Monday, September 29, 2014

BLIND ALGORITHM

“Paint with an airbrush!”
“Yes but all that paint-scatter?”
“Mask the edges!”
“But…but!”
An un-blinded Algorithm


We employ methodologies with limited views and with one broad stroke of the brush to wipeout any hidden flaws. The truth seeks but under the colossal weight of dried ink it remains muffled and hidden, like a masterpiece painting it lies submerged under the spray of a modern airbrushed abstract. Eventually the leveling scythe of assumptions and probability science shows its obverse edge.
What if… we had a blind algorithm that went about sniffing through large pieces of data, snaking its way and exploiting each path, determining the cost of each path and all successor events that preceded and followed in each of those paths to arrive at a goal that no one pre-selected, in other words, blind vectoring into a sea of options. The blind algorithm would blind the researcher and would dive down into the sea of amorphous data. The Artificial Intelligence would guide it through the maze just as a modern day Robotic vacuum cleaner dodges and bumps against furniture in a room. This would prevent the ebb and fracture of the scientific culture currently in progress.


Hamlet:
O God, I could be bounded in a nutshell, and count myself a
king of infinite space—were it not that I have bad dreams.

Guildenstern:
Which dreams indeed are ambition, for the very
substance of the ambitious is merely the shadow of a dream.

What would happen?

We might get results that would surprise us all. It might eliminate certain prejudices of thought. It might conflate some, inflate others and deflate concretely held paradigms. It might through aggregation of such information form a shape more akin to reality then prophesied through the false gods of statistical fiat.

What then?

Would humanity consider those potential alternatives via a more clear vision rather than the dark lenses of doubt? I am afraid so. The well entrenched busy-bodies would still want to extract their pound of flesh, but their premise would be mortally weakened. Their narcissistic grist would be reduced and their mills dried would seek redemption. To reduce the risk of such posturing or "gaming" the system with the algorithm, one might consider sending a second algorithm-bot which could constantly modify the prime algorithm's behavior when under threat from outside manipulations.

http://youtu.be/BsCeNCVb-d8

Humans love to seek the truth; beneath the stone, the dark side of the moon, the distance from the moon and the elliptical orbit of the planets. They desire real evidence but often fail in their goals mired in the gutter of soft, pliable and manipulated evidence. Medical literature is bugged with a significant amount of pseudo-science. This form of pseudoscience comes from selected variable sources that attempt to create a reality that is nonexistent. These useless dribblings on our zeitgeist mar the tattered tapestry of our being even further.


A blind algorithm run amuck in a Data-warehouse would produce some sparks of discontent as it bumps against dead ends, ricochets through the “bump and grind” and the stochastic information finds the critical path to a heretofore unrealized solution. This ultimate critical path would use efficiency, expediency and find pecuniary limits to realize the least resistant and best pathway. Or, then it might just prove an existing paradigm. Such a confirmation would equally have immense credibility and usage. The flowering colorful proofs from random analytics would shed more light and do more for humanity than the gunmetal gray of a postured regulatory missive!

Imagine if a large pool of patient data demographics that included age, sex, race etc. and in addition family history, dietary history, exercise habits, thrill seeking or a quiet lifestyle, use of any prescribed and over the counter medication and myriad of other information is floating around in the dark unreflective waters. The blind algorithm would tease outputs that we may not have contemplated. Instead of selected data, univariate analytics or even controlled multivariate analytics, the randomness of “chew and spit” of the esoteric data for the “right taste” could/would reveal outputs of immeasurable weights and benefit…or not. It certainly would be worth the endeavor.  variables would then indeed be variables, not chosen and picked like fruit from a tree, the correlations would indeed be obvious and used within the algorithm and the regressions would point to the future with a focused light. The p-values would have meaning and the Confidence Intervals would be tightly bound. Even Fat tails would be obvious and not hidden under the weight of mathematical jujitsu to make “nice.”

