ENCORE #80! – Dealing With Restless Limb Syndrome…

From the first moment my wife discovered she had breast cancer, there was a deafening silence from the men I know. Even ones whose wives, mothers or girlfriends had breast cancer seemed to have received a gag order from some Central Cancer Command and did little more than mumble about the experience. Not one to shut up for any known reason, I started this blog…That was four years ago – as time passed, people searching for answers stumbled across my blog and checked out what I had to say. The following entry appeared in January of 2015.

First of course, the definition: “Restless legs syndrome (RLS) also known as Willis-Ekbom disease (WED) or Wittmaack-Ekbom syndrome, is a neurological disorder characterized by an irresistible urge to move one's body to stop uncomfortable or odd sensations. It most commonly affects the legs, but can affect the arms, torso, head, and even phantom limbs. Moving the affected body part modulates the sensations, providing temporary relief.”

Once again, this is something my wife has struggled with. But instead of breast cancer causing it, it has exacerbated it. She’s had RLS her whole life (at least since she was six years old!) Breast cancer – double mastectomy, aggressive tri-weekly chemotherapy (Taxotere + Adriamycin + Cytoxan and the next day, neulasta), followed by five years of anastrazole – just made it...weirder.

I first experienced when we got married. At night, before falling asleep, she would move her legs in order to “short-circuit” the odd sensations. That seemed to work. Then the cancer diagnosis and treatment and as of right now, it has manifested itself by odd sensations in her LEFT arm. This is odd because the removal of sentinel nodes and the resulting lymphedema was in the RIGHT pit and arm (sounds like a medieval British pub, doesn’t it...).

Current research suggests “...exercise, avoiding RLS precipitants (caffeine, alcohol, antidepressants, antihistamines); exercise; counter stimulus to sensory symptoms (hot or cold baths, limb massage, compression stockings, counter-pulsation devices); herbal medicines and acupuncture; and cognitive behavioral therapy.”

Her first “go to” was to up her calcium intake: “Dehydration, prolonged sitting, or not getting enough potassium, calcium or magnesium in your diet can be associated with leg cramps. So can certain medications -- including diuretics, beta blockers and other blood pressure drugs. Sometimes, these cramps also may be related to an underlying metabolic condition, such as an underactive thyroid (hypothyroidism) or a parathyroid condition. Diabetes or other conditions that disrupt your metabolism can also cause muscle cramps.”

The calcium chews she’d been doing were originally to counter the bone debilitation caused by the chemotherapy, so she stopped for a while. The RLS increased and now she uses the calcium chews as well as a hot water bottle to lower the intensity of the sensations.

As I wrote earlier, we’ve also started a regimen of exercise together – alternating strength training (after a visit with the Planet Fitness trainer) and cardio – we usually do a half an hour of stationary biking. The hot water bottle was a “new development” and has been remarkably effective.

I’ll note here something we HAVE NOT tried, but is a recent development: “In 2014, the FDA approved a device that provides electrical stimulation to the legs as a non-medication treatment for restless legs syndrome. Studies suggest this treatment can be quite helpful. Although it is generally well tolerated, it occasionally causes a temporary worsening of symptoms, leg cramps, soreness and motion sickness.” My guess is that this is an outgrowth of the device developed for those who suffer from chronic pain, what’s called Microcurrent Electrical Therapy.

Taken all together, the “therapies” seem to be working for the time being. It’s also light years better than adding ANOTHER pill to her already abundant storehouse!

Resources: http://effectivehealthcare.ahrq.gov/index.cfm/search-for-guides-reviews-and-reports/?productid=1328&pageaction=displayproduct, http://articles.chicagotribune.com/2012-04-13/lifestyle/sns-201204131600--tms--mayoclnctnmc-a20120413apr13_1_leg-cramps-restless-legs-syndrome-calf-muscles, https://www.intelihealth.com/article/restless-legs-syndrome

Image: https://c2.staticflickr.com/6/5527/10893068965_1d328e8f71_b.jpg

BREAST CANCER RESEARCH RIGHT NOW! #59: Lymph Node TRANSPLANT!

