eSource and the Paperless Clinical Trial


Target e*CTR® (eClinical Trial Record) is revolutionizing the way clinical research is being conducted at Target Health Inc. for both our big pharma, mid-size pharma and biotech clients. We are saving clients around $8,000-$10,000/site/year and have reduced the need for filing cabinets at the clinical sites, client headquarters and at our offices in NY. Target e*CTR® can also be integrated with any EDC software with no change in the behaviors of current and future users.


Beyond the cost savings, benefits include:


1. Improved site/sponsor relationships
2. Efficiency improvements at the clinical sites can see more study subjects in a day since there is virtually no need to transcribe data
3. Ability to make faster, mid-course corrections
4. Improved data quality (w/associated cost savings)
5. Focusing on things that matter means more effective allocation of resources


For more information about Target Health contact Warren Pearlson ( 212-681-2100  ext. 104). For additional information about software tools for paperless clinical trials, please also feel free to contact Dr. Jules T. Mitchel or Ms. Joyce Hays. The Target Health software tools are designed to partner with both CROs and Sponsors. Please visit the Target Health Website

“Cancer Can Teach Us About Our Own Evolution“ – Paul Davies PhD


Cancer cells come pre-programmed to execute a well-defined cascade of changes.


By asking ourselves why cancer might exist, we can get a glimpse of life in a bygone biological age


Medical science treats cancer as a 1) ___ in which rogue cells proliferate uncontrollably, running amok around the body. Therapy focuses on killing the cancer before it kills the host. Unfortunately, the emphasis on cancer cells as defective loose cannons is at odds with the stubborn way they outwit both the body’s defenses and current treatments. Cancer is such a ruthless adversary because it behaves as if it has its own fiendishly cunning agenda. Cancer cells come pre-programmed to execute a well-defined cascade of changes, seemingly designed to facilitate both their enhanced survival and their dissemination through the 2) ___. There is even an air of conspiracy in the way that tumors use chemical signals to create cancer-friendly niches in remote organs.


In the frantic search for an elusive “cure“, few researchers stand back and ask a very basic question: why does cancer exist? What is its place in the grand story of life? Astonishingly, in spite of decades of research, there is no agreed theory of cancer, no explanation for why, inside almost all healthy 3) ___, there lurks a highly efficient cancer subroutine that can be activated by a variety of agents – radiation, chemicals, inflammation and infection. Cancer, it seems, is embedded in the basic machinery of life, a type of default state that can be triggered by some kind of insult. That suggests it is not a modern aberration but has deep evolutionary roots, a suspicion confirmed by the fact that it is not confined to 4) ___ but is widespread among mammals, fish, reptiles and even plants. Scientists have identified genes implicated in cancer that are thought to be hundreds of millions of years old. Clearly, we will fully understand cancer only in the context of biological history.


Two relevant evolutionary transitions stand out. The first occurred over 2 billion years ago, when large, complex cells emerged containing mitochondria – tiny factories that supply energy to the cell. Biologists think mitochondria are the remnants of ancient 5) ___. Tellingly, mitochondria undergo systematic changes as cancer develops, profoundly altering their chemical and physical properties.


For most of Earth’s history, life was confined to single-celled organisms. Over time, however, a new possibility arose. Earth’s atmosphere became polluted by a highly toxic and reactive chemical – oxygen – created as a waste product of photosynthesis. Cells evolved ingenious strategies to either avoid the accumulating 6) ___ or to combat oxidative damage. But some organisms turned a vice into a virtue and found a way to exploit oxygen as a potent new source of energy. In modern organisms, it is mitochondria that harness this dangerous substance to power the cell.


With the appearance of energized oxygen-guzzling cells, the way lay open for the second major transition relevant to cancer – the emergence of multi-cellular organisms. This required a drastic change in the basic logic of life. Single cells have one imperative – to go on replicating. In that sense, they are immortal. But in multi-celled organisms, ordinary cells have outsourced their immortality to specialized germ cells – sperm and eggs – whose job is to carry genes into future generations. The price that the ordinary cells pay for this contract is 7) ___; most replicate for a while, but all are programmed to commit suicide when their use-by date is up, a process known as apoptosis. And apoptosis is also managed by mitochondria.