Studies of coffee, chocolate and red wine proving goodness for the heart created through selected dataset by those industries to prove the primary aim of the researcher would indeed be a thing of the past. As John Ioannidis points out currently 54% of the studies are not validated or reproducible lends further credence to blinding the algorithm for real “Evidence’ in Evidence Based Medicine!
In the end, the numbers themselves do not deny us our humanity but the calculated decision to stop being human but the complete devotion to reliance on an obtuse and self-motivated junk science.
Let us therefore use the combinatorial force of computer science for the purpose it was designed. Let us start looking for the keys to reality in the dark and not only under the lamplights. Let us use Big Data for all its worth! 


We all have dreams…

http://youtu.be/Gm1f6ojwuAc

Wednesday, September 17, 2014

OBESITY AND CANCER

 The Cancer Prevention Study II (CPS II) examined the risk of cancer mortality in obese men and women in the U.S. They reported that obesity is associated with a significant increase in mortality from multiple cancers, including esophageal, colorectal, liver, gallbladder, pancreatic, breast, endometrial, cervical, ovarian, renal, brain, kidney, and prostate cancer; non-Hodgkin lymphoma; and multiple myeloma.

 It has been estimated that overall overweight and obesity cause approximately 20% of all cancer cases.  International Agency for Research on Cancer has reported that obesity causes 39% of endometrial cancer cases.

Asia-Pacific Cohort Collaboration set out to to specifically examine the association of cancer mortality with BMI. They reported a significant increase in the risk of mortality from colon, rectal, postmenopausal breast, ovarian, cervical, and prostate cancer and leukemia in overweight and obese individuals from this population.

The CPS II study examined the association between diabetes and cancer mortality in 467,922 men and 588,321 women in the U.S. After 16 years of follow-up, they found a significantly increased risk of mortality from bladder, colon, pancreatic, and liver cancer in men and from pancreatic, colon, and breast cancer in women with diabetes. In the CPS II study, an inverse association was found between diabetes and prostate cancer mortality.

After 26 years of follow-up, in addition to finding an increased risk of mortality from bladder, pancreatic, breast, liver, and colon cancers, they reported that diabetes was associated with an increased risk of oral and pharyngeal cancer, breast cancer in men, and endometrial cancer in women.
The Metabolic Syndrome and Cancer Project (Me-Can) cohort in Austria, Sweden, and Norway is examining the association between the metabolic syndrome as a whole and its individual components on the risk of cancer. From this cohort, the investigators have reported that higher glucose levels were associated with an increased risk of liver, gallbladder, respiratory, and thyroid cancer and multiple myeloma in men, and pancreas, bladder, endometrial, cervical, and stomach cancer in women.

Syllogisms aside, if infections cause inflammations, by Giuseppe Peano’s logic, cancer must to some degree come from an infection.

A more apt question would be; does inflammation promote cancer? The answer to this statement is more apt to be a yes.

The most well-known is the disease Ulcerative Colitis. In this disease there is generalized inflammation of the colon.  This constant inflammation leads to intestinal crypt deformation and a 43% chance of colon cancer within 25-35 years.

PMNs produce enzymes/cytokines to evoke the inflammatory and immune response. The immune cells are provoked via a protein product liberated by the (TAM1) or T cell activated Macrophages. This product is called TNFa. TNFa promotes another agent called NFkB that sends signals to the immune system via IL6 (a cytokine). This signal essentially motivates the immune system with an “intruder alert” warning.

In the immune system, the NFkB is designed to eradicate the potential for injury but in the tissues the mischief it creates is a whole different ballgame.

This leads to the continuous inflammatory response and further production of the TNFa and by shared cross-talk the production of NFkB in the infected tissue cells. 

The overabundance of the NFkB leads to signaling via the STAT3 and IL6. The latter agent induces COX2, which stimulates the Prostaglandin E or PGE. This final agent then provokes the inflammatory response. The continued inflammation leads to a constant provocation of the tissue cells and a self-sustained vicious cycle of cytokine production that induces the cells to grow or proliferate. Somewhere in that confluence of this potpourri of enzymes, a genetic mutation lives or occurs and a cancer is born.

