CenterWatch Interview – Risk-based Monitoring and eSource


On 28 October 2013, Dr. Jules T. Mitchel was interviewed by CenterWatch Weekly where they asked the following 5 questions. Take a look at the article for the responses.



1. How has your CRO grown and evolved to specialize in eClinical trials in the metropolitan New York City area?

2. A major focus for Target Health is the development of the “Paperless Clinical Trial,“ and under your leadership there have been significant efforts to seamlessly combine direct data entry (DDE) into an eClinical trial record. Explain the major advantages plus the barriers to DDE adoption by sponsors.

3. Going the next step of combining DDE into an eCinical trial record would include electronic medical records and the technology solutions EDC provides. Have there been U.S. and European regulatory issues over this truly paperless process, and how have sites reacted to it?

4. Target Health and LifeOnKey, a developer of electronic health records, received a $900,000, two-year award from the BIRD Foundation to integrate EMR with EDC systems in clinical trials in which investigators will maintain original source records and sponsors will not have exclusive control of source data. Explain this strategy.

5. At a recent Global Clinical Trials conference, you spoke out about the challenges and the need to use technology better for risk-based monitoring. What can we expect from CROs in terms of lowering the research burden or cost?



New York at Night – View From Target Health (24th Floor) ©Target Health Inc, 2013


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.

Adrenoleukodystrophy (how much do you know about orphan diseases?)


White matter, with reduced volume and increased signal intensity. The anterior white matter is spared. Features are consistent with X-linked adrenoleukodystrophy


Adrenoleukodystrophy (ALD), also known as X-linked adrenoleukodystrophy, ALD, X-ALD, adrenomyeloneuropathy, AMN, Siemerling-Creutzfeldt disease or bronze Schilder disease, is a rare genetic (inherited) disorder characterized by the breakdown or loss of the myelin sheath surrounding nerve cells in the brain and progressive dysfunction of the adrenal gland. ALD is the most common peroxisomal inborn error of metabolism, with an incidence estimated between 1:20,000 and 1:50,000. It does not have a significantly higher incidence in any specific ethnic groups. ALD is one of a group of genetic disorders called the leukodystrophies that cause damage to the myelin sheath of the nerve fibers in the brain. The myelin sheath is a fatty covering which acts as an electrical insulator.


There are several forms of ALD:


The classic childhood form, which is the most severe and affects only boys, may occur between ages 4 and 10. It affects only boys because the 1) ___ is on the X chromosome. Features of this form may include visual loss, learning disabilities, seizures, dysarthria (poorly articulated speech), dysphagia (difficulty swallowing), deafness, disturbances of gait and coordination, fatigue, intermittent vomiting, melanoderma (increased skin pigmentation), and progressive dementia. The most common symptoms are usually behavioral changes such as abnormal withdrawal or aggression, poor memory, and poor school performance.


Women carriers: Another form of ALD is occasionally seen in women who are carriers of the disorder. Symptoms are mild and may include spastic paraparesis of the lower limbs, ataxia, hypertonia (excessive muscle tone), mild peripheral neuropathy, and urinary problems.


The milder adult-onset form typically begins between ages 21 and 35. Symptoms may include leg stiffness, progressive spastic paraparesis (stiffness, weakness and/or paralysis) of the lower extremities, and ataxia. Although adult-onset ALD progresses more slowly than the classic childhood form, it can also result in deterioration of 2) ___ function.


Neonatal (newborn) ALD affects both male and female babies. Symptoms may include mental retardation, facial abnormalities, seizures, retinal degeneration, hypotonia (low muscle tone), hepatomegaly (enlarged liver), and adrenal dysfunction. This form is usually quickly progressive. The treatment for all forms of ALD is symptomatic and supportive. Physical therapy, psychological support, and special education may be useful for some individuals. The prognosis for patients with ALD is generally poor due to progressive neurological deterioration. Death usually occurs within 1 to 10 years after the onset of 3) ___.


Myelin is the insulating sheath surrounding nerve cells. It is the white matter coating our nerves, enabling them to conduct impulses between the brain and other parts of the 4) ___. It consists of a layer of proteins packed between two layers of lipids. Myelin can be destroyed by hereditary neuro-degenerative illnesses such as ALD, and also by acquired diseases such as multiple sclerosis. There is no known cure for demyelinating illnesses.



