10 Steps to Consider to Fund and Provide Health Care for All

 

By Joyce Hays, MS and Jules Mitchel, MBA, PhD

 

Since we are all going to be a patient at multiple points in our lives, policy makers must support healthcare as a right rather than a choice. Therefore, from a strict business perspective, we must all pay for the right to have healthcare when we need it, and thus be part of the risk pool. It should not matter whether one is 1) working for a company that does or does not provide health insurance; 2) a sole practitioner; 3) unemployed; or 4) for whatever reason unable to work and pay premiums. The issue is, therefore, how to make healthcare universally available, and how to fund healthcare and health insurance premiums. While there are many more issues that must be addressed, here are 10 ideas that could make a difference right away:

  1. All citizens should have the same healthcare benefits provided to all members of congress who work for us. And that all American citizens, through their tax dollars, pay for the insurance that all of the congress enjoys.

 

  1. As taxpayers, we fund the critical research performed and supported by the National Institutes of Health (NIH), as well as other government agencies such as the Department of Defense (DoD). As a result, and as a return on our investment (ROI), a royalty from licenses/sales and any financial transactions related to any pharmaceuticals and devices that received funding from any government agency be allocated directly to healthcare services to all of our citizens.

 

  1. To encourage well educated US citizens, with good jobs that yield tax dollars, we should provide automatic paths to: work visas and to citizenship for any foreign college student graduating with a minimum of a B average, and for any graduate student receiving an advanced degree.

 

  1. As part of attending a medical school, tuition-free PLAN, all physicians must return to their solemn commitment and passion to assure that healthcare is available for those who need it, which is all of us.

 

To accomplish this, physicians should be required to provide services at public clinics in underserved geographical areas 1 day per week, on a salary basis, in return for the free medical school tuition. Additional salaries can be paid to those who want to commit more time to the public clinics, and additional insurance can be bought by patients who want “concierge” medicine, private rooms in hospitals, etc. When I was at Pfizer Pharmaceuticals, all licensed full-time physicians and pharmacists working at the company were allowed, on company time, to provide medical services one half day per week. The Pfizer Medical Director I worked for provided these services at a rheumatology clinic at Elmhurst Hospital in Queens, a city hospital. Similarly, many at Pfizer in Groton CT worked at Yale, Hartford Hospital, and Connecticut Children’s Medical Center at no cost to the institutions.

 

  1. The U.S. should open more medical school slots for future physicians which will allow for more staffing of the public clinics.

 

  1. The U.S. should encourage the use of telemedicine and remote medical devices to reduce patient travel for office visits.

 

  1. The U.S. should allow for more mobility by physicians across state line, all states respect medical and healthcare licenses issued by any other state.

 

  1. The U.S. should extend the patent life of life-saving drugs and devices.

 

  1. Health Insurance should be funded like term Life Insurance in that once the policy is bought, the premiums, which are paid for life, are also fixed for life. Therefore, the younger you are, the less expensive the premiums. Cash value may also accrue as the population becomes healthier.

 

  1. Climate change brings with it more virulent microbes. This is a new challenge to U.S. health agencies and to U.S. security. Common sense tells us that the healthier all Americans are, as a group, the greater chance to keep individuals healthy. When Americans as a group have access to healthcare, we, as a country are better able to handle pandemics, like the Zika virus, from becoming a nationwide disaster. This is the final reason to provide healthcare to all Americans and not just to a few.

 

For more information about Target Health contact Warren Pearlson (212-681-2100 ext. 165). 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.

 

Joyce Hays, Founder and Editor in Chief of On Target

Jules Mitchel, Editor

QUIZ

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First Drug for Aggressive MS Wins FDA Approval

Editor’s note: For us at THI, the Hauser goal and its challenges, reads like an exciting adventure story. Couldn’t put it down.

 

Graphic credit: Mikael Häggström – Public Domain, Wikipedia Commons

 