It appears that the NFkB causes about 500 different reversible and irreversible actions within the cellular DNA through epigenetics (Modulating the gene function by virtue of minor or major pressures from micro RNA, Histones etc. imposed on the genome) So not only is this cascade in flow, but other mechanisms are also being cumulated and promoted.

Specific COX-2 inhibitors (Celexecob) including aspirin and other NSAIDs (Advil. Aleve etc.) the increased incidence of polyp formation and cancer is reduced many-fold in patients with ulcerative colitis, in Familial Polyposis Coli and Inflammatory Bowel Disease.

Interestingly, the mitochondria undergo stresses via infection and inflammation by releasing Reactive Oxygen Species (ROS) and Reactive Nitrogen Species (RNS). 80% of all ROS is produced by the mitochondria. These reactive or nascent radical elements (when released within the mitochondria) lead to damage to the mitochondrial DNA (mtDNA), which leads to loss of energy needed for cell growth and function, cell senescence and finally cell death. In the aging process, mtDNA damage occurs over decades. While in infection-inflammation scenario the time is shorter. These ROS and RNS liberations are directly related to the TNFa and NFkB production.

Breast Implants: Recent studies have shown a higher risk of Malignant Lymphoma arising in the breasts of patients with breast implants. Questions remain as to the inflammatory link as the probable causality.

Mutation of the c-Myc and the K-Ras genes lead to the production of TNFa and NFkB, both within the tissue cells and the mitochondria spontaneously thus liberating the ROS and RNS (Oxidative Stressors)

Aspirin. A large meta-analysis of eight studies done by Rothwell et al revealed that those individuals talking daily aspirin had a 60% lower risk of colo-rectal cancer and a 30% lowered risk of other solid malignancies.

Natural agents: Fruits, vegetables, legumes and spices are notable in their ability to reduce inflammatory response.

Curcumin used in curry has been shown to decrease the levels of Y+TNFa and NFkB in the blood of individuals consuming curcumin when exposed to inflammatory provocations. In addition there was a reduction by 40% of abnormal crypt formation in the intestines of patients with inflammatory bowel disease (IBD), which also is proof positive.

Green Tea, Red wine, grape juice and other bioflavonoid also reduce the ROS liberation and the inflammatory response.

Hippocrates: Let food be thy medicine and medicine be thy food.”

Potential mechanisms:
Increased insulin secretion from the pancreas into the portal circulation may lead to increased hepatic growth hormone–mediated synthesis of IGF-1. High-normal levels of insulin, C-peptide, and IGF-1 have been associated with an increased risk of certain cancers in epidemiological studies.

An analysis of 12 prospective studies reported that men with serum IGF-1 levels in the highest quintile of the population range had an odds ratio of 1.38 for developing prostate cancer, compared with men with the lowest IGF-1 levels not all studies have reported positive findings.

In vitro, both IGF-1 and insulin stimulate the proliferation of tumor cells lines. In vivo animal studies have demonstrated that endogenous hyperinsulinemia increases the growth and metastasis of mammary tumors, while increased circulating IGF-1 levels increased the growth and metastases of colon cancers in mice.

Many tumors are known to overexpress the IR, and some studies have reported that higher expression of the IR is associated with a worse prognosis.

Therefore, in obesity, diabetes, and the metabolic syndrome, glucose may be playing a role in concert with hyperinsulinemia, inflammation, adipokines, and altered estrogen levels.

Estrogen:
Similarly, increased endogenous estrogen levels have been reported to increase the risk of postmenopausal breast cancer twofold. Obesity has long been known to be associated with increased circulating estrogen levels, due to increased aromatase activity in adipose tissue. In addition, insulin-resistant women have suppressed hepatic production of sex hormone–binding globulin, leading to increased levels of free estrogen. More recent studies have also demonstrated that obese women express increased levels of aromatase in breast stromal tissues, the expression of which is increased by inflammatory mediators including TNF-α, IL-1β, prostaglandin E2, and cyclooxygenase-2 (COX-2)
The estrogen receptor (ER) and IGF-1R are known to have significant cross-talk in the normal mammary gland and breast cancer.

