime.

Directly after Jo and Steve, we flew to Fort Worth for Officer’s parent’s 50th anniversary 6/25 and stayed nearly a week.  Sister Elaine & Ian hosted dinner at Bizzi's Bistro, Daddy made a chicken soup dinner, Qwirkle, assembling chairs, Daddy & Charlotte took us to Dixie Belle, we treated to Luby’s, and Sister Susan & Dan treated us to Sunny Street Café.

July was full.  Officer was sick near the beginning.  Mary from Tucson came nearby, to Palm Springs, so Daddy Barry went to see her.  We both volunteered in the Leather Realm at Pride.  And then Daddy Barry’s 20-year-old nephew Dylan died of a fentanyl overdose.  Just a kid.  So sad.


The big thing in August was Opa had cataract removal surgery on her right eye, and Daddy Barry resumed art classes.

In September dog visited for a week, and Melissa hosted tea and games.  In medical news, we changed to Trintellix as my primary antidepressant.  It worked well, adding shine and some energy back to my days.  We also shifted from generic methylfolate to Deplin.  And I resumed making music.  Plus we went on motorcycle rides.  Below is a photo from one beautiful Santa Ana morning.



In October my iPhone 5 fully died and got replaced by one of the large-screen iPhone 7 Pluses.  Boy do I like having more screen real estate.  Lester, John and Kent’s dear big girl dog, died.  We made floor and plaster repairs after the kitchen faucet failed.  Took Patrick and JT to Gospel Brunch at Lip’s as a going away party.  Listened to Mike’s 5th Step.  Gary and Mark over for Qwirkle.  Patrick & JT lunch @ Salsa Fiesta.  Roadkill & Kevin’s for dinner.  Lunch with Tom.  Men’s naked yoga.  ENT & 14 days of Levaquin.  Vigilance while Daddy Barry had coffee with Zane.  John & Kent over.  Safer sex talks with Daddy Barry, Frank, Chuck and Daddy Barry’s primary care physician.  New starter on the Kawasaki.  New stereo in the car, and replacing it (a JVC/Kenwood) with one with better software (a Pioneer); and adding a subwoofer.  Frank’s leather cover ceremony in Palm Springs.  Halloween costume party dance at the Alano Club.  Adding music to Daddy Barry’s iPhone via iTunes.

November was impressive.  We reconnected with Harvey, who helped introduce Daddy Barry and me, and had coffee with him and his partner Michael @ Lestat's on University.  My quarterly primary care physician appointment.  Training on the History of HIV/AIDS at The Center.  Cigars and Boots.  Bear Night dance.  Farrah over for brunch + Qwirkle.  Looking after Molly.  Annual music.  Closing two financial accounts in our further consolidation.  Taking on slave frank as my leatherslave >:  )  Daddy Barry to Foxhole.  Dan’s 17 year cake.  Kane & Steve's Annual Extravaganza.  XPS8100 hard drive crash – which took a week to restore; thankfully we had multiple recent backups on two different external hard drives.  Movie:  Fantastic Beasts and Where to Find Them.  Thanksgiving at Aunt Sonia’s.  Sinus CT.  Lunch at Chuck and Frank’s with their artist and photographer friends.  Sister Elaine broke her arm and wrist.  Daddy Barry had a consult with Nelson Vergel, a specialist on HIV+ nutrition, supplements and working out.  And I got Huntington’s Disease genetic results of “39 matches”  40 is a definitive you’re-going-to-have-symptoms level.  Here’s what I wrote my psychiatrist, and an article recommended by my doctor about this strong gray zone:


Dear Dr. ______,


My mom's side of the family has Huntington's Disease.  I've had what may be some symptoms for years; jerky chorea in my legs, shaky hands, awkward gait.  At my last quarterly primary care doctor appointment earlier this month I requested the genetic test.  Definitive diagnosis is a 40.  I came back with a 39.  Just got the details today.  Been doing some reading.  This was particularly interesting, from further down in the section on Signs and Symptoms :


Reported neuropsychiatric manifestations are anxietydepression, a reduced display of emotions (blunted affect), egocentrismaggression, and compulsive behavior, the latter of which can cause or worsen addictions, including alcoholismgambling, and hypersexuality.[10] Difficulties in recognizing other people's negative expressions have also been observed.[17]


My therapist had previously mentioned I seemed to have a blunted affect and difficulties in recognizing other people's negative expressions in relation to Barry, whom he also counsels.  Thought you'd want to know.