Multiple sclerosis is the most common autoimmune disorder affecting the central 1) ___ system. The name multiple sclerosis refers to the scars (sclerae – better known as plaques or lesions) that form in the nervous system. In 2013, about 2.3 million people were affected globally with rates varying widely in different regions and among different populations. That year about 20,000 people died from MS, up from 12,000 in 1990. While the cause is not clear, the underlying mechanism is thought to be either destruction by the immune 2) ___, or failure of the myelin-producing cells. Proposed causes for this include genetics and environmental factors such as being triggered by a viral infection.
Apart from demyelination, the other sign of the disease is inflammation. Fitting with an immunological explanation, the inflammatory process is caused by T cells, a kind of lymphocyte that plays an important role in the body’s defenses. T cells gain entry into the brain via disruptions in the blood-brain 3) ___. The T cells recognize myelin as foreign and attack it, explaining why these cells are also called “autoreactive lymphocytes”. The attack of myelin starts an inflammatory processes, which triggers other immune cells. The blood-brain barrier is a part of the capillary system that prevents the entry of T cells into the central nervous system. It may become permeable to these types of cells secondary to an infection by a virus or bacteria. After it repairs itself, typically once the infection has cleared, T cells may remain trapped inside the 4) ___. There is no known cure for multiple sclerosis. Treatments attempt to improve function after an attack and prevent new attacks. Medications used to treat MS, while modestly effective, can have side effects and be poorly tolerated.

 

Nerve axon with myelin sheath. Graphic credit: Public Domain, Wikipedia Commons

 

Forty years ago, one of Dr. Stephen Hauser’s first patients was a young Harvard Law School graduate and White House aide with a case of multiple 5) ___ that raced like a brush fire through her brain. She quickly lost her ability to speak, swallow, and breathe. She got married in a wheelchair in her hospital room, tethered to breathing and feeding tubes and dressed in her wedding gown. “We had nothing to treat her with,” recalled Hauser, now director of the Weill Institute for Neurosciences at the University of California, San Francisco. It was such a searing moment for the young doctor, then at the beginning of his neurology training, that he decided to dedicate his career to MS research. Last week, after decades of false starts, struggles to persuade disbelieving colleagues, and a tortuous path through the maze of drug discovery – Roche Holding AG, announced that the FDA 6) ___and ___ ___ had approved its new drug for MS based on Hauser’s research. Researchers say the medication is a significant improvement over other treatments for the debilitating disease, which afflicts more than 400,000 Americans.

 

The drug, called ocrelizumab, takes a different approach than the more than a dozen other MS drugs on the market. It blocks certain immune system cells called B cells that Hauser’s lab discovered play a critical role in the disease. The other drugs target the immune system’s T cells, long thought to be the main culprit in MS. The FDA approved ocrelizumab for treatment of primary-progressive MS, making it the first drug ever approved for the most aggressive form of the disease. It is marked by a gradual worsening of neurological symptoms, especially difficulty walking and in some patients paralysis below the waist, and accounts for between 10-15% of MS cases.

The decision was based largely on results of a 732-patient clinical trial that showed primary-progressive patients on the drug were about 25% less likely to have their disability worsen. The FDA also cleared the drug for the more common relapse-remitting form of the disease, which is characterized by inflammatory attacks that trigger such early symptoms as vision problems, tingling in the feet, weakness, and muddled thinking.

 