Cytokines:
Obesity is considered a state of chronic inflammation. In obesity, adipocytes increase in size and have a greater number of macrophages. Adipose tissue macrophages secrete a number of inflammatory molecules including IL-6 and TNF-α.

Increased IL-6 levels have been implicated in the pathogenesis of hepatocellular carcinoma and ovarian, prostate, and breast cancer.

IL-6 has also been implicated in the development of breast cancer metastases by inducing changes in cells that lead them to have greater invasive and migration properties: a phenomenon known as epithelial-mesenchymal transition. TNF-α has also been seen to play a role in tumor promotion. TNF-α is associated with increased colon tumor growth in animal models and with more aggressive prostate cancer and in breast adipose tissue has been shown to increase the expression of aromatase. 
Studies have demonstrated cross-talk between IL-6 and epidermal growth factor receptor signaling in epidermal growth factor receptor–driven breast cancer.

Knocking down IL-6 was also associated with a decrease in the number of tumor-associated macrophages. Tumor-associated macrophages are a source for cytokines and TNF-α and may contribute to tumor growth and metastases.

Low adiponectin levels and high leptin have been associated with an increased risk of colorectal cancers in a cohort study nested within the Women’s Health Initiative cohort. Leptin is also a proangiogenic factor and increases the expression of matrix metalloproteases (MMP-2 and MMP-9) that are important for cell invasion.

The bottom line is simple: Obesity is linked with chronic Inflammation and the latter drives the wheel of misfortune (cancer).

"Live Long and Prosper: Eat less (consider fasting a few days a month a prelude to healthy living), Exercise more (Walking daily for an hour) and De-stress a bit (don't take everything seriously)."

References:

Calle EE, Rodriguez C, Walker-Thurmond K, Thun MJ. Overweight, obesity, and mortality from cancer in a prospectively studied cohort of U.S. adults. N Engl J Med 2003;348:1625–1638

Wolin KY, Carson K, Colditz GA. Obesity and cancer. Oncologist2010;15:556–565

 Parr CL, Batty GD, Lam TH, et al., Asia-Pacific Cohort Studies Collaboration. Body-mass index and cancer mortality in the Asia-Pacific Cohort Studies Collaboration: pooled analyses of 424,519 participants.Lancet Oncol 2010;11:741–752

Coughlin SS, Calle EE, Teras LR, Petrelli J, Thun MJ. Diabetes mellitus as a predictor of cancer mortality in a large cohort of US adults. Am J Epidemiol 2004;159:1160–1167

Campbell PT, Newton CC, Patel AV, Jacobs EJ, Gapstur SM. Diabetes and cause-specific mortality in a prospective cohort of one million U.S. adults.Diabetes Care 2012;35:1835–1844

Stocks T, Rapp K, Bjørge T, et al. Blood glucose and risk of incident and fatal cancer in the metabolic syndrome and cancer project (me-can): analysis of six prospective cohorts. PLoS Med 2009;6:e1000201

Roddam AW, Allen NE, Appleby P, et al. Insulin-like growth factors, their binding proteins, and prostate cancer risk: analysis of individual patient data from 12 prospective studies. Ann Intern Med 2008;149:461–471

Novosyadlyy R, Lann DE, Vijayakumar A, et al. Insulin-mediated acceleration of breast cancer development and progression in a nonobese model of type 2 diabetes. Cancer Res 2010;70:741–751

Ferguson RD, Novosyadlyy R, Fierz Y, et al. Hyperinsulinemia enhances c-Myc-mediated mammary tumor development and advances metastatic progression to the lung in a mouse model of type 2 diabetes. Breast Cancer Res 2012;14:R8

Wu Y, Yakar S, Zhao L, Hennighausen L, LeRoith D. Circulating insulin-like growth factor-I levels regulate colon cancer growth and metastasis.Cancer Res 2002;62:1030–1035

Mathieu MC, Clark GM, Allred DC, Goldfine ID, Vigneri R. Insulin receptor expression and clinical outcome in node-negative breast cancer.Proc Assoc Am Physicians 1997;109:565–571

