Rosa Rubicondior: Incompetent Design - Failing To Plan Is Planning to Fail

Thursday, 13 March 2025

Incompetent Design

Failing To Plan Is Planning To Fail
And A Fatal Cancer Is The Result

Stress

Chronic stress and obesity work together to accelerate pancreatic cancer development and growth, study finds | UCLA Health

It’s a fundamental principle of management that failing to plan is, in effect, planning to fail. The future is inevitable, so preparation for it is essential.

Creationism’s supposed designer, however, is claimed to be both omniscient and omnipotent — fully aware of the future and capable of shaping it. In fact, many fundamentalist believers assert that this designer has a specific plan for each individual, meaning it doesn’t just foresee the future but actively creates it.

Logically, then, an intelligent, all-knowing creator should have planned accordingly, yet the evidence suggests otherwise. Our bodies are poorly adapted to endure the demands of modern urban life in a technologically advanced society, indicating a lack of foresight in their design.

The alternative explanation? This designer was fully aware of our future needs but deliberately created a body ill-suited for them.

What information do you have on the types and causes of pancreatic cancers?

Pancreatic cancer is a complex disease with multiple subtypes and causes. It is one of the most aggressive cancers, often diagnosed late due to a lack of early symptoms. Here’s a breakdown of its types and causes:

Types of Pancreatic Cancer

Pancreatic cancers can be broadly categorized into exocrine and endocrine (neuroendocrine) tumours, based on the type of cells they originate from.

Exocrine Pancreatic Cancers (Most Common)

These arise from the exocrine cells, which produce digestive enzymes.

Pancreatic Ductal Adenocarcinoma (PDAC) - The most common type (>90% of cases). It starts in the ducts of the pancreas.
Acinar Cell Carcinoma - Rare; arises from enzyme-producing cells.
Adenosquamous Carcinoma - A rare and aggressive form with both glandular and squamous components.
Colloid Carcinoma - Less aggressive; arises from mucin-producing cells.
Giant Cell Tumours - Extremely rare and aggressive.

Pancreatic Neuroendocrine Tumours (PNETs)

These develop from hormone-producing endocrine cells and can be functional (producing hormones) or non-functional (not producing hormones).

Insulinomas - Produce insulin, causing hypoglycaemia.
Gastrinomas - Cause excess stomach acid (Zollinger-Ellison syndrome).
Glucagonomas - Lead to high blood sugar and skin rash.
VIPomas - Affect fluid balance, causing diarrhea.
Somatostatinomas - Disrupt digestion and hormone regulation.

Causes and Risk Factors

The exact cause of pancreatic cancer is not always clear, but several risk factors contribute:

Genetic and Hereditary Factors

Inherited Mutations - BRCA1, BRCA2, PALB2, STK11 (Peutz-Jeghers syndrome), and PRSS1 (hereditary pancreatitis).
Family History - First-degree relatives with pancreatic cancer increase risk.

Environmental and Lifestyle Factors

Smoking - One of the strongest modifiable risk factors.
Obesity and Poor Diet - Linked to chronic inflammation and insulin resistance.
Chronic Pancreatitis - Persistent inflammation increases cancer risk.
Diabetes Mellitus - Type 2 diabetes, especially if recently diagnosed, can be both a risk factor and an early symptom.
Excessive Alcohol Consumption - Contributes to pancreatitis and increases risk.

Biological and Disease-Related Factors

Age - Most cases occur in people over 60.
Gender - Slightly more common in men.
Race/Ethnicity - Higher incidence in African Americans.
Infections - Helicobacter pylori and hepatitis B/C have been linked to increased risk.

Recent Findings: Stress and Obesity as Risk Factors

Recent studies suggest that chronic stress and obesity may contribute to pancreatic cancer through:

Inflammation - Stress-related hormones (cortisol) and chronic obesity promote inflammation, which can drive cancerous changes.
Insulin Resistance - Excess body fat leads to insulin resistance and increased insulin-like growth factor (IGF-1), which can fuel tumour growth.
Immune Suppression - Chronic stress weakens the immune system, reducing its ability to fight off early cancerous cells.

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Information Continually updated

Whichever view creationists choose, scientists have now uncovered how chronic stress and obesity sometimes combine to trigger pancreatic cancer.

Chronic stress and obesity work together to accelerate pancreatic cancer development and growth, study finds
UCLA investigators uncover how stress and obesity activate similar pathways to fuel pancreatic cancer growth

A new study led by UCLA investigators suggests that chronic stress and an unhealthy diet may work together to fuel the early development of pancreatic cancer, shedding light on how lifestyle factors contribute to one of the deadliest malignancies.
In preclinical models, researchers identified a key molecular mechanism by which stress and obesity trigger changes in pancreatic cells that may lead to cancer. Specifically, stress-related neurotransmitters and obesity-related hormones were found to activate a protein called CREB, which is linked to cancer cell growth, through different biological pathways. Stress hormones activate the β-adrenergic receptor/PKA pathway, while obesity-related signals mainly use the PKD pathway. This suggests that both stress and obesity can fuel pancreatic cancer growth through similar mechanisms.

