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This Is Your End: Heart Disease or Cancer

Yesterday, we discussed Americans’ declining life expectancy. Today, we’ll explore the endpoint that’s ever closer and how we’ll get there. But cheer up: We have good news, too.

There really is no “good” way to die. We’re all going to do it. As of today, death is inevitable.

Some ways are more hideous than others, particularly the torturous variety such as “scaphism,” allegedly designed and practiced by the ancient Persians so the subject would suffer as much as possible before succumbing.

The good news is that none of us will likely meet our end by scaphism (or “the boats” — click here for a not-so-pretty picture, as strictures of time, space, and good taste rule out a full description).

Nor, for 99.99%, of us will it be through any of the other “top 10 worst ways to die” – radiation, burning, decompression, crucifixion, the electric chair, lethal injection, decapitation, dehydration, and starvation.

No, we’re actually highly likely to die from either heart disease or cancer, which, combined, account for 46% of U.S. deaths in 2014.

The end will come after a long, physically and emotionally taxing battle, marked by periods of optimism and pessimism, invasive tests and treatments, isolation and alienation, and, finally, realization of our mortality.

All we can really hope is that our doctors know how to manage the pain.

So we may not be consumed by insects or suffer for the few seconds that science suggests we would if our heads were separated by sharp force from our torsos.

Ours will be a special kind of modern torture, the consequence, in many cases, of decisions we made and behaviors we adopted all on our own.

No, we’re actually highly likely to die from either heart disease or cancer, which accounted for 46% of U.S. deaths combined in 2014.

Sure, some of us are genetically predisposed to defective vessels, leaky valves, or holes in the heart. And certain cancers may run in families, or we may be exposed to harmful substances without our knowledge.

But what we eat, drink, smoke, whether we exercise: These are all variables that we can, in general, control. It’s a complex causational stew that includes social and environmental factors as well as scientific ones, but we individuals can do better for our own sake.

And then there’s what happens when we finally make it to the hospital.

Innovation in heart disease treatment is a subject we’ve not yet covered. We’ll get to it.

We have, however, devoted significant pixels to cancer and cutting-edge research into its cure.

There’s good news on this front, and there’s bad news.

Let’s start with the bad — an object lesson on the special kind of modern torture that leads us to explore revolutionary ways to treat diseases without obvious solutions.

As you may have read, Seattle-based Juno Therapeutics Inc. (JUNO) recently experienced another major setback in the Phase II clinical trial of its CAR-T (chimeric antigen receptor T-cell) cancer immunotherapy treatment, JCAR015.

Two more patients suffered swelling of their brains and subsequently died. The incidents follow three similar deaths that led to a suspension of the clinical trial in July.

Once again, Juno has suspended the Phase II trial.

Juno attributed the July deaths to the introduction of the chemotherapy drug fludarabine to its “Rocket” trial for B-cell acute lymphoblastic leukemia (ALL).

It changed the protocol, removing fluradabine from the trial. Now we know that fluradabine was not the sole cause of the cerebral edema that caused patients’ deaths.

And that raises the question whether the Food and Drug Administration (FDA) should have done more to understand a phenomenon that is clearly not monocausal before it lifted the July suspension on Juno’s Phase II trial.

Two more patients suffered swelling of their brains and subsequently died. The incidents follow three similar deaths that led to a suspension of the clinical trial in July.

Maxim Jacobs, a health care analyst at Edison Investment Research who researches oncology drugs, posed key rhetorical questions for STAT: “What did the FDA review during that period from when the hold was announced to when it was lifted? What exactly was the decision-making process? What was the logic behind going so quickly toward lifting the hold?”

The FDA has yet to comment on the recent Juno clinical trial deaths.

Juno’s ambitious goal of getting an approved therapy to market in 2017 is in jeopardy. Its stock price has certainly reflected the company’s recent clinical difficulties.

It closed at $22.98 on November 22. But it gapped down to $21.33 at the open on November 23 and is now trading at $17.75. Juno’s 52-week high is $49.72, which it achieved June 6, 2016.

Juno sold 11 million shares at $24 on its December 18, 2014, initial public offering. The stock immediately surged when it began trading on Friday, December 19, 2014, opening at $39. It ended 2014 at $52.22.

The stock followed that trajectory to an all-time high of $69.28 on June 5, 2015.

Juno’s future may lie with other therapies, including JCAR014 for patients with chronic lymphocytic leukemia (CLL) and JCAR017 for patients with relapsed/refractory diffuse large B-cell lymphoma (DLBCL).

“New research has identified the cells responsible for this process in oral tumors, and also a promising way to stop it.”

Of course, that’s little consolation for Juno shareholders who’ve been with the stock for more than 12 months. It may, however, offer some upside for particularly aggressive traders.

And then there are patients and families, including Max Vokhgelt’s father, who wants to know how his son could go from telling his grandmother “in five or six days, I will be cancer-free” to dying within a few days of that phone call.

But in an effort to end on a positive note:

Metastasis, the spreading of cancer cells to other parts of the body, is the main cause of cancer-related death. New research has identified the cells responsible for this process in oral tumors, and also a promising way to stop it. The key lies in the cells’ ability to absorb dietary fatty acids — particularly palmitic acid, a major component in palm oil. Metastasis-initiating cells have high levels of the fatty acid receptor CD36 and seem to rely on certain fatty acids to thrive. Blocking the CD36 receptor prevented human oral cancer transplanted into mice from spreading, and a similar effect was found in melanoma and breast cancer cells.

That’s the introduction to an interview of Salvador Aznar Benitah and Gloria Pascual of the Institute for Research in Biomedicine in Barcelona conducted by ResearchGate’s Katherine Lindemann.

Benitah, Pascual, and their fellow researchers may have discovered the key to the development of antimetastatic therapies. Cutting off certain fats stops metastasis.

The full research paper is available here.


Writes space historian and writer Andrew Chaikin in a piece for Scientific American, Godspeed, John Glenn — the Quintessential Astronaut“:

The more I’ve come to know about John Glenn and what he did, the more I’ve come to see him as the quintessential astronaut.

Glenn was a man who seemed to be driven by one overriding purpose: to utilize his abilities to the fullest extent possible and to increase what he once called “mankind’s ever broadening store of knowledge.” He welcomed the unknown and longed to explore it. Without planning it, or even realizing it, he was preparing for his Mercury mission for most of his adult life.

No one could have imagined then that more than three decades later a 77-year-old Glenn would shatter all preconceptions of age by venturing into space for a second time. I was lucky enough to witness his launch on space shuttle Discovery, watching him and his six crewmates leave the planet atop brilliant pillars of fire. And when it was over, I was able to turn to a fellow journalist and say, as I had not known to do in 1962, “John Glenn is in orbit.”

Smart Investing,

David Dittman
Editorial Director, Wall Street Daily

David Dittman

, Contributing Writer

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