Lorenzo’s Oil is a combination of a 4:1 mix of erucic acid and oleic acid, extracted from rapeseed oil (canola) and olive oil designed to normalize the accumulation of the very long chain fatty acids in the brain thereby halting the progression of adrenoleukodystrophy (ALD). In the United States, Lorenzo’s oil is currently only available to patients taking part in a clinical trial as it has not yet been approved by the U.S. Food and Drug Administration (FDA) for marketing.


In ALD pre-symptomatic boys, Lorenzo’s Oil has been reported to often (but not always) prevent the onset of the disease by stopping the body from producing the very long chain fatty acids, whose buildup leads to demyelination. It is specific to ALD, does not repair 5) ___, and does not have any known effect on other demyelinating disorders.




At least 70% of patients with childhood cerebral ALD (CCALD) and adrenomyeloneuropathy (AMN) have clinical and biochemical evidence of primary adrenocortical insufficiency. Primary adrenocortical insufficiency may also be the only clinical manifestation of 6) ___. Recently, screening of at-risk family members showed there was a high prevalence of unrecognized adrenocortical insufficiency in asymptomatic boys with X-ALD (age: 4.5+3.5 years). At baseline, 81% had impaired adrenal function. Serum ACTH was elevated in 69% patients and the ACTH stimulation test was abnormal in 43% of patients. By the end of the follow-up (2+1.7 years), 86% patients had borderline or clear adrenal insufficiency (age of onset: 4.8+3.7 years). A key finding was that 70% of the patients studied by 2 years of age already showed increased serum ACTH levels. This is a very important finding, as unrecognized 7) ___ insufficiency frequently can result in morbidity and even mortality. Careful monitoring, early identification of impaired adrenal reserve, and timely initiation of therapy can prevent this.


Plasma ACTH is the most sensitive laboratory marker for adrenocortical dysfunction in children, adolescents and adults and serial measurement i.e. every 6 months is recommended to identify the patients with (sub clinical) adrenal involvement.


Adrenal hormone therapy is mandatory to all X-ALD patients who have adrenal insufficiency, and it may be lifesaving.


Although it is generally thought not to alter neurological progression two recent reports documented moderate improvement in evoked responses and motor function in patients with adrenomyeloneuropathy. Unlike the affected men clinical overt adrenocortical insufficiency is exceptionally rare in female carriers. Studies in a large group of carriers demonstrated that adrenocortical insufficiency is present in about 1% of females with X-ALD.

VLCFA and adrenocortical cells



There are several reasons for the impaired steroid synthesis in patients with X-ALD. Very long chain fatty acids (VLCFAs) accumulate in the adrenocortical cells and have a direct toxic effect on intracellular membranes and enzymes. Characteristic lamellar lipid inclusions ultimately leading to cell death can be seen (see picture). Accumulation of VLCFAs in the outer cell membranes of the adrenocortical cells hinder the capacity of the adrenocortical 8) ___ to respond to ACTH.


ALD is caused by mutations in ABCD1, a peroxisomal membrane transporter protein, located on the X chromosome. The exact mechanism of the pathogenesis of the various forms of ALD is not known. Biochemically, individuals with ALD show very high levels of unbranched, saturated, very long chain fatty acids, particularly cerotic acid (26:0). The level of cerotic acid in plasma does not correlate with clinical presentation. Treatment options for ALD are limited. Dietary treatment is with Lorenzo’s 9) ____. For the childhood cerebral form, stem cell transplant and gene therapy are options if the disease is detected early in the clinical course. Adrenal insufficiency in ALD patients can be successfully treated.


Because the characteristic elevations associated with ALD are present at birth, well before any symptoms are apparent, there have been methods developed in the interests of including it in 10) ___ screening programs. One of the difficulties with ALD as a disease included in universal newborn screening is the difficulty in predicting the eventual phenotype that an individual will express. The accepted treatment for affected boys presenting with the cerebral childhood form of the disease is a bone marrow transplant, a procedure which carries significant risks. However, because most affected males will demonstrate adrenal insufficiency, early discovery and treatment of this symptom could potentially prevent complications and allow these patients to be monitored for other treatment in the future, depending on the progression of their disease. Because 30-60% of X-ALD patients develop adrenal insufficiency before the onset of neurological symptoms, a young man or boy with primary 11) ___ insufficiency should always be tested for ALD.