Cancer involves a breakdown of the covenant between germ cells and the rest. Malignant cells disable apoptosis and make a bid for their own immortality, forming 8) ___ as they start to overpopulate. In this sense, cancer has long been recognized as a throwback to a “selfish cell“ era. But recent advances in research permit us to embellish this picture. For example, cancer cells thrive in low-oxygen (even zero-oxygen) conditions, reverting to an earlier, albeit less efficient, form of 9) ___ known as fermentation. Biologists are familiar with the fact that organisms may harbor ancient traits that reflect their ancestral past, such as the atavistic tails or supernumerary nipples some people are born with. Evolution necessarily builds on earlier genomes. Sometimes older genetic pathways are not discarded, just silenced. Atavisms result when something disrupts the silencing mechanism.


Charles Lineweaver, of the Australian National University, and Dr. Paul Davies have proposed a theory of cancer based on its ancient evolutionary roots. They think that as cancer progresses in the 10) ___ it reverses, in a speeded-up manner, the arrow of evolutionary time. Increasing deregulation prompts cancer cells to revert to ever earlier genetic pathways that recapitulate successively earlier ancestral life styles. They predict that the various hallmarks of cancer progression will systematically correlate with the activation of progressively older ancestral genes. The most advanced and malignant cancers recreate aspects of life on Earth before a billion years ago.


Ancient genes remain functional only if they continue to fulfill a biological purpose. In early-stage embryo development, when the basic body plan is laid down (also in 11) ___-oxygen conditions, incidentally) ancestral genes help guide developmental processes before being switched off. Every human, for example, possesses tails and gills for a time in the womb. Significantly, scientists have recently identified examples of early-stage embryonic genes being reawakened in cancer. The deep links between evolutionary biology, developmental biology and cancer have huge implications for therapy, and also provide an unexpected reason to study 12) ___. By unraveling the details of cancer initiation and progression, scientists can open a window on the past through which we can gain tantalizing glimpses of life in a bygone age. Source: Paul Davies, The Guardian


ANSWERS: 1) disease; 2) bloodstream; 3) cells; 4) humans; 5) bacteria; 6) oxygen; 7) death; 8) tumors; 9) metabolism; 10) body; 11) low-oxygen; 12) cancer

Paul Davies PhD (1946 to present)


Paul Davies is a physicist, writer, professor, broadcaster, and founder/director of the Beyond Center for Fundamental Concepts in Science at Arizona State University. His latest book is The Goldilocks Enigma: Why Is the Universe Just Right for Life? His research interests are in the fields of cosmology, quantum field theory, and astrobiology. He has proposed that a one-way trip to Mars could be a viable option. In 2005, he took up the chair of the SETI: Post-Detection Science and Technology Task group of the International Academy of Astronautics. He is also an adviser to the Microbes Mind Forum.


Davies was brought up in Finchley, London, and attended Woodhouse Grammar School on Woodhouse Road. In 1970, he completed his PhD under the supervision of Michael J. Seaton and Sigurd Zienau at University College London. He then carried out postdoctoral research under Fred Hoyle at the University of Cambridge.


Davies’ inquiries have included theoretical physics, cosmology, and astrobiology and his research has been mainly in the area of quantum field theory in curved spacetime. His notable contributions are the so-called Fulling-Davies-Unruh effect, according to which an observer accelerating through empty space will perceive a bath of thermal radiation, and the Bunch-Davies vacuum state, often used as the basis for explaining the fluctuations in the cosmic background radiation left over from the big bang. A paper co-authored with Stephen Fulling and William Unruh was the first to suggest that black holes evaporating via the Hawking effect lose mass as a result of a flux of negative energy streaming into the hole from the surrounding space.


Davies has had a longstanding association with the problem of time’s arrow, and was also an early proponent of the theory that life on Earth may have come from Mars cocooned in rocks ejected by asteroid and comet impacts. During his time in Australia he helped establish the Australian Centre for Astrobiology. Davies was a co-author of Felisa Wolfe-Simon on the Science article “A Bacterium That Can Grow by Using Arsenic Instead of Phosphorus.“


Davies is now Principal Investigator at Arizona State University’s Center for Convergence of Physical Science and Cancer Biology. This is part of a program set up by the National Institutes of Health’s National Cancer Institute to involve physicists in cancer research which has set up a network of 12 Physical Sciences-Oncology Centers.