Since I came back with a 39, just shy of 40, my PCP Dr. _____ recommended the article below, from


If I were planning on having children this would be horrible news.  Though I'm not, it's still spooky nonetheless.  Still absorbing all this.


The genetic 'gray area' of Huntington's disease: what does it all mean?


Intermediate alleles and reduced penetrance – the genetic 'gray area' of Huntington’s disease, explained

By Dr Nayana Lahiri on April 22, 2011Edited by Dr Jeff Carroll

By popular request, a special feature article on the often confusing topic of ‘intermediate alleles’ and ‘reduced penetrance’ – the genetic ‘gray area’ that frequently comes up in discussions around genetic testing for Huntington’s disease.

Having a genetic test for Huntington’s disease is an extremely worrying time. The only thing you want to hear when you go for the result is whether or not you are going to develop HD. Most people do get a clear answer to this question, but for a small minority, the answer is not quite as simple because they receive a result in the ‘gray’ area known as either a ‘reduced penetrance allele’ or an ‘intermediate allele’. The meaning of these results can be confusing, but we hope this article will help set things straight.

The Genetic Basics

Small, medium or large? HD genetic test results in the ‘intermediate’ or ‘reduced penetrance’ range can be confusing

Genes are made up of the genetic material called DNA. DNA is the code for all life and is made up of a combination of 4 ‘letters’ - A, C, G and T. Scientifically, these genetic letters are called ‘nucleotide bases’.

The HD gene provides the code for the huntingtin protein, and everyone inherits two copies of the gene - one from each parent. The genetic mutation that causes HD is a long sequence of repeated C-A-G nucleotides in the HD gene.

Scientists love jargon, and sometimes use the term ‘allele’ instead of gene; but basically these terms mean the same thing.

The number of CAG repeats in the HD gene determines whether or not someone will develop HD during their lifetime. Everyone has two copies of the HD gene - one from their father and one from their mother. HD testing involves measuring the CAG repeat length in both HD genes of an individual, using DNA obtained from a blood sample.

The number of CAG repeats in an HD gene can range from less than 10 to more than 120. The average number of CAG repeats is around 17. HD is a ‘dominant’ disease, which means that an individual only needs one of their two HD genes to have a larger-than-normal number of CAG repeats for them to develop the disease.

Two facts are quite straightforward:

If both copies of a person’s HD gene contain 26 or fewer repeats, they will not develop HD, and nor will any of their children.


If one copy of an person’s HD gene has 40 or more repeats, they will develop HD in their lifetime, and each of their children will have a 50% risk of inheriting the expanded HD gene.

An HD gene with 40 or more repeats is called a full penetrance gene. That means the person will definitely develop HD in their life, as long as they don’t die prematurely of another cause.

The ‘Gray area’

The clinical meaning of results becomes more complicated when the HD gene has a repeat length between 27 and 39 CAGs - often described as the ‘gray area’.

People with an HD gene containing between 36 and 39 repeats are in the ‘reduced penetrance’ range. Some people in this range will develop symptoms of the disease, while others won’t.

Unfortunately, it’s impossible to predict which people with a reduced penetrance gene will or won’t develop the disease. If symptoms do occur, they tend to begin later in life and are generally less severe.

Children of an individual with an HD gene in the ‘reduced penetrance’ range are each at 50% risk of inheriting a gene with either ‘reduced’ or ‘full’ penetrance.

‘Intermediate alleles’, on the other hand, have repeat lengths between 27 and 35 CAGs. People with an intermediate allele will not develop HD themselves, but there may be a risk of HD developing in their children.

What about Future Generations?

The number of CAG repeats in an HD gene can be unstable when the gene is passed on to the next generation. That means the number of CAG repeats can increase or decrease when the gene is passed from parent to child.

We don’t know for sure why the HD gene is unstable, but we think it has something to do with how accurately DNA is copied by cells. If you were asked to type ‘CAG’ 50 times, you might find that you actually end up typing a couple of extra ‘CAGs’ by accident, or a couple too few. The machinery in cells that copies DNA also makes mistakes when copying long lengths of repetitive DNA.