ANSWERS: 1) gene; 2) brain; 3) symptoms; 4) body; 5) myelin; 6) X-ALD; 7) adrenocortical; 8) cells; 9)) oil; 10) newborn; 11) adrenal

Augusto Odone, the Father Who Fought for Lorenzo’s Oil (1933-2013)



Augusto Odone with Lorenzo, his son who died in 2008Photo: via Myelin Project


Augusto Daniel Odone was born in Rome on March 6, 1933, to Angelo and Maria Odone. His father was a general in the Italian Army, and his mother was a novelist. He grew up in Gamalero, in northwest Italy, received a law degree from the University of Rome and studied at the University of Kansas on a Fulbright scholarship. He worked for a bank that specialized in reconstruction and development in southern Italy before joining the World Bank in 1969. Augusto Odone, with no medical training, flouted scientific protocol and doctors’ advice to help concoct an experimental medicine that extended the life of his terminally ill son and inspired a Hollywood film, “Lorenzo’s Oil,“ died on Friday, October 25th in Acqui Terme, in northern Italy. He was 80.



Mr. Odone (pronounced oh-DOH-nay), an analyst for the World Bank who specialized in East African economies, and his American-born wife, Michaela, a translator and linguist, became known internationally both for the ingenuity of the medicine they invented and for the bitter criticism they leveled at a medical establishment that they saw as hidebound and aloof. The hit 1992 film based on their story, which starred Nick Nolte and Susan Sarandon, in turn drew criticism from medical experts for portraying scientists as unfeeling, and for suggesting that Lorenzo’s Oil was a cure.


Lorenzo’s Oil did not cure Lorenzo Odone, the couple’s son, who died in 2008 at age 30 from a rare neurological disease known as adrenoleukodystrophy (ALD). But the movie, directed by George Miller, a former physician, produced a wave of financing for research that has confirmed the benefits of Lorenzo’s Oil in some cases, and has led to more promising treatments.


In the summer of 1983, Lorenzo, a precocious boy who spoke three languages, and loved opera, started kindergarten that fall. Yet rather than thriving, Lorenzo experienced numerous problems, having temper tantrums, slurring his words and even falling on two occasions. Doctors initially suspected a difficult adjustment to a new country and school. But Lorenzo grew progressively sicker. When a neurologist finally made the diagnosis, in April 1984, when Lorenzo was 6, the news was terrible: ALD, a genetic disorder of young boys in which the myelin that protects the nerves of the brain and spinal cord becomes progressively damaged. Lorenzo, doctors said, would gradually lose his ability to see, hear, eat and walk. Death would soon follow. Doctors predicted he would not survive childhood. After scouring medical journals and consulting scientists and doctors, he taught himself enough science that in 1987 he came up with a concoction derived from natural cooking oils. He turned to a British scientist to produce an edible version.


The family took Lorenzo to Baltimore to see the world’s top ALD specialist, Dr. Hugo Moser. Dr. Moser entered Lorenzo in a clinical trial of a special diet to try to lower the elevated level of very-long-chain fatty acids in the blood of affected boys. But it did not work. It was here that the Odones went from ordinary to extraordinary parents. Refusing to believe that there was nothing else to be done, they became fixtures at the nearby library of the National Institutes of Health in Bethesda, Md. Among the things the Odones discovered was that scientists across the globe who were working on ALD and other so-called demyelinating diseases had never actually attended a conference together. Not only did the Odones arrange this, in October 1984, but they began to study ALD themselves, asking probing questions of the scientists, generating hypotheses about the cause of the disease and beginning to develop possible therapies. When asked why he and Michaela did this, Mr. Odone, in typically modest fashion, said “We love this kid, and we don’t want to lose him.“ After scouring medical journals and consulting scientists and doctors, Odone taught himself enough science that in 1987 he came up with a concoction derived from natural cooking oils. He turned to a British scientist to produce an edible version.