Davies’ talent as a communicator of science has been recognized in Australia by an Advance Australia Award and two Eureka Prizes, and in the UK by the 2001 Kelvin Medal and Prize by the Institute of Physics, and the 2002 Faraday Prize by The Royal Society. Davies received the Templeton Prize in 1995.


Davies wrote an article in the Wall Street Journal where he stated that he supported the ?arsenic can replace phosphorus’ idea of Felisa Wolfe-Simon because “I had the advantage of being unencumbered by knowledge. I dropped chemistry at the age of 16, and all I knew about arsenic came from Agatha Christie novels.“ He also made the statement, “Well, I would be astonished if this was the only arsenic-based organism on Earth and Felisa just happened to scrape it up from the bottom of Mono Lake on the first try, It’s quite clear that it is the tip of an iceberg. I think it’s a window into a whole new world of microbiology.“ In the same vein, in an article in The Guardian, Davies suggests that the origin of life will be uncovered through information theory rather than chemistry. Concerns have been raised about his responsibility as one of Wolfe-Simon’s co-authors.


The basis of a new theory of cancer is developed by Paul Davies and Charles Lineweaver in the following paper published in the journal of Physical Biology:




The genes of cellular cooperation that evolved with multicellularity about a billion years ago are the same genes that malfunction to cause cancer. We hypothesize that cancer is an atavistic condition that occurs when genetic or epigenetic malfunction unlocks an ancient ?toolkit’ of pre-existing adaptations, re-establishing the dominance of an earlier layer of genes that controlled loose-knit colonies of only partially differentiated cells, similar to tumors. The existence of such a toolkit implies that the progress of the neoplasm in the host organism differs distinctively from normal Darwinian evolution. Comparative genomics and the phylogeny of basal metazoans, opisthokonta and basal multicellular eukaryotes should help identify the relevant genes and yield the order in which they evolved. This order will be a rough guide to the reverse order in which cancer develops, as mutations disrupt the genes of cellular cooperation. Our proposal is consistent with current understanding of cancer and explains the paradoxical rapidity with which cancer acquires a suite of mutually-supportive complex abilities. Finally we make several predictions and suggest ways to test this model.


To read more, click on this link for the entire paper:


From the (UK) Telegraph, By Paul Davies


When President Nixon declared war on cancer 40 years ago, he also sanctioned one of the biggest research programs in history. The budget of America’s National Cancer Institute (NCI) is now $5 billion a year, more than NASA spends on space exploration. Cancer accounts for a large slice of research funds in most other developed countries, too: Cancer Research UK, for example, has a budget of 500 million British pounds a year. But despite this vast investment, the long-awaited “breakthrough“ remains elusive. Although certain drugs (often very expensive) can prolong life, the brutal truth is that most patients diagnosed with metastatic cancer today fare little better than their counterparts did decades ago. And as life expectancy rises, more people will die of cancer. Given the escalating costs of treatment, the economic impact is unsustainable.


I became embroiled in this depressing story four years ago when I was called out of the blue by the deputy director of the NCI, Anna Barker. Dr Barker talked about the glacial pace of clinical progress and her frustration that, even with some of the world’s finest minds involved, no light could be discerned at the end of the tunnel. Her question to me was: “Can physicists help?“


I explained that my career was focused on quantum mechanics, cosmology, black holes. “I know nothing about cancer,“ I said. “It doesn’t matter!“ was her response. Physicists, she pointed out, think about the world in a distinctive way. They have elucidated the secrets of the atom and probed the farthest reaches of the cosmos, and have a good track record at cracking tough, complex problems. It was not so much new technology that she was after, but insights from our problem-solving approach.


Two years later, in a bold attempt to exploit this untapped expertise, the NCI created 12 centers of physical science and oncology, and I found myself directing the one at Arizona State University. So, how are we getting on?


Well, one of the virtues of being unencumbered by much knowledge of a subject is the ability to come at it afresh, to see it through different eyes. The basic story of cancer is very simple. Somewhere in the body, cells start to proliferate uncontrollably. If unchecked, they spread to other organs and colonize them. At that stage, the patient’s prospects are grim. Yet nobody has a convincing explanation for why this happens. The individual steps can be partially explained in terms of changes in the cells. But precisely why a cell from, say, a breast duct or the prostate gland starts roaming the body to make a home in the liver or the lung – a process called metastasis – remains a mystery.