From the first moment my wife discovered she had breast cancer, there was a deafening silence from the men I know. Even ones whose wives, mothers or girlfriends had breast cancer seemed to have received a gag order from some Central Cancer Command and did little more than mumble about the experience. Not one to shut up for any known reason, I started this blog…

Every month, I’ll be highlighting breast cancer research that is going on RIGHT NOW! Harvested from different websites, journals and podcasts, I’ll translate them into understandable English and share them with you. Today: Lymph Node Transplant…

The process of transferring lymph nodes from various parts of the body has been going on for nearly ten years now with varying rates of success.

Let me be clear before I go any further, according to the most recent article I could find, most of the patients experienced a decrease in the dimensions of the lymphedema-affected limb. The most successful transfers happened in the arms; less successful were the transfers affecting lymphedema of the leg.

Even though the transfers were successful, THIS WAS NOT A MIRACLE CURE!

Swelling in the arm was at best reduced by “…29.1% (Stage II) and 17.9% (Stage III) (P < 0.05).” To give you a reference point, my wife’s current arm swelling is 40 cm around (at the bicep). Depending on the stage she’s in, that would be a reduction from 40 cm to (Stage II) 40 cm – 11.64 cm = 28.36 or (Stage III) 40 cm – 7.16 = 32.84. Let’s say that a successful lymph node transfer would result in the arm going from 40 cm around to 30 cm around. In the case of my wife, the affected arm would still be slightly larger than the unaffected arm, BUT the difference would be less noticeable. My wife asked about the stretched skin from the lymphedema, but I will need to do research on THAT subject at a later time.

HOW is it done?

From the article referenced below: “…functioning lymph nodes were transplanted from the outer groin area [other possible sites for node removal include the base of the neck; around the stomach; around the intestines; or those around the appendix then]into the wrist…[the] transfer surgery is done through an incision…with the aid of loupe magnification…then the targeted lymph nodes [are] carefully dissected out, along with the veins and artery and some surrounding tissue…blood vessels [a]re reconnected under microscopic magnification…”

After the surgery is completed – and the person in this article said it was “painless”, though I can’t imagine how it could be! – “…the transplanted lymph nodes are reestablished…acting as a physiological ‘sponge’ to drain the excessive lymphedema fluid…[in]to [nearby veins]...”

The study reference below was published in November of 2017 and included some 80 or so patients with lymphedema. It didn’t specify in the abstract how many of them had suffered from breast cancer. I can only imagine that SOME of them had.

The third article referenced was published in July of 2016. Even so, it states clearly: “Although results are promising, VLNT is relatively new and thus still in the exploratory stage…we do not know exactly which subset of patients with lymphedema will benefit most from the procedure. In order to tease out these answers we need ongoing, coordinated outcomes reporting, basic science research on mechanisms of action in VLNT and an increased understanding of the pathobiology of lymphedema.”

Hopeful? ABSOLUTELY! But still not a panacea – a cure all – for those suffering lymphedema.

Resources: http://www.health24.com/Medical/Cancer/News/first-lymph-node-transplant-for-cancer-patient-a-success-20171023, https://www.cancercenter.com/video/treatments-technology/vascularized-lymph-node-transfer/, https://www.ncbi.nlm.nih.gov/pubmed/27270748, https://consultqd.clevelandclinic.org/2016/07/qa-vascularized-lymph-node-transfer-lymphedema-cancer/

Image: https://static1.squarespace.com/static/51c16910e4b014f2c800eb39/t/5262c442e4b04c04f40cf61f/1409593462984/VLNT+Israel.png

ENCORE #79! – Weight Training Can HELP Stop Or Reduce Lymphedema

From the first moment my wife discovered she had breast cancer, there was a deafening silence from the men I know. Even ones whose wives, mothers or girlfriends had breast cancer seemed to have received a gag order from some Central Cancer Command and did little more than mumble about the experience. Not one to shut up for any known reason, I started this blog…That was four years ago – as time passed, people searching for answers stumbled across my blog and checked out what I had to say. The following entry appeared on 11/2/2014. (http://www.breastcancer.org/research-news/exercise-program-successful-in-life)

Exercise and breast cancer – at first thought, you might say, “What!!!!!” The implication of a breast cancer diagnosis or treatment, brings to mind hospital beds, recuperation, and convalescence.