There have been other examples of this type of activism. Also in the mid-’80s, people with AIDS were becoming experts regarding their disease, advocating – often angrily – for increased research funding, faster approval of drugs and entrance into experimental protocols. Still, many physicians, as well as the parents of boys with ALD, resented what the Odones were doing. Yet by 1986, the Odones had achieved the unthinkable. They had deduced that a mixture of two cooking oils, oleic acid (olive oil) and erucic acid (canola oil), competitively inhibited the enzymes that overproduced the very-long-chain fatty acids that destroyed the myelin. They had begun to feed the oil to Lorenzo through the stomach tube he used for eating. By this time, Lorenzo was blind, mute, largely deaf and wheelchair bound.


In 1990, the Australian film director George Miller, best known for the “Mad Max“ movies, contacted the Odones. He had heard their story and wanted to make a Hollywood film based on Lorenzo’s story. Released in 1992 and starring Nick Nolte as Augusto and Susan Sarandon as Michaela, “Lorenzo’s Oil“ was an unabashed paean to the love and determination that the Odones had shown their son. One reviewer said it was “an inspirational drama that is truly inspiring.“ In the book, When Illness Goes Public, author, Barron H. Lerner MD, discusses how many of the film’s scenes were inaccurate or misleading. For example, doctors had never tried to deny Lorenzo’s Oil to a segment of boys with ALD in order to conduct a randomized clinical trial. Nor had it been proven that the oil successfully treated the disease, as the film implied.


But these details were not the crucial aspects of Lorenzo’s story. What Dr. Lerner witnessed when he visited the Odones in 2005 was quite remarkable. Michaela had died of cancer in 2001, but Lorenzo was alive at age 26, defying the gloomy prognosis the Odones had received two decades before. He did not interact with Lerner and lay the entire time in a chair. However, Augusto interacted with him frequently and believed that his son could understand him and still appreciated classical music and books. The most indelible image was of Augusto leaning down next to his grown son, quietly speaking with him and kissing him. Lorenzo died in 2008 at age 30.


“Lorenzo never regained his faculties,“ said Cristina Odone, one of Mr. Odone’s two children from a previous marriage, in a phone interview. But she added: “If you had ever walked into the room and seen how Lorenzo responded to the way my father and Michaela embraced him in life, wrapped him in love, you would see he was a living being who knew he was loved. That’s what they gave him, but it was very difficult.“ By the late 1980s – distilling what they had learned, as they later recalled, through doggedness, serendipity and ignorance of their own limits – the Odones, with a few scientist allies, developed a chemical compound that seemed to slow Lorenzo’s disease. They called the medicine, an extract of acids in olive and rapeseed (canola) oils, Lorenzo’s Oil. It apparently worked by breaking down the long-chain fatty acids that are considered a major cause of damage to nerve cells in people with ALD.


The compound has been the subject of long-term studies, one still in progress. Another, completed in 2005, found that Lorenzo’s Oil helped children with ALD if used before they started showing symptoms, but that it was less effective once the degenerative process had begun. The Food and Drug Administration still considers the treatment experimental. The current scientific consensus is that while it may prolong the lives of boys like Lorenzo, it does not really reverse the effects of ALD. However, astoundingly, it does prevent the onset of the disease in susceptible boys in at least two-thirds of cases.


Before the doctors could do so, Augusto Odone had guessed right. Hundreds of boys are alive and well today as a result.


J. Michael Bishop, an American microbiologist who shared the 1989 Nobel Prize in Medicine, and others in medical research, were upset by a particular viewpoint in the film “Lorenzo’s Oil,“ – a viewpoint found to be encapsulated by one particular line spoken late in the film by Lorenzo’s father: “These scientists have their own agenda, and it is different from ours.“ And, yet, later, in The Bulletin of the American Academy of Arts and Sciences in 1995, Dr. Bishop cautioned fellow scientists against dismissing the public sentiment the film conveyed. “Here is a warning science cannot take lightly,“ he wrote, “a warning to explain ourselves more clearly, a warning even to change some of our ways.“


In the summer of 2010, two years after Lorenzo’s death, Augusto Odone sold his home in Virginia and moved to Acqui Terme in his native Italy, near his father’s village of Gamalero where he lived when he was young. He died there on October 25, 2013, at the age of 80, and was survived by the son and daughter from his first marriage, as well as a grandchild by his daughter, journalist Cristina Odone. Today, Odone’s work lives on through The Myelin Project, an organization that aims to accelerate research on myelin repair in neurological diseases. The project is funded through royalties earned on the patent for Lorenzo’s oil.