Most research has focused on cancer as a human disease. But tumors are also widespread among animals and plants, suggesting that they have deep evolutionary roots. Cancer is such a formidable adversary because it is a fundamental part of the story of life itself, and I believe it can be properly understood only by seeing the grand evolutionary picture. The earliest traces of life on Earth date back 3.5 billion years, but only about a billion years ago did complex, multi-celled organisms begin to evolve. This was a profound transition. Single cells have but one imperative – to replicate. They are, in effect, immortal. But when cells first formed co-operative assemblages, a new deal was struck. Most organisms outsourced their immortality to specialized germ cells (e.g. sperm and ova), and in return accepted death for themselves. Thus a typical tissue cell might reproduce a handful of times and then die.


Organisms police this contract with a variety of regulatory systems, including specialized genes that suppress runaway growth. I believe that cancer is a breakdown in this contract, initiated when a common-or-garden cell refuses to die on cue and embarks on its own agenda. It would be a mistake, however, to suppose that cancer merely represents a cell that has “gone wrong“, and started running amok in the body. In fact, cancers possess a surprising degree of organization. As they become more malignant, they deploy sophisticated tricks designed to evade the body’s defenses and enhance their own prospects. This pre-programmed box of tricks is what makes combating them such a challenge.


Together with Charles Lineweaver at the Australian National University, I have been developing a theory of cancer based on the concept that it is an evolutionary throwback to our earliest ancestors. About 600 million years ago, there appeared a riot of modern-looking metazoa (the multi-celled creatures that make up the bulk of the animal kingdom), with many specialized cell types and organs. But this explosion didn’t happen in a vacuum. Hundreds of millions of years before, they – we – had precursors: clumps of semi-organized cells forming robust, tumor-like forms. Our bodies are replete with ancestral genes that evolution has built on. These genes are retained because they are active in the early stages of embryo development, when the basic body plan is being laid down. Curiously, human embryos temporarily develop gills and tails, representing long-lost features of our evolutionary history. Normally these ancient genes are silenced thereafter. But Lineweaver and I have proposed that cancer results from an accidental reawakening of the earliest metazoan genes, the ones programmed to build the sort of structures that inhabited Earth millions of years ago. Rather like a computer starting up in safe mode after an error of some sort, cancer may be a reversion to a tried-and-tested ancestral lifestyle in response to a physical stress such as a carcinogen. By connecting the dots of evolutionary, developmental and cancer biology, we have come to view cancer not so much as a disease to be cured as a condition to be controlled. Like ageing, cancer must be accepted as part of life. But by careful management, its effects can be mitigated. For example, 90 per cent of cancer deaths result from metastasis. Slowing or arresting this spread would make a big difference.


Even when cancer cells make a home in a remote organ, the micro-tumors often fail to progress, or may lie dormant. Many people who appear to have survived unscathed eventually succumb when the cancer returns years or even decades later, with enhanced malignancy. If we can understand how these micro-tumors remain in equilibrium with their environment, we could work to extend that quiescent phase. After all, a cancer that reappears after 50 years instead of five is not too serious a health risk. The great advantage here is that such improvements could come without requiring us to unravel fully the stupendously complex innards of cancer cells, with their myriad genetic and chemical pathways and survival mechanisms. If Lineweaver and I are right, and a special cassette of ancient genes drives the basic behavior of cancer, then we will have a well-defined target for therapy. The challenge is to find a way to seize control of the cassette’s operating system and tweak it to do our bidding, by reducing the cancer cells’ wanderlust or keeping the micro-tumors stable.


Cancer touches all of us. Public health programmers, such as the campaign against smoking, have had a big impact. And a handful of cancers are, in effect, curable. But headway against this scourge has stalled, and requires some radical new thinking, including concepts that cross subject boundaries and emphasize control over cure. The NCI’s bold initiative of inviting perspectives from physical science needs to become an integral part of the next phase of cancer research.