When Hauser began his quest for better MS remedies in the late 1970s, the prevailing belief was that T cells were the sole offenders behind MS. That would turn out to be wrong. T cells, as well as B cells, are key components of the arsenal the immune system uses to detect, hunt down, and kill viruses, bacteria, and other “foreign” invaders that harm the body. The focus on T cells grew in part from researchers’ longtime use of a mouse model with a T cell-driven condition called experimental allergic encephalomyelitis, or EAE, to study and develop drugs for the disease. Like multiple sclerosis, EAE is characterized by inflammation of the brain and spinal cord, but there, the similarities end. Hauser’s mentor, the late Harvard neurologist Dr. Raymond Adams, told him there was little resemblance between the two conditions. “It really didn’t look like MS at all,” Hauser said. So, his first task was to develop a new animal 7) ___ for the disease. It took a decade, but eventually he and his lab came up with a guinea pig-sized monkey called a marmoset that was able to develop MS that looked just like the human version. Then, in a series of experiments, they tried to induce the disease by transferring myelin-targeted T cells into the animals. It didn’t work. Next, when they tried certain antibodies that are produced by B cells, that didn’t work. Finally, when they used both T cells and the B cell antibodies together, the animals developed MS. The experiments showed that MS wasn’t fueled just by T cells, and Hauser’s lab identified B cells and their related antibodies as promising new drug targets. At first, it seemed Hauser’s timing was fortuitous. In 1997, as his group’s research was coming together, the FDA approved the first treatment directed against B cells. It was a genetically engineered antibody called rituximab, from Genentech and its partner Idec Pharmaceuticals Corp. The drug was for non-Hodgkin lymphoma, but its approval meant an off-the-shelf therapy was available to test their B cell hypothesis in MS patients. Hauser and other researchers then applied for a grant from the NIH, 8) ___ ___of ___ to run a pilot study of rituximab in people. The NIH said no. The idea was “biologically implausible,” Hauser said they were told. In 2001, Hauser asked Genentech to fund the study. Initially, he met resistance there as well, he said. A team of outside experts the company assembled to evaluate the proposal rated its chances of success at less than 15%. However, in 2003, after 18 months of discussions, Genentech agreed to a trial. Just as the decision came down, news came from the East Coast that Biogen, the dominant player in drugs for MS, had agreed to merge with Idec, gaining Idec’s rights to rituximab in the process. Working out details with a new corporate partner further delayed the start of the study, Hauser said. The next hurdle was the FDA, which also had to approve the trial. Hauser and his colleagues proposed a one-year, placebo-controlled trial with two infusions of rituximab six months apart. They would measure the effect of the treatment on formation of new MS lesions in the brain as determined by MRI after a year. They thought the treatment would have a gradual impact on inflammation and that they would need at least a year to see whether the drug was working. But the FDA said it wouldn’t be 9) ___ to keep patients with active relapsing MS on placebo for a year. Instead, the agency permitted only a single dose of the drug. The researchers would have to measure its effectiveness after just 24 weeks. The study enrolled 104 patients, 69 of whom were treated with rituximab. The moment of truth came in late September 2006 when the researchers “unblinded” the data. What they saw astonished them. The formation of new brain lesions in the rituximab patients was reduced by 91% compared with those on placebo. The size of the effect was “unprecedented” in MS, Hauser said. The study showed not only that B cells were critical players in the disease, but that when B cells were depleted by the drug, brain inflammation was almost immediately shut down. However, it would take a much larger Phase 3 trial to win FDA approval, but he figured rituximab would be available to MS patients within four years — by about 2010. But, Genentech said that they had another molecule that was better suited for MS. Ocrelizumab had a key advantage over rituximab, which, like other monoclonal antibodies developed during the early days of the technology, is comprised of part human and part mouse protein. Over time, some patients develop immune responses to the mouse component, leading to problematic side effects or undercutting the drug’s benefits. In contrast, ocrelizumab, like most newer genetically engineered drugs, is fully humanized and much less likely to trigger an immune response in patients. These were among reasons Genentech decided to place its bet for MS on the new agent, Hauser said. He agreed that ocrelizumab would likely prove a better drug – both for Genentech and for MS patients. But he believed it would further delay getting a B cell therapy to patients. Then in 2009, Roche, which had long held a majority stake in Genentech, moved to take over the rest of the company. After the acquisition closed, Roche quickly announced that the MS program would move forward. The Phase 3 studies that led to FDA approval were launched in 2011. The results, which for the studies of relapsing patients were a near-replication of the rituximab findings from 2006, were published by the New England Journal of Medicine in December. The two Roche-funded studies involving a total of 1,656 patients with relapsing MS showed the drug cut annualized relapse rates for such patients almost in half compared with a commonly used treatment called Rebif. The formation of new lesions in the brain and spinal cord – the key marker of inflammation – was reduced by more than 94% compared to patients on Rebif.

 

Side effects of the drug were generally mild or similar to comparator agents, but studies raised the possibility of a slightly elevated risk of cancer on the drug, a concern doctors are certain to keep an eye on as use of the medicine grows.

 

B Cells:

 

B cells are a type of white blood cell and, specifically, a type of lymphocyte. Many B cells mature into what are called plasma cells that produce antibodies (proteins) necessary to fight off infections while other B cells mature into memory B cells. All the plasma cells, descended from a single B cell, produce the same antibody which is directed against the antigen that stimulated it to mature. The same principle holds with memory B cells. Thus, all of the plasma cells and memory cells “remember” the stimulus that led to their formation. The maturation of B cells takes place in birds in an organ called the bursa of Fabricus. B cells in mammals mature largely in the bone marrow. The B cell, or B lymphocyte, is thus an immunologically important cell. It is not thymus-dependent, has a short lifespan, and is responsible for the production of immunoglobulins. It expresses immunoglobulins on its surface. Validation of the B cell’s role in MS poses an intriguing question for MS researchers. The fact is, Hauser said, that most of the immune system cells found in MS lesions are T cells. So, what are B cells doing? Hauser suspects they are “orchestrating” the process by which 10) ___ do their damage. Many other MS drugs, he added, while viewed as targeting T cells, also interfere with B cells. “Ocrelizumab’s success has led to a rethinking of how the other MS therapies may be working,” he said. Credit: Ron Winslow, 2017, www.statnews; Wikipedia

 