Sources: The New York Times, October 29 and 30, 2012: Paul Vitello, Barron H. Lerner, MD, professor of medicine and population health at the New York University School of Medicine, is the author of “When Illness Goes Public“ and the forthcoming “The Good Doctor“, as well as the Myelin Project.

Click on the two video links, below, to hear more


Candidate Vaccine Against Respiratory Syncytial Virus


According to a report in the journal Science (31 October 2013), an experimental vaccine to protect against respiratory syncytial virus (RSV), a leading cause of illness and hospitalization among very young children, has elicited high levels of RSV-specific antibodies when tested in animals. The respiratory syncytial virus (RSV) is responsible for a common childhood illness. There is no vaccine available to prevent RSV infection.


In the United States, RSV infection is the most common cause of bronchiolitis (inflammation of small airways in the lungs) and pneumonia in children less than one year old and the most common cause for hospitalization in children under five. Worldwide, it is estimated that RSV is responsible for nearly 7% of deaths in babies aged 1 month to 1 year; only malaria kills more children in this age group. Others at risk for severe disease following RSV infection include adults over age 65 and those with compromised immune systems.


Earlier this year, the VRC team obtained atomic-level details of an RSV protein — called the fusion (F) glycoprotein — bound to a broadly neutralizing human RSV antibody. The protein-antibody complex gave scientists their first look at the F glycoprotein as it appears before it fuses with a human cell. In this pre-fusion shape, F glycoprotein contains a region vulnerable to attack by broadly neutralizing antibodies (antibodies able to block infection from the common strains of RSV).


Once RSV fuses with a cell, this vulnerable area, named antigenic site zero by the researchers, is no longer present on the rearranged F protein. In natural RSV infection, the immune system produces antibodies against both the pre-fusion and post-fusion forms of F glycoprotein. But the antibodies to antigenic site zero, which is only present on the pre-fusion form, have much stronger neutralizing activity. Therefore, a vaccine against RSV would have greater chance of success by eliciting antibodies directed at F glycoprotein in its pre-fusion configuration.


The current publication describes how the authors used this structural information to design and engineer F glycoprotein variants that retained antigenic site zero even when no antibody was bound to it. The goal was to create stable variants that could serve as the foundation for a vaccine capable of eliciting a potent antibody response. The authors designed more than 100 variants; of these, three were shown by X-ray crystallography to retain the desired structure. The engineered variants were then used as vaccines in a series of experiments in mice and rhesus macaques.


In mice and macaques, it was found that the more stable the protein, the higher the levels of neutralizing antibodies elicited by vaccination. The levels of antibody made in response to one of the engineered F glycoproteins were more than 10 times higher than those produced following vaccination with post-fusion F glycoprotein and well above levels needed to protect against RSV infection.

Effects of Closure of Live Poultry Markets on Poultry-to-Person Transmission of Avian Influenza A H7N9 Virus


Transmission of the novel avian influenza A H7N9 virus seems to be predominantly between poultry and people. In the major Chinese cities of Shanghai, Hangzhou, Huzhou, and Nanjing -where most human cases of infection have occurred – live poultry markets (LPMs) were closed in April, 2013, soon after the initial outbreak, as a precautionary public health measure. As a result, a study published online in The Lancet (31 October 2013), was performed to quantify the effect of LPM closure in these cities on poultry-to-person transmission of avian influenza A H7N9 virus.


The authors obtained information about every laboratory-confirmed human case of avian influenza A H7N9 virus infection reported in the four cities by June 7, 2013. This information came from a database built by the Chinese Center for Disease Control and Prevention. They used data for age, gender, location, residence type (rural or urban area), and dates of illness onset, and obtained information about LPMs from official sources. They then constructed a statistical model to explain the patterns in incidence of cases reported in each city on the basis of the assumption of a constant force of infection before LPM closure, and a different constant force of infection after closure. The model was fitted with Markov chain Monte Carlo methods.