Paul Davies is founder/director of the Beyond Center for Fundamental Concepts in Science at Arizona State University. For more details, see


Paul Davies address: Breast Cancer Deadline 2020


Paul Davies: New Scientist, “Cancer from a physicist’s perspective: a new theory of cancer“

Renal Artery Stents Lead To Similar Outcome vs. Medication-Only


The narrowing and hardening of one or both renal arteries, known as renal artery stenosis, occurs in 1 to 5% of people who have high blood pressure, or hypertension. An estimated 78 million Americans have hypertension, according to the AHA, and as many as 3.9 million people in the United States may have renal artery stenosis. Renal artery stenosis can lead to conditions such as chronic kidney disease and can appear alongside conditions including coronary artery disease. Effective treatment of renal artery stenosis can improve blood pressure control, stabilize kidney function, and reduce incidence of serious cardiovascular events.


According to the study’s authors, between 1996 and 2000, there was a 364% jump in renal artery stenting procedures for Medicare beneficiaries. The procedure involves inserting a metal mesh tube into an artery to open the clogged passageway. Now, according to findings that were presented last week at the American Heart Association (AHA) 2013 Scientific Sessions in Dallas, a commonly used stenting procedure to treat plaque build-up in the renal artery appears to offer no significant improvement when added to medication-based therapy.


The Cardiovascular Outcomes in Renal Atherosclerotic Lesions study, known as CORAL, studied 947 patients whose plaque build-up in the renal artery narrowed the blood vessel by 60% or more. Participants, whose average age was 69 years, had renal artery stenosis and either systolic blood pressure of 150 mmHg or higher while taking two or more drugs or Stage 3 (moderate) chronic kidney disease. Researchers from more than 100 institutions randomly assigned participants to receive medical therapy only or medical therapy plus a stent. The research team examined the effect of the two treatment options on a combination of cardiovascular and renal outcomes that included death from renal or cardiovascular causes; heart attack; hospitalization for congestive heart failure; progressive renal insufficiency; or renal replacement therapy, which includes the need for dialysis or renal transplantation. Results showed that during an average follow-up period of 43 months, 35.1% of patients who received medical therapy and stents experienced one of the negative endpoints versus 35.8% of patients who received medication alone.

Chelation Therapy Reduces Cardiovascular Events for Older Patients with Diabetes

Chelation is a chemical process in which a substance is delivered intravenously to bind atoms of metals or minerals, and hold them tightly so that they can be removed from the body. Chelation is conventionally used as a treatment for heavy metal poisoning, although some people use chelation as an unapproved and unproven treatment for conditions like heart disease. Chelation therapy is not approved by the FDA to treat heart disease. However, use of chelation therapy to treat heart disease and other health problems grew in the United States between 2002 and 2007 by nearly 68% to 111,000 people, according to the 2008 National Health Statistics Report.


From 2003 to 2010, 1,708 adults aged 50 and older were enrolled in TACT, of whom 633 had diabetes. Study participants had suffered a heart attack 6 weeks or more before enrollment (on average, the heart attack occurred about 4.5 years earlier). The participants were assigned randomly to receive 40 infusions of disodium EDTA chelation solution or a placebo solution. Patients also were randomly assigned to receive high doses of oral vitamins and minerals or an identical oral placebo. Most participants also took standard medicines for heart attack survivors, such as aspirin, beta blockers, and statins. They were followed for a minimum of 1 year and up to 5 years, with followup ending in October 2011.


TACT was not designed to discover how or why chelation might benefit patients with diabetes


According to analyses of data from the National Institutes of Health-funded Trial to Assess Chelation Therapy (TACT), chelation treatments reduced cardiovascular events, such as heart attacks, and death in patients with diabetes but not in those who did not have diabetes. However, researchers say more studies are needed before it’s known whether this promising finding leads to a treatment option. The diabetes subgroup analysis of TACT was presented at the American Heart Association’s Scientific Sessions 2013. TACT is a study supported by NIH’s National Center for Complementary and Alternative Medicine (NCCAM) and National Heart, Lung, and Blood Institute (NHLBI).


TACT’s initial report was published in the March 27, 2013, issue of The Journal of the American Medical Association. This previous report showed that infusions of a form of chelation therapy using disodium ethylene diamine tetra-acetic acid (EDTA) produced a modest but statistically significant reduction in cardiovascular events in all EDTA-treated participants. However, further examination of the data showed that patients with diabetes were significantly impacted by chelation therapy while patients without diabetes were not. The patients with diabetes, which made up approximately one third of 1,708 participants, demonstrated a 41% overall reduction in the risk of any cardiovascular event; a 40% reduction in the risk of death from heart disease nonfatal stroke, or nonfatal heart attack; a 52% reduction in recurrent heart attacks; and a 43% reduction in death from any cause. In contrast, there was no significant benefit of EDTA treatment in the subgroup of 1,045 participants who did not have diabetes.