Not hitting the weight room!

But this study, while it’s neither large nor longitudinal for more than a year, seems to indicate that gentle weight training has a good chance of either preventing the occurrence of lymphedema or reducing it.

We’re NOT talking pumping iron, here folks! In the words of the study: “As in PAL [Physical Activity and Lymphedema Trial], the researchers found that the Strength After Breast Cancer program didn’t increase the risk of lymphedema and helped ease lymphedema symptoms. The women were also stronger at the end of the program and felt better about their bodies.”

Does this mean you have to join a gym and get into those leotards and exercise?

Not necessarily. Simply returning to moderate exercise after breast cancer treatment and surgery is GOOD: “...one study found that women who followed a slow, progressive strength-training program lowered their risk of developing lymphedema by 35 percent; women who had at least five lymph nodes removed and started lifting weights reduced their risk by 70 percent.”

                                                                                                                                 

As well, the article goes on to talk about other aspects of exercise after breast cancer and as always, do so with your doctor’s knowledge and under her supervision. Even so, “Increased physical activity after cancer treatment has been consistently linked to better physical function, reduced fatigue, and bodily pain...Compared to sedentary women, regular exercisers, who have been diagnosed with breast cancer, have a much lower risk of breast cancer recurrence, breast cancer death, and all causes of death.”

And NOT just the wives/girlfriends/moms/sisters, gentlemen! We need to exercise as well to maintain our health and support our women!

Capisce? (From Neapolitan capisci, the second-person present-tense form of capire (“to understand”), from Latin capere (“to grasp, seize”).)

Resource: http://www.acefitness.org/acefit/fitness-fact-article/3320/exercise-for-breast-cancer/

Image: https://c2.staticflickr.com/6/5527/10893068965_1d328e8f71_b.jpg

GUY’S GOTTA TALK ABOUT…Alzheimer’s #13 – Research Into Diabetes Leads To Possible Treatment for Alzheimer’s!

Dad’s diagnosis of Alzheimer’s stayed hidden from everyone until I took over the medical administration of my parents in 2015. Once I found out, there was a deafening silence from most of the people I know even though virtually all of them would add, “My _____ had Alzheimer’s…” But there was little help, little beyond people sadly shaking heads. Or horror stories. Lots of those. Even the ones who knew about the disease seemed to have received a gag order from some Central Alzheimer’s Command and did little more than mumble about the experience. Not one to shut up for any known reason, I started this part of my blog…

I’ll also be trying to keep up with current research in Alzheimer’s treatments as well as research into understanding exactly what the diseases does…and I’ll be looking HARD for research on Alzheimer’s prevention – as that one has some real importance for me and my siblings.

Today, I’ve found some hopeful research on “curing” the disease. Mind you, it’s ONLY in the mouse-testing phase, but given the number of people suffering from it, it would seem to me that finding a way to prevent Alzheimer’s from occurring in the first place would be high on SOMEONE’S research list.

Here’s the actual, untranslated abstract (sort of like the summaries we had to do in middle school about the books we read):