A total of 85 human cases of avian influenza A H7N9 virus infection were reported in Shanghai, Hangzhou, Huzhou, and Nanjing by June 7, 2013, of which 60 were included in the main analysis. Results showed that closure of LPMs reduced the mean daily number of infections by 99% in Shanghai, by 99% in Hangzhou, by 97% in Huzhou, and by 97% in Nanjing. Because LPMs were the predominant source of exposure to avian influenza A H7N9 virus for confirmed cases in these cities, it was estimated that the mean incubation period was 3.3 days (1.4-5.7).


According to the authors, LPM closures were effective in the control of human risk of avian influenza A H7N9 virus infection in the spring of 2013, and in the short term, LPM closure should be rapidly implemented in areas where the virus is identified in live poultry or people. In the long term, the authors suggested that evidence-based discussions and deliberations about the role of market rest days and central slaughtering of all live poultry should be renewed.

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


Designating an Orphan Product: Drugs and Biological Products


The following is the list of US Orphan Designations Target Health assisted our client to obtain:


1. Gaucher Disease-NDA – NDA Approved

2. Hereditary angioedema – NDA Approved

3. Growth Hormone (in development)

4. Burn progression in hospitalized patients (in development)

5. Debridement of 3rd degree burns (in development; approved in Europe)

6. Scleroderma (in development)

7. Alagille Syndrome

8. Caries prevention, head and neck cancer

9. Cushing’s syndrome secondary to ectopic ACTH secretion

10. Edema-related effects in hospitalized patients with 3rd degree burns

11. Osteonecrosis of the jaw


The Orphan Drug Act (ODA) provides for granting special status to a drug or biological product (“drug“) to treat a rare disease or condition upon request of a sponsor. This status is referred to as orphan designation (or sometimes “orphan status“). For a drug to qualify for orphan designation both the drug and the disease or condition must meet certain criteria specified in the ODA and FDA’s implementing regulations at 21 CFR Part 316. Orphan designation qualifies the sponsor of the drug for various development incentives of the ODA, including tax credits for qualified clinical testing. A marketing application for a prescription drug product that has received orphan designation is not subject to a prescription drug user fee unless the application includes an indication for other than the rare disease or condition for which the drug was designated.


A sponsor seeking orphan designation for a drug must submit a request for designation to OOPD with the information required in 21 CFR 316.20 and 316.21. Each designation request must stand on its own merit. Sponsors requesting designation of the same drug for the same rare disease or condition as a previously designated product must submit their own data and information in support of their designation request. The granting of an orphan designation request does not alter the standard regulatory requirements and process for obtaining marketing approval. Safety and effectiveness of a drug must be established through adequate and well-controlled studies.

(source: FDA Website)

Creamy Celery Root Skordalia


Photo: Joyce Hays, ©Target Health Inc. 2013


Skordalia (skor-thal-YAH) is a tasty Greek vegetarian dip/spread/sauce, that is a delicious accompaniment to fish or cooked vegetables. It can also stand alone as a dip for pita bread, breadsticks and crudit?s. The Greek recipes call for potatoes or bread. In this recipe, celery root is substituted for starchy potatoes. Also, to boil potatoes or substituting for them, with celery root,, water is used, but I prefer to steam veggies or boil in chicken stock. Also, if thinning down is needed, I use chicken stock or broth, rather than water.



4 large garlic cloves

1/2 cup extra-virgin olive oil

3/4 pound celery root

Pinches Salt (optional) & black pepper (grind to your taste)

2 Tablespoons sliced blanched almonds

3 Tablespoons fresh lemon juice

Chicken stock or broth, to boil the celery root (Broth: use low fat, low sodium)



1. Preheat the oven to 350?. In a small saucepan, cover the garlic with the oil and simmer over low heat until the garlic is tender, about 12 minutes. Let the garlic stand in the oil. 


2. Using a sharp knife, peel the celery root and cut into 1-inch cubes. In a saucepan, cover the celery root with water or chicken stock and bring to a boil. With a pinch of salt, simmer over moderate heat until tender, 25 minutes. Drain and spread out on a work surface or baking sheet. Let dry for 5 minutes. 