Toniolo PG, Levitz M, Zeleniuch-Jacquotte A, et al. A prospective study of endogenous estrogens and breast cancer in postmenopausal women. J Natl Cancer Inst 1995;87:190–197

Le TN, Nestler JE, Strauss JF 3rd, Wickham EP 3rd. Sex hormone-binding globulin and type 2 diabetes mellitus. Trends Endocrinol Metab2012;23:32–40

Guo Y, Xu F, Lu T, Duan Z, Zhang Z. Interleukin-6 signaling pathway in targeted therapy for cancer. Cancer Treat Rev 2012;38:904–910

Sullivan NJ, Sasser AK, Axel AE, et al. Interleukin-6 induces an epithelial-mesenchymal transition phenotype in human breast cancer cells.Oncogene 2009;28:2940–2947

Flores MB, Rocha GZ, Damas-Souza DM, et al. Obesity-induced increase in tumor necrosis factor-alpha leads to development of colon cancer in mice. Gastroenterology 2012;143:741–753 

Rokavec M, Wu W, Luo JL. IL6-mediated suppression of miR-200c directs constitutive activation of inflammatory signaling circuit driving transformation and tumorigenesis. Mol Cell 2012;45:777–789

Kim SW, Kim JS, Papadopoulos J, et al. Consistent interactions between tumor cell IL-6 and macrophage TNF-α enhance the growth of human prostate cancer cells in the bone of nude mouse. Int Immunopharmacol2011;11:862–872

Ho GY, Wang T, Gunter MJ, et al. Adipokines linking obesity with colorectal cancer risk in postmenopausal women. Cancer Res2012;72:3029–3037

Vona-Davis L, Rose DP. Angiogenesis, adipokines and breast cancer.Cytokine Growth Factor Rev 2009;20:193–201

Weinberg F, Hamanaka R, Wheaton WW, et al. Mitochondrial metabolism and ROS generation are essential for K-ras-mediated tumorogenicity. Proc Natnl Acad Sci USA 2010;107:8788-93

Prasad S, Ravindran J, Aggarwal BB,  NFkB and cancer: how intimate is this relationship? Mol Cell Biochem. 2010;336:25-37.

Kamp Dw, Shacter E, Weitzman SA. Chronic inflammation and cancer: the role of the mitochondria. Oncology 2011;25:400-13.

Aggarwal BB. Nuclear factor kappaB: the enemy within. Cancer Cell 2004;6:203-8

Grivennikov SI, Greten FR, Karin M. Immunity, inflammation and cancer. Cell 2919;140:883-99.

Montavani A, Garland C, Allavavena P. Molecular pathways and targets in cancer related inflammation. Ann Med 2010;42:161-70.

Ekbom A. Risk of cancer in ulcerative colitis. J Gasterointest Surg. 1998:2:132-13.

Weinberg F, Chandel NS. Reactive oxygen species dependent signaling regulates cancer. Cell Mol Life Sci. 2009;66:663-73.

Balkwill F. Tumor Neoosis Factor and cancer. Nat Rev Cancer. 2009;’9:361-71.
Gullett NP, Ruhul Amin AR, Bayraktar S, et al. Cancer prevention with natural compounds. Semin Oncol. 2010;37:258-81

Aggarwal BB, Kumar A, Bharti AC. Anticancer potential of curcumin: preclinical and clinical studies. Anticancer Res. 2003;23:363-98

Carroll RE, Benya RV, Turgeon DK, et al. Phase IIa clinical trial of curcumin for the prevention of colorectal neoplasia. Cancer Prev Res (Phila). 2011;4:354-64.

Popivanova BK, Kitamura K, Wu Y, et al. Blocking TNF-alpha in mice reduces colorectal carcinogenesis associated with chronic colitis. J Clin Invest. 2008;118:560-70

http://www.aacr.org/Newsroom/Pages/News-Release-Detail.aspx?ItemID=582&utm_source=social&utm_medium=twitter&utm_content=can&utm_campaign=newsrelease#.U-4EhPldU_5






Friday, September 12, 2014

TIME to say "HELLO"

Can we quantify and qualify everything we do?

Is that a good thing?