ANSWERS: 1) nervous; 2) system; 3) barrier; 4) brain; 5) sclerosis; 6) Food and Drug Administration; 7) model; 8) National Institutes of Health; 9) ethical; 10) T cells

Stephen L. Hauser MD (1949 to Present)

Photo credit: UCSF Medical Center, https://commons.wikimedia.org/w/index.php?curid=15734615

 

Stephen L. Hauser is the Robert A. Fishman Distinguished Professor and Chair of the Department of Neurology at the University of California, San Francisco (UCSF), where his work has focused on immune mechanisms and multiple sclerosis (MS). Hauser is a principal investigator of a large multinational effort to identify genetic effects on MS, and part of the team that identified that humoral immune mechanisms are important in the pathogenesis of MS lesions, leading to the development of B-cell based therapies for MS. He has contributed to the establishment of nationwide and international genetics consortia that have identified more than 50 gene variants that contribute to MS risk.

 

Using comparative genomics between African-American and Caucasian MS populations, Hauser’s group was able to identify HLA-DRB1 as the primary MS signal in the MHC, and also fine map other secondary loci in this region.

 

In 2007, as a senior organizer of the International Multiple Sclerosis Genetics Consortium (IMSGC), Dr. Hauser helped identify the first two non-HLA genes involved in MS susceptibility, IL-2R (CD25) and IL-7R (CD127). In 2010, his laboratory published the complete genome sequences and the epigenome of identical twins discordant for MS. By mid-2011 more than fifty MS associated risk alleles were identified, and by now nearly the entire array of common variants associated with MS susceptibility have now been mapped. Hauser also has focused on the role of the B cell and immunoglobulin in the pathogenesis of the disease. He developed and characterized an MS disease model that replicated the core feature of vesicular demyelination previously observed in MS, and demonstrated that this pathology resulted from the synergistic effects of autoreactive T-cells and pathogenic autoantibodies.

 

In 1999, Hauser published work identifying specific myelin reactivity of these autoantibodies deposited in areas of myelin damage in MS brains. Hauser translated this finding into a new potential therapy for MS. He led a large-scale clinical trial with rituximab, a chimeric monoclonal antibody that depletes CD20+ B cells, and demonstrated robust efficacy in relapsing remitting MS. A second trial in primary progressive MS reported in 2009 that rituximab may similarly be effective in patients with primary progressive MS who also have evidence of ongoing inflammatory CNS disease. More recently, a third clinical trial with a fully humanized anti-CD20 monoclonal antibody, ocrelizumab, replicated the results of the rituximab trial in relapsing remitting MS. With the MS Bioscreen project, Hauser has pioneered precision medicine for complex diseases like MS, creating an “actionable digital growth-chart for complex traits”

 

Hauser is a graduate of MIT (Phi Beta Kappa) and Harvard Medical School (Magna Cum Laude). In 2010 Hauser was appointed to the Presidential Commission for the Study of Bioethical Issues. He is a co-editor of the textbook Harrison’s Principles of Internal Medicine and past editor-in-chief of the Annals of Neurology. Hauser trained in internal medicine at the New York Hospital-Cornell Medical Center, in neurology at the Massachusetts General Hospital (MGH), and in immunology at Harvard Medical School and the Institute Pasteur in Paris, France, and was a faculty member at Harvard Medical School before moving to UCSF. Hauser received the 2013 Charcot Award from the Multiple Sclerosis International Federation, the Jacob Javits Neuroscience Investigator Award, and the John Dystel Prize for Multiple Sclerosis Research. In 2011 he delivered the Robert Wartenberg Lecture at the American Academy of Neurology, an honor given for excellence in clinically relevant research. Hauser is also the chair of the Committee on Gulf War and Health Outcomes for the Institute of Medicine and a Fellow of the American Academy of Arts and Sciences and the Association of American Physicians.
In addition to the research of Dr. Hauser, there is a long history of studying MS called by some: the Viking Gene.

 

Detail of Robert Carswell’s drawing of MS lesions in the brain stem and spinal cord (1838). Credit: Wikipedia

 