In mouse experiments, a high-fat diet alone led to the growth of precancerous pancreatic lesions. However, when the mice also experienced social isolation stress, they developed even more advanced lesions.

The study also found that social isolation had a stronger impact on cancer development in female mice compared to male mice. The researchers hypothesize that women’s biological response to stress, possibly influenced by estrogen and increased β-adrenergic receptor activity, may make them more susceptible to stress-related cancer risks.

IMPACT
The findings suggest that stress hormones and obesity-related hormones activate key cancer-promoting pathways, potentially accelerating the onset of pancreatic cancer. One possible solution, researchers suggest, is to explore the use of existing medications to reduce this risk. Since β-adrenergic receptors play a crucial role in stress-related cancer growth, commonly used beta-blockers, which are drugs prescribed for high blood pressure, could be repurposed to help mitigate these effects.

JOURNAL
The study was published in Molecular Cancer Research.

AUTHORS
The study’s first authors are Xiaoying Sun, a postdoctoral researcher in the departments of medicine and surgery at UCLA, and Yaroslav Teper, a project scientist at David Geffen School of Medicine at UCLA. The senior authors are Dr. Guido Eibl, professor in residence in the department of surgery at UCLA Health, and Dr. Enrique Rozengurt, distinguished professor of medicine and chief of research in the division of digestive diseases at UCLA. Other coauthors, all from UCLA, are James Sinnett-Smith, Mineh Markarian, Dr. Joe Hines and Dr. Gang Li. Eibl, Rozengurt, Hines and Li are also members of the UCLA Health Jonsson Comprehensive Cancer Center.

Abstract
One of the deadliest types of cancer is pancreatic ductal adenocarcinoma (PDAC). Chronic stress and obesity are recognized as risk factors for PDAC. We hypothesized that the combination of stress and obesity strongly promotes pancreatic cancer development and growth. Here, we show that the stress mediator norepinephrine and the β-adrenergic receptor agonist isoproterenol rapidly stimulate cyclic adenosine monophosphate response element-binding protein (CREB) phosphorylation at Ser133 in human PDAC cells. Exposure to the nonselective β-adrenergic receptor antagonist propranolol or selective antagonists, including nebivolol, atenolol, or ICI118551, blocked CREB phosphorylation elicited by norepinephrine or isoproterenol in PDAC cells. Stimulation of PDAC cells with neurotensin, a neuropeptide implicated in obesity and PDAC, also stimulated CREB phosphorylation at Ser133. Mechanistically, norepinephrine induced CREB phosphorylation at Ser133 via PKA, whereas neurotensin promoted CREB phosphorylation predominantly through protein kinase D. Our results indicate that CREB is a point of signal convergence that mediates proliferation in PDAC cells and raised the possibility that stress and diet cooperate in promoting PDAC in vivo. To test this notion, mice expressing KrasG12D in all pancreatic lineages (KC mice) and fed an obesogenic high fat, calorie diet that promotes early PDAC development were subjected to social isolation stress. We show that social isolation stress induced a significant increase in the proportion of advanced PDAC precursor lesions (pancreatic intraepithelial neoplasia) in KC mice subjected to an obesogenic high fat, calorie diet.

Implications:
Our data imply that chronic (social isolation) stress cooperates with diet-induced obesity in accelerating the development of pancreatic cancer.

Sun, Xiaoying; Teper, Yaroslav; Sinnett-Smith, James; Markarian, Mineh; Hines, O. Joe; Li, Gang; Eibl, Guido; Rozengurt, Enrique (2025)
Stress and Obesity Signaling Converge on CREB Phosphorylation to Promote Pancreatic Cancer
Molecular Cancer Research 23(3) 236-249; DOI: 10.1158/1541-7786.MCR-24-0785.

© 2024 American Association for Cancer Research.
Reprinted under the terms of s60 of the Copyright, Designs and Patents Act 1988.

It doesn't take a genius to understand that an intelligent designer should have, and in the case of creationism's putative designer god, could have, anticipated the future needs of the body it was designing and ensured it was robust and resilient enough to withstand what was in store for it as society progresses. The alternative is, of course, that it knew exactly what the human body's future needs would be but chose to withhold its ability to cope with it for some unfathomable but malevolent intent.

Of course, this ability is not available to a natural process operating without a plan and with no foresight, and no mechanism for selecting for fitness in a future environment, so creationists have a clear choice here between an incompetent and/or malevolent god and a natural process being the reason our bodies are so poorly designed to cope with a modern lifestyle.

My book, The Body of Evidence: How the Human Body Refutes Intelligent Design contains very many more examples of how the human body is poorly designed, compared to what an intelligent, omnibenevolent designer would have produced, had it been intelligently designed.

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