According to the authors, although subgroup analyses of clinical trials do not provide definitive answers, they are very useful in identifying future research questions, and this analysis suggests strongly that more research is needed to examine possible benefits of chelation in diabetics and the potential mechanisms.

TARGET HEALTH excels in Regulatory Affairs. Each week we highlight new information in this challenging area.

FDA Allows Marketing of Four “Next Generation“ Gene Sequencing Devices

The FDA has allowed marketing of four diagnostic devices that can be used for high throughput gene sequencing, often referred to as “next generation sequencing“ (NGS). These instruments, reagents, and test systems allow labs to sequence a patient’s DNA (deoxyribonucleic acid). The new technology also gives physicians the ability to take a broader look at their patients’ genetic makeup and can help in diagnosing disease or identifying the cause of symptoms.


“NGS is changing the way we look at genomics,“ said Alberto Gutierrez, Ph.D., director of the Office of In Vitro Diagnostics and Radiological Health in FDA’s Center for Devices and Radiological Health. “Before NGS, sequencing genes associated with a particular disease was a long and costly process. Today, we have the capability to read and interpret large segments of DNA very quickly in a single test and this information-rich technology is becoming more accessible for use by physicians in the care of their patients.“


Two of the newly cleared devices are used to detect DNA changes in the cystic fibrosis transmembrane conductance regulator (CFTR) gene, which can result in cystic fibrosis (CF), an inherited chronic disease that affects the lungs, pancreas, liver, intestines, and other organs of those who inherit a faulty CFTR gene from both parents. More than 10 million Americans are CF carriers and approximately 30,000 children and adults in the U.S. are affected with CF. Most children with CF are diagnosed by age 2 and the average life span for people with CF who live to adulthood is approximately 37 years.


The cleared devices include:


1. The Illumina MiSeqDx Cystic Fibrosis 139-Variant Assay, which checks specific points in the patient’s CFTR gene sequence to detect known variants in the gene. Information about which DNA changes are associated with symptoms of cystic fibrosis is found in the Clinical and Functional TRanslation of CFTR database (CFTR2).


2. The Illumina MiSeqDx Cystic Fibrosis Clinical Sequencing Assay, which sequences a large portion of the CFTR gene to detect any difference in the CFTR gene compared to a reference CFTR gene.


Data submitted by Illumina for their cystic fibrosis tests included comparisons of the sequence results to Human Genome Build 19, a reference representation of the human genome. In addition, Illumina evaluated the performance of its instrument and reagent systems against a publically available quality-weighted human reference genome that was created through collaboration between the FDA and the National Institutes of Standards and Technology (NIST).


The FDA also granted de novo petitions for the Illumina MiSeqDx instrument platform and the Illumina Universal Kit reagents, two devices that make up the first FDA-regulated test system that allows laboratories to develop and validate sequencing of any part of a patient’s genome. The Universal Kit reagents isolate and create copies of genes of interest obtained from patient blood samples, and the MiSeqDx platform analyzes the genes. The software compares the patient’s genomic sequence to a reference sequence and reports back any differences between the patient and the reference.


The FDA reviewed the Illumina MiSeqDx instrument platform and the Illumina Universal Kit reagents through its de novo classification process, a regulatory pathway for some novel low-to-moderate risk medical devices that are not substantially equivalent to an already legally marketed device. For the de novo petitions, the FDA based its decision on the demonstrated performance of the MiSeqDx instrument and Universal Kit reagent systems across numerous genomic segments spanning 19 human chromosomes.


Illumina MiSeqDx instrument platform, Universal Kit reagents, MiSeqDx Cystic Fibrosis 139-Variant Assay, and MiSeqDx Cystic Fibrosis Clinical Sequencing Assay are manufactured by Illumina, Inc. in San Diego, Calif.

Pumpkin Cake for Thanksgiving Desert


Warm pumpkin cake, with a dollop of fat-free cool whip, and thin slices of fresh sweet ripe persimmon. Photo, ©Joyce Hays, Target Health Inc.