Robert Carswell (1793-1857), a British professor of pathology, and Jean Cruveilhier (1791-1873), a French professor of pathologic anatomy, described and illustrated many of the disease’s clinical details, but did not identify it as a separate disease. Specifically, Carswell described the injuries he found as “a remarkable lesion of the spinal cord accompanied with atrophy”. Under the microscope, Swiss pathologist Georg Eduard Rindfleisch (1836-1908) noted in 1863 that the inflammation-associated lesions were distributed around blood vessels. The French neurologist Jean-Martin Charcot (1825-1893) was the first person to recognize multiple sclerosis as a distinct disease in 1868. Summarizing previous reports and adding his own clinical and pathological observations, Charcot called the disease sclerose en plaques. The first attempt to establish a set of diagnostic criteria was also due to Charcot in 1868. He published what now is known as the “Charcot Triad”, consisting in nystagmus, intention tremor, and telegraphic speech (scanning speech) Charcot also observed cognition changes, describing his patients as having a “marked enfeeblement of the memory” and “conceptions that formed slowly”. Diagnosis was based on Charcot triad and clinical observation until Schumacher made the first attempt to standardize criteria in 1965 by introducing some fundamental requirements: Dissemination of the lesions in time (DIT) and space (DIS), and that “signs and symptoms cannot be explained better by another disease process”. Both requirements were later inherited by Poser criteria and McDonald criteria, whose 2010 version is currently in use. During the 20th century, theories about the cause and pathogenesis were developed and effective treatments began to appear in the 1990s.
Historical cases

Photographic study of locomotion of an MS female patient with walking difficulties created in 1887 by Muybridge. Photo credit: Wikipedia
There are several historical accounts of people who probably had MS and lived before or shortly after the disease was described by Charcot. A young woman called Halldora who lived in Iceland around 1200 suddenly lost her vision and mobility but, after praying to the saints, recovered them seven days after. Saint Lidwina of Schiedam (1380-1433), a Dutch nun, may be one of the first clearly identifiable people with MS. From the age of 16 until her death at 53, she had intermittent pain, weakness of the legs, and vision loss – symptoms typical of MS. Both cases have led to the proposal of a “Viking gene” hypothesis for the dissemination of the disease. Augustus Frederick d’Este (1794-1848), son of Prince Augustus Frederick, Duke of Sussex and Lady Augusta Murray and the grandson of George III of the United Kingdom, almost certainly had MS. D’Este left a detailed diary describing his 22 years living with the disease. His diary began in 1822 and ended in 1846, although it remained unknown until 1948. His symptoms began at age 28 with a sudden transient visual loss (amaurosis fugax) after the funeral of a friend. During his disease, he developed weakness of the legs, clumsiness of the hands, numbness, dizziness, bladder disturbances, and erectile dysfunction. In 1844, he began to use a wheelchair. Despite his illness, he kept an optimistic view of life. Another early account of MS was kept by the British diarist W. N. P. Barbellion, nom-de-plume of Bruce Frederick Cummings (1889-1919), who maintained a detailed log of his diagnosis and struggle. His diary was published in 1919 as The Journal of a Disappointed Man.

Higher Death Rate Among Youth With First Episode Psychosis

 

A new study, published online in the Schizophrenia Bulletin (6 April 2017), shows that young people experiencing first episode psychosis have a much higher death rate than previously thought. The study used insurance claims data to identify approximately 5,000 young people aged 16-30 who had been diagnosed with a first episode of psychosis in 2008-2009, and used data from the Social Security Administration to identify deaths in this population within 12 months of the initial psychosis diagnosis. Results showed that the 12-month mortality rate for these young people — from any cause — was at least 24 times higher than their peers in the general population. In the general United States population, only individuals over age 70 come close to a similar 12-month mortality rate.

 

In addition to mortality, the study examined the health care that individuals received in the 12 months after the initial psychosis diagnosis. Those data showed that young people with a new psychosis diagnosis had surprisingly low rates of medical oversight and only modest involvement with psychosocial treatment providers. Overall, 61% of them did not receive any antipsychotic medications, and 41% did not receive any psychotherapy. Those who died within 12 months of diagnosis received even less outpatient treatment and relied more heavily on hospital and emergency care.
According to the authors, the study underscores that young people experiencing psychosis warrant intensive and proactive treatments, services and supports.

ONCOLOGY

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Cancer Death Rates Continue to Decline

 

According to the latest Annual Report to the Nation on the Status of Cancer, 1975-2014, published early online in the Journal of the National Cancer Institute (JNCI; 31 March 2017), overall cancer death rates continue to decrease in men, women, and children for all major racial and ethnic groups. The report finds that death rates during the period 2010-2014 decreased for 11 of the 16 most common types of cancer in men and for 13 of the 18 most common types of cancer in women, including lung, colorectal, female breast, and prostate cancers. Meanwhile, death rates increased for cancers of the liver, pancreas, and brain in men and for liver and uterine cancer in women. The report finds overall cancer incidence rates, or rates of new cancers, decreased in men but stabilized in women during the period 1999-2013.

 

The Report to the Nation is released each year in a collaborative effort by the American Cancer Society; the Centers for Disease