3. While the celery root is cooking, spread the almonds in a pie plate and toast in the oven for about 7 minutes, until golden. Let cool.


4. Transfer the celery root to a food processor.


5. Using a slotted spoon, add the cooked garlic, then add the toasted almonds and lemon juice and puree. With the machine on, slowly, pour in the garlic-infused olive oil.


6. Taste, then season, to your taste, the skordalia with salt (optional). If the skordalia is too thick, gradually, while whisking, stir in 1/4 cup of water or chicken broth and serve.


The skordalia can be refrigerated overnight. Reheat gently.


Try this garlic spread with roasted beets, fish, chicken, pita, sesame breadsticks, etc.


Information About Celery Root



Celery Root is believed to date back to the 7th century BC growing as wild celery; traces of it were found at the tomb of the Pharaoh Tutankhamun whom died in 1323 BCE. It didn’t make its way into modern kitchens until the early 1600’s. Even though celery root is associated with other root vegetables it has a certain flair that other root vegetables don’t have, mostly because French chefs have made it such an honored vegetable to pair with many other food items.


California cultivates and produces the most celery root on the market today, harvesting over 26 acres in the year 2008, followed by Michigan, harvesting 1,800 acres. Celery root can be grown year round in suitable climates.


Celery root, which is also known as “celeriac“, is low in cholesterol and saturated fat and is found to be an excellent source of riboflavin, calcium, Vitamin B6, magnesium, phosphorus, and an excellent source of potassium, Vitamins A, C, and K, as well as dietary fiber. In a study done at Harvard Medical School it was shown that vitamin B6 could help prevent colon and or rectal cancer in women. Vitamin B6 is vitally important for proper immune health and also is essential in the health of red blood cells, muscles, and nerves.


Vitamin C is also an immune building vitamin which helps to fight off potentially harmful infections by building a strong and healthy immune system. Celery root is high in dietary fiber which helps to maintain a well working digestive tract. It is high in potassium which helps to send and receive neurotransmissions throughout the body. Celery root is loaded with dietary fiber which helps to maintain a healthy digestive system. Because celery root has a high content of Vitamin B6 along with the high content of dietary fiber, the consumption of celery can greatly decrease your chances of colon cancer. The content of Vitamin C in celery root helps to build a strong immune system by fighting off harmful free radicals that damage cells and are said to cause many types of cancer. Riboflavin, also found in celery root, helps to convert the food you eat into energy to be stored and used as needed. Individuals whom exercise on a regular basis would be wise to include celery root into their diet as a much needed source of energy is provided to the tissues and muscles from the riboflavin that is found in celery. Because celery root is low in cholesterol and saturated fats, its consumption can help reduce heart related diseases such as heart attacks and clogging of the arteries from cholesterol build up.


Celery Root (celeriac) is a great substitute for potatoes. It can be cooked in many of the same ways as potatoes, but is a far healthier alternative. Here’s a quick nutritional summary from Nutrition Data that compares celery root to a comparable amount of potato:




Celery Root*


Calories 42 118
Carbohydrates 9g 27g
Dietary Fiber 2g 2g
  *1 cup celery root (155g)

boiled, drained with no salt

**1 potato (136g)

, boiled in skin with no salt


Celeriac is:

1. Low in Saturated Fat and Cholesterol

2. High in Vitamin C, Vitamin K, Phosphorus, Potassium, Dietary Fiber, Vitamin B6, Magnesium and Manganese


This dip is a nice change from hummus. The flavor of the celery root is more delicate. At the last minute, if you want to add more garlic, simply squeeze the juice of a garlic clove, into the mixture, rather than going through cutting again. This celery root dip can also be used as a topping for fish and cooked vegetables.


We had this dip as an appetizer with pieces of warm pita bread and a lively oaky cabernet. Then lamb patties, (lamb mixed with chopped pistachios and garnished with pomegranate arils), saffron rice and broccoli saut?ed in olive oil and garlic. We had our usual fresh blueberry dessert topped with no-fat cool whip.


Hope you’re having a relaxing weekend with lots of laughing, keeping the endorphin levels up!