1 box yellow cake mix (18 oz)
1 box instant butterscotch pudding (3.4 oz)
1/4 cup canola oil
1/4 cup water
1 cup canned pumpkin
2 teaspoons pumpkin pie spice
4 eggs
1 cup (salt-free) walnuts, chopped coarsely
1 cup (salt-free) walnuts, chopped very fine (for inside pan & sprinkles)
3 Tablespoons brown sugar substitute
1 container fat-free cool whip (topping)


Cake batter, before adding coarsely chopped walnuts — Photo: ©Joyce Hays, Target Health Inc.




In a large mixing bowl, combine the first seven ingredients. Beat on low speed for 30 seconds. Then beat on medium speed for 4 minutes.

When beating is done, add the coarsely chopped walnuts and stir them into the mixture.

Pour into a (canola oil) greased cake pan that you add the very finely chopped walnuts to. Shake the pan so that the walnuts begin to stick to and cover the pan, all over. Bake at 350’F for 50-55 minutes. Test with a tooth pick. Insert near center. When it comes out clean, cake is done.

Before you take the cake out of the oven, in a small bowl add the brown sugar substitute with the finely chopped walnuts and mix together. Now, sprinkle this mixture, slowly, over the top of the cake. Return to oven to brown slightly, for 5 to 8 minutes. Check oven to be sure nothing burns, and remove when done.

Cool cake in pan for 15 minutes. Then move to wire rack to cool completely.


Tame your craving, to top servings with vanilla ice cream and use fat-free cool whip as a topping instead, along with thinly sliced ripe persimmon, in season now.


Just out of oven, after sprinkling walnuts & brown sugar substitute,

on top of pumpkin cake to caramelize a bit. Photo: ©Joyce Hays, Target Health Inc.

Here is a Thanksgiving dessert that tastes best served warm. IMO, the no-fat cool whip and thin slices of ripe Persimmon, enhance the flavor of the warm pumpkin cake. Although a slice of this cake is about 275-300 calories, it’s less than pecan pie or pumpkin pie. The pumpkin flavor of this warm cake is full and luscious. A sweet dessert wine would go well, like the Italian dessert wine, Vin Santo.  My own preference for dessert wine, is that the wine be sweeter than the dessert. 

This cake is not too sweet, so could even be served the next morning with coffee, and would be wonderful for brunch, breakfast, and afternoon tea.


A glass of Vin Santo with its characteristic amber color.


Although the style of making wine from dried grapes has been around almost as long as wine has been made, there are many theories on how the particular name Vin Santo or “holy wine“ came to be associated with this style of wine in Italy. The most likely origin was the wine’s historic use in religious Mass, where sweet wine was often preferred.

One of the earliest references to a “vinsanto“ wine come from the Renaissance era sales logs of Florentine wine merchants who widely marketed the strong, sweet wine in Rome and elsewhere. Eventually the term “vinsanto“ became almost an umbrella name for this style of wine produced elsewhere in Italy. When the Greek island of Santorini came under rule of the Ottoman Empire, the ruling Turks encouraged the island’s wine production of a sweet dessert wine made from dried grapes. Over the next few centuries, this wine became known as Vin Santo and was widely exported to Russia where it became a principal wine in the celebration of Mass for the Russian Orthodox Church.

Other, likely apocryphal, stories on the name’s origin attributes its naming to the work of a 14th-century friar from the province of Siena who would use the leftover wine from Mass to cure the sick. The miraculous healing became associated with the santo or “holy“ wine and the name Vin Santo was allegedly born.  Another 14th century story involving John Bessarion, a patriarch of the Greek Eastern Orthodox Church. According to legend at the Ecumenical Council of Florence of 1349 a local Florentine wine called Vin Pretto (pure wine) was served. After trying the wine, Bessarion is said to have liked the wine and remarked that it was like Xanthos, alluding to the famous straw wine of Thrace, (though some sources said he described the wine as Xantho or “yellow“). The Florentine locals thought they heard the patriarch describe the wine as Santo and they accordingly started promoting the wine as a “holy wine“. Another theory for the name association often touted is the tradition of starting fermentation around All Saint’s Day and bottling the wine during Easter week.

Here in New York, we are definitely thankful for all that we have and all that we’re able to do.  We wish everyone a happy Thanksgiving weekend!  And, of course, Bon Appetit!