Think about the latest craze about wearables. Our heart rates, respirations, movements are being monitored and stored in some digital universe for retrieval later by us or someone else all the time. There are methods measuring the measures that measure our progress or lack thereof. There is a constant cacophony of “talking heads” on television that it is a must for the 21st Century being to make certain that each step is quantified, each wink immortalized, each view in the mirror, mirrored to the world and each thought expressed. The makers of the wearables are eager to have you buy the latest greatest gizmo and attach it to your limb, body, ear or eye in the hopes of gathering data about the “pathetic’ populace that is so out of touch with itself in staying healthy. In so doing they are tethering us into this virtual world of electronic emptiness.


I wonder…

What did the older generations do?

Really what did they do?

Asking a 90 year old and his response is simple. “We played stick ball in the streets and our elders watched from the sidelines keeping a watchful eye on traffic.” He added, “”We played football with a stuffed toy, or jumped in a brook nearby to cool down.”


Really?

“Yes and we were as thin as rails.” I could throw a stick like a javelin, hurl a ball as a hammer throw and swim like a fish in a lake. Yes we did all that and more!” He closes his eyes to the present in search of a distant but a pleasing past.

Now we have a constant flow of gadgets and gizmos galore that a 3 year-old can expertly navigate to the latest You-Tube video of Disney character in under ten seconds and there sit with eyes staring at the flicker of the screen, mesmerized by the limits of time during which the adult seeks refuge in their virtual world transgressions.

Is the progress we seek that is around us today, the progress we sought in days past? Apparently it is, after all we are here. The verse has changed. Maybe it needs a revision?

Asking a 20 year old and her response is simpler. “Umm…” as her eyes are glazed over by the flicker of her computer screen.

We want connections, we want to be liked for all the selfish reasons, we want to have a constant wave of onlookers that give “thumbs up” and a one word response of “Great, Brilliant, Excellent,” or the implied sentiment thru, “LOL, LMAO or some other contrived messaging that appeals to the vacuous nature of such connections.” We fear direct contact for fear of appearing stupid, or quiet or humble. We fear our real life persona might not hold up the candle to the digital persona we have crafted. And we are constantly in the narcissistic jungle of “how much and how many” virtual beings we have. Whereas taking a "selfie" is an immediacy for gratification, drawing a sketch is losing oneself on the road less traveled, which brings with it unimaginable happiness and satisfaction.

Maybe it is time to recognize that measuring, messaging and living in the digitally archived virtual world is not the real reality. It limits activity, which limits the fecundity of the brain and makes us all lethargic. This virtual existence damages our real connections, isolates us into compartments and groups and cabals that function to self-glorify. It makes for an under-nourished mind, a weaker thought and a “followers” instinct-a drone, rather than a leader’s virtue.  

Maybe we should learn to “feel” the touch, “hear” the angst of another being and “see” the wonder in someone’s eyes. And from there gather what is and what needs to be.

Maybe it is time to power down the wearables. Shut the flicker on the screen. Stop looking at the digital world for a response and move into existential reality.

Maybe it is time to say, “FUGGADABOUTIT!”

And maybe it is time to say, “HELLO!”


.....Rather than just write it an be governed by "Morons," Peter Drucker's term for computers.

Sunday, September 7, 2014

SOLITUDE, the Power of SILENCE and the neon gods!

Several years ago upon walking into the room of an elderly patient in the hospital, the noise of my heels on the floor startled her out of a sleep state or so I thought. I apologized and she shrugged it off. She was 91 years old with a long history of chronic leukemia. Two days later, I happen to walk into the room when her husband who was 90 years sat by her bedside. He was holding her hand and as I approached she was again startled out of her reverie. Again with deep apologies I examined her and noted her progress and left the room. She continued to improve and was discharged a few days later. I realized as I reflect back on that time; the power of silence.

There is something to be said about the power of silence. We are constantly inundated with powerful messaging, the clink and clang of technology, the seduction of verbal contact, the force to communicate to everyone, to no one in particular or just reclaim the beast of “being alive.” Where has all that solitude gone?