Changes in repeat length are called ‘expansions’ when more CAG repeats are passed to the next generation, and ‘contractions’ when fewer CAG repeats are passed to the next generation.

The unstable HD gene causes problems when it comes to predicting what will happen to the next generation. Although people with intermediate alleles (27 to 35 repeats) will never experience HD symptoms themselves, the repeat inherited by their children can be longer than their own. Their children are at risk of inheriting a reduced penetrance or full penetrance gene.

In the same way, someone with a reduced penetrance gene (36 to 39 repeats) can pass on a full penetrance gene to a child, if the gene expands.

A table summarizing the different possible results of a predictive HD gene test.

A few factors can influence whether expansion occurs. The first is the starting length of the CAG repeat. Normal repeat lengths of 26 or less are stable, and don’t change when passed on. But full penetrance genes - those with repeat lengths of 40 or more - are more likely to expand in the next generation.

Intermediate and reduced penetrance alleles are generally more stable than full penetrance genes, but can still expand, giving rise to longer repeat lengths in the next generation.

Other factors influencing CAG repeat expansion are the sex and age of the parent. Fathers are much more likely than mothers to pass on an HD gene with an expanded number of CAG repeats. However, the sex of the children doesn’t make a difference.

Older fathers are more likely than younger fathers to pass on an expanded copy. This may be because new sperm are made throughout a man’s lifetime, allowing more DNA copying mistakes as the man gets older.

Currently, it’s not possible to estimate the exact risk of CAG repeat expansion, for people with intermediate or reduced penetrance alleles. However, the risk that people with intermediate or reduced penetrance alleles will pass on an expanded allele to their children is thought to be small.

The importance of family history.

It’s possible to develop HD even if there are no known family members with the condition. Around 10% of people with HD don’t have a family history.

Sometimes, that’s because a parent or grandparent was wrongly diagnosed with another condition like Parkinson’s disease, when in fact they had HD. Now that we have a reliable genetic test, this doesn’t happen as often as it used to.

In other families, HD appears for the first time because a parent who would have developed HD died from another cause before they started showing symptoms, but had already passed the gene on to their children.

Another way that HD can occur in a family with no previous history is when a new genetic mutation for HD occurs. New mutations come from intermediate alleles. They happen when a parent with an intermediate allele (27-35 repeats) passes on an expanded allele in the HD range. Later in life, the son or daughter will develop HD, but the parent with an intermediate allele will remain symptom-free. Intermediate alleles are often identified in parents whose children have a new HD mutation.

Intermediate alleles aren’t just found in families where a new mutation has been identified - they can also crop up in families where HD is known about. This happens when someone with an intermediate allele, who’s not from an HD family, has children with someone who has a fully penetrant allele.

If one of that couple’s children decides to have HD genetic testing later, they might learn that they didn’t inherit the HD gene from their HD-affected parent, but did inherit an intermediate allele from the other parent. Families are often surprised to learn that there is an intermediate allele on the non-HD side - but in fact, this is the most common way intermediate alleles for HD are identified.

It’s not currently possible to estimate the exact risk that someone with an intermediate or reduced penetrance allelewill pass an expanded allele to their children. The risk is small, but further research in this area is underway.


A small number of people having a test for HD will have a result which falls into the ‘gray area’ area of intermediate alleles and reduced penetrance.

Someone with an intermediate allele (27-35 CAG repeats) will not develop HD. Their children have a low risk of inheriting a gene with an increased number of CAG repeats, in either the reduced or full penetrance range.

Someone with a reduced penetrance allele (36-39) may or may not develop HD in their lifetime. Their children are at a 50% risk of inheriting an HD gene with either reduced or full penetrance.

Intermediate and reduced penetrance alleles mean that predictive test results are not always black or white. Researchers are working to understand these ‘gray area’ genes better, so we are better able to prepare people for testing and explain results to patients and their families.


HDBuzz thanks Alicia Semaka for her expert advice about intermediate allele risk. Alicia is a genetic counsellor at the Centre for Molecular Medicine and Therapeutics, University of British Columbia, who studies genetic risk in HD.

The authors have no conflicts of interest to declare. For more information about our disclosure policy see our FAQ...


In December Harvey and Michael (taking the photo, below) hosted a handsome holiday dinner.  Not long after, we flew east to spend the rest of the holiday with family.


As always, may this find you happy & well.



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