“Type 2 diabetes mellitus (T2DM) is a risk factor for Alzheimer disease (AD). Previous studies have shown that the incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) that have anti-diabetic properties show very promising effects in animal models of AD. Glucagon (Gcg) is a hormone and growth-factor, and the Gcg receptor is expressed in the brain. Here we test the effects of a triple receptor agonist (TA), which activates GLP-1, GIP and glucagon receptors at the same time. In the present study, the effects of the TA were evaluated in the APP/PS1 transgenic mouse model of AD. The TA was injected once-daily (10 nmol/kg i.p.) for two months. The results showed that treatment with TA significantly reversed the memory deficit in the APP/PS1 mice in a spatial water maze test. Moreover, the drug reduced levels of the mitochondrial pro-apoptotic signaling molecule BAX, increased the anti-apoptotic signaling molecule Bcl-2 and enhanced the levels of BDNF, a key growth factor that protects synaptic function. Levels of synaptophysin were enhanced, demonstrating protection from synaptic loss that is observed in AD. Neurogenesis in the dentate gyrus was furthermore enhanced as shown in the increase of doublecortin positive cells. Furthermore, TA treatment reduced the total amount of β-amyloid, reduced neuroinflammation (activated microglia and astrocytes), and oxidative stress in the cortex and hippocampus. Thus, these findings show that novel TAs are a promising lead for the design of future treatment strategies in AD.”

Like I used to do for my wife’s breast cancer diagnosis and treatments, I’m going to make an attempt to translate this. [To lend a little bit of credibility: I have a BS in Biology and an MS in School Counseling. I have been a science geek since I was a teenager, I love language, and I read and understand technical papers in both fields. Science is full of jargon – but all jargon is, is an attempt to communicate something as precisely as possible. You can probably find someone else to translate for you, but they’d need more schooling than I’ve had…]

The abstract begins by saying that people who are Type 2 diabetic (This means that they started having insulin problems AFTER adolescence. Type 1 diabetics were called “juvenile onset” at one time) have a higher risk of getting Alzheimer’s. It’s not a guarantee (and my dad wasn’t diabetic), but there’s an increased risk there.

The researchers made a “cocktail” of three different hormones that would lock into the brain

Research has shown that two hormones that prevent people from becoming diabetic, ALSO appears to protect people from developing Alzheimer’s. In the abstract, they name the hormones, then abbreviate them, then continue to use LOTS of abbreviations (for example, AD = Alzheimer’s Disease).

One of the hormones contributes to growth in the human body. When the hormone travels to the brain, there is a SPECIFIC site that it can hook into that is there; the hormone can then signal the brain to grow more nerve cells that connect you to your memories. The other two are the ones that protect the body from becoming diabetic.

The researchers injected a mixture of the hormone and diabetes protectors into mice every day for two months. At the end of that period, a NUMBER of really good things had happened!

First of all, the treatment reversed memory loss! Moreover, the drug reduced the molecule that makes a brain cell commit suicide and increased the amounts of molecules that both stop the brain cell suicide and created TWO chemicals that stimulates growth and a chemical that protects the nerves from attack by the molecule that starts the cell-suicide process.  It also acts on a part of the brain called the “hippocampus” (I know, sounds like a place where zoo animals go to school). It causes the growth of new nerves in a place called the “dentate gyrus” (NOT someone who meditates on dentures), a place the guides the “formation of new episodic memories, the spontaneous exploration of novel environments, and other functions.” The injections reduced the amount of brain plaque that has become associated with Alzheimer’s, and finally made the swelling in the lining of the nerves go down.

All-in-all, the research delivered a lot of what researchers are looking for. HOWEVER – this is at the “injecting mice stage”. It’s a long, long way away from the “Hey, Doc! Can I get me a set of those daily injections so I can get my memory back?” In other words, this research won’t lead to a competitor for PREVAGEN (a miracle drug (ABSOLUTELY NOT BEING SERIOUS HERE!!!). It’s years from being a real, clinical treatment.

Then again, it’s way better than the bad news we’ve been feasting on since the first attempt to deal with the beta-amyloid plaques and Tau protein tangles the first Alzheimer’s drug tried to attack in 1987…three decades ago.

I’m not going to hold my breath. As with any research on finding a cure for any disease or condition, much remains to be seen.

Resource: http://www.sciencedirect.com/science/article/pii/S0006899317304596?via%3Dihub

Image:  http://az616578.vo.msecnd.net/files/2016/06/25/6360242025150255191939281878_Alzheimer-disease-patients.jpg