A person seeking solitude was at first considered a hermit, now he or she is considered an antisocial and in some circles labeled as an anomaly of human behavior. Yet we are forever trying to hide in our rooms, bury our ears beneath pillows to drown out the noise, wear noise-cancelling headsets, turn up the volume of the music that feels good to drown out the cacophony of daily life. Why?

There must be an edge to silence over noise!

What is it?

In Finland the power of branding to increase tourism has taken on a whole new meaning. The country has espoused and advertises the “Silence” to attract tourists as the quiet getaways from the humdrum of daily chaos. And they are winning over the hearts and minds of their segmented population. Wealthy citizens of this world buy islands to escape the ticker-tape of life. Why?

Children growing up, sleep for 12-14 hours a day during their first year of life, this sparks neural growth and their brains increase three times in neural density and synaptic connections. Mice brains relegated to silence also grow more neuronal density. In humans, with neuronal density and a plethora of new synaptic connections, new ideas take shape from old memories and experiences that are stored within. From new ideas come new actions and the world changes! We make better decisions away from the constant noise that robs us of our peace and inner strengths.

Professional skiers, swimmers, runners, and other athletes before any performance will close their eyes and imagine their moves. Why? Because in the quiet of their brain they are able to evoke the countless hours of positive imagery developed and stored during practice and training. Some wear headsets tuned to their favorite music, others just the noise-cancelling headsets for silence.


As the daily grind and the cacophony to join this that and the other, to be known, to be heralded, to be retweeted, to be liked or to be commented about takes over our being, but through it all, the quiet seems also to have a quiet resurgence. In the 1980s 9% of the adult population was single now that number has steadily climbed to 16%. Solitude is not an illness or a disease of the mind. It is a conscious voluntary act of living in harmony. Just like silence is not measurable in ounces or pounds, in dollars and cents or in good and bad, solitude too is without metrics, except maybe in happiness!

http://youtu.be/4zLfCnGVeL4

Solitude and silence does not mean the absence of love and friendship. It means the opposite: tethered to the wings of silence, the two achieving greater heights in thought, in friendship, in love, in affection and in living.


The 90 year old lived for a few more years in the firm and ever present loving hand of her husband. When they passed away it was within a month of each other. The transference of the sole energy of each other’s silent love ceased and life became meaningless for the survivor. Their love was in the silence and their touch.

Tuesday, September 2, 2014

BARBARIC

Some things are patently wrong and require the conscious to speak out...


I read about the King family that is awaiting extradition to the United Kingdom after taking their child out of the UK hospital where the child was denied the benefit of Proton beam Therapy for a diagnosis of Medulloblastoma (a brain tumor). It does not matter whether Proton Beam Therapy will cure or even extend survival of the child for that matter. What is important is that the King family’s desired to seek help on their own dime and not on the public dole, outside the reaches of the NHS and this want should not be the purview of any authority, state or liege.

What is beguiling is the long heavy arm of the law going after the parents whose only intent is to save their child. The father sold a home to have the money so he could seek Proton Beam therapy in one of the close neighboring European Countries. The parents decided to take the child out of the UK hospital in search for the medical help they sought. What could be wrong with that? The Public Healthcare of the National Health Services of the United Kingdom comes to mind? A denied need by the Central Planners cannot be overturned even if one wants to spend one’s own money? It is a system of Cost Control on the treatment of malignant illness! “No, that is not in the rule book, Sir!”

It brings the bile wave crashing at one’s conscience’s shores to allow something like this to happen. It is a travesty to prevent someone to seek a different modality of care. To exercise the long arm of the law and the heavy hand of the enforcers in order to quell such a desire is beneath a country that has always dedicated itself to Liberty and Freedom.

These might be the times the future will look upon with tinted shades. The darkness itself appears deadly and the only way to visit the present in the future will be to avoid it.


The King family now awaits extradition orders while the Spanish judge has enforced that the King family is barred from visiting the child and the child is now a ward of the court. A travesty upon travesty! What on earth is going on in these so-called “civilized societies” is nothing less than a value proposition that borders on barbaric.

Maybe sense will prevail. Just maybe?