Body Was Created for Healing Itself
New discoveries point out automatic mechanisms for repair and health.
Could disease result from failure of these processes?
Were our bodies designed for self-repair? Evolutionists insist that what we have is all that natural selection gave us, including disease and death, so get used to it.
Hints of a better existence can be glimpsed, though, in some animals like salamanders that can regrow limbs, and mammals such as naked mole rats that seem immune from cancer. Indeed, we would be dead already were it not for countless repair mechanisms that are constantly at work. These include mechanisms within the cell, like multiple DNA Damage Repair (DDR) systems, and mechanisms at the macro level, like blood clotting and the immune system. Some recent news items hint that life could be healthier by boosting some of these built-in mechanisms.
This experimental drug could change the field of cancer research (National Public Radio, 7 June 2022).
An amazing report about a new cancer treatment hit numerous news sites on June 7 from the prestigious Memorial Sloan Kettering Cancer Center in New York. In a clinical trial, all 14 patients with rectal cancer who were treated with dostarlimab had complete remission. That’s 100% of patients who saw 100% of their tumors disappear—an unheard of success rate. It’s “what cancer doctors’ dreams are made of,” remarked lead researcher at Sloan-Kettering, Dr Andrea Cercek.
Watch a must-see clip by Dr Cercek on OANN as she glows with excitement about this unexpected outcome. Listen to four of the patients on Science Alert, who all look and feel great after the treatment. A concise video by Roman Balmakov of the Epoch Times, with quotes from Dr Cercek and from the paper in New England Journal of Medicine, premiered on June 9th, sharing what is known so far and the multiple ways in which this discovery portends hope for other cancer patients. “It’s absolutely incredible,” Cercek gleamed.
The treatment involved 6 months of injections with monoclonal antibodies (remember those during Covid?), specially designed to boost the population of existing antibodies so that the body’s immune system attacks and kills the cancer cells. It’s a type of immunotherapy, meaning that it helps the body do what it is already capable of doing, “unlocking the body’s natural immune system to fight cancer,” as Cercek explains. For patients lacking the gene for mismatch repair, “it revs up the immune system” that already can tell the cancer cell is foreign and must be destroyed.
The treatment had low toxicity and required no debilitating chemotherapy or radiation. Although the drug was designed for cancers resulting from defects in the Mismatch Repair System in cells, which when broken accelerates mutations leading to cancer, Cercek feels confident that what is being learned in this study will lead to treatments for other cancers, too. The OANN report says that dostarlimab could be available within a year.
What this means for our current focus is two things: (1) a healthy body with a healthy genome already has mechanisms for repairing DNA mismatch defects, and when that doesn’t work, (2) the body has an immune system able to recognize the problem and destroy the incipient cancer cells. If both those were in original working order, no therapy would have been needed. The body would keep itself healthy.
A surprise in the eye: long-lived T cells patrol the cornea (Nature, 3 June 2022).
“Scientists previously thought that specialized immune cells did not reside in the transparent cornea,” begins this news item. They were wrong: long-lived T cells, part of the immune system, have been found in the front surface tissue of the eye: the cornea, where they patrol for trouble. Long-lived T cells, the report says, “swiftly attack pathogens they have previously encountered — a process called ‘immune memory’.”
The researchers then used live-cell imaging to observe the corneas of six healthy adults. They found cells similar in shape, size and speed to the patrolling T cells in mice. It was a “lightbulb moment”, says Mueller. “We were somewhat surprised and pleased to see that there is, indeed, an immune memory” in the cornea, says Mueller, who is now working on obtaining tissue from organ donors to confirm the exact type of the patrolling cells in people.
The article says that this finding may lead to treatments for the painful viral infection known as shingles—which sometimes attacks the eye as well as the skin—and other diseases like chronic dry eye, cornea loss and implant rejection, as well as certain autoimmune diseases. Those T cells were patrolling the cornea all the time and scientists didn’t know it. When diseases occur, has something gone awry with those T cells?
Unprecedented Case Series Advances Promise of Phage Therapy (University of California San Diego Health, 9 June 2022).
Another natural protection against disease involves—of all things—viruses. Before getting into the discovery, hear some astonishing facts about a type of virus called a phage (feyj) that invades bacteria and kills them. (Note: it’s OK to skip over the e-word evolved, which contributes nothing to the story).
Bacteriophages are viruses that have evolved to target and destroy specific bacterial species or strains. Phages are more abundant than all other life forms on Earth combined and are found wherever bacteria exist. Discovered in the early 20th century, they have long been investigated for their therapeutic potential, but increasingly so with the rise and spread of antibiotic-resistant bacteria.
Phages look remarkably artificial, like miniature lunar landers attaching to the surface of nanoscopic planets. Powerful motors in the capsid inject their DNA into the bacterium, where they commandeer the bacterial genome and use it to make copies of themselves. Bursting the bacteria, they emerge in large numbers to invade other bacteria. It’s a powerful and rapid response to a bacterial infection. It seems made to order for treatment of disease but successes have been few so far. The new clinical trial at UCSD yielded promising results when 20 patients were given phages over a six-month period.
The authors reported no adverse reactions to phage therapy in any of the patients, regardless of type of bacterial infection, types of phages used or method of treatment. Eleven of the 20 patients displayed some measure of symptom improvement or reduced bacterial presence. Five patients had inconclusive outcomes and four exhibited no response to treatment.
This initial success could lead to stronger doses, now that the patients suffered no ill effects. If readers can hold their nose at the credit given to evolution, the report ends with reasons why phages work so well:
“In phages, evolution has produced an effective killer of bacteria, one that offers enormous potential in the worldwide fight against antibiotic resistance. This paper is a glimpse of what might and can be. It starts with NTM infections, but the number of antibiotic-resistant bacterial species out there is large and growing. This is another step, an important one, in a fight that will likely never end.”
Assuming that evolution invented phages, though, makes no sense. Phages need bacteria to work, but both phages and bacteria are irreducibly complex. Both are functional arrangements of many sophisticated parts. A better explanation is that phages keep bacterial numbers in check, which might otherwise overwhelm animal hosts. This requires additional sophistication for monitoring and recognizing the difference between beneficial and harmful strains.
Primary cilia in satellite cells are the mechanical sensors for muscle hypertrophy (PNAS, 7 June 2022)
Briefly considered, this paper explains why exercising muscle makes it grow bigger. Most cells have primary cilia that act like antennas to the outside world. In muscle cells, these primary cilia signal the interior of the cell that they need to grow strong, a benefit called hypertrophy.
Muscle atrophy is characterized by loss of lean muscle mass and increased weakness. Physical exercise is the primary intervention to improve muscle strength and endurance in healthy individuals. However, some people are so-called exercise resistant, with underlying mechanisms unclear. We discover that the cilia of skeletal muscle satellite cells are indispensable mechanical sensors for exercise-induced muscle hypertrophy and, potentially, could be targeted for future interventions to ameliorate muscle atrophy or mimic exercise-induced beneficial effects in persons unable to exercise or responding poorly to exercise.
What this means is that weakness and atrophy, such as in muscular dystrophy, can occur from damage to those cilia. ID advocate Dr Michael Behe pointed to cilia as irreducibly complex systems, both in the way they function and in the way they are constructed (se his books Darwin’s Black Box and The Edge of Evolution). Normally, those cilia are part of complex signal transduction systems. When they work, the messages are communicated between outside and inside the cell. All is well, and physical activity builds muscle mass. That was the plan; disease comes from the breakdown of well-designed systems.
We live in a fallen world. The curse God put on the world when Adam and Eve sinned could have involved judgments of omission instead of commission: God releasing his hands on some of the built-in mechanisms for health, letting nature take its course through entropy, including mutational burden. Consider, by analogy, how in the case of sinners who did not acknowledge their Creator in Romans 1:22, God “gave them up” to dishonorable passions, “receiving in themselves the due penalty for their error.”
Another factor of the curse might have involved granting Satan limited ability to bring pain on mankind—the book of Job being a case study.
And yet “God did not leave himself without witness,” Paul said to pagans in Lystra in Acts 14, “for he did good by giving you rains from heaven and fruitful seasons, satisfying your hearts with food and gladness.” He also gave man healing hands and a moral compass to try to slow down some of the effects of the curse. His merciful benevolence to all the world did not leave man without hope. He loved mankind so much it cost him his Son! But as the Son was raised, we also can be raised to newness of life (Romans 6). Death and Satan will not get the last word.
These reports are both instructive and encouraging. At best, though, they are only temporary. They can only delay the inevitable. In the meantime, don’t expect your body to get out of this world alive. The way of life is through the narrow gate (Matthew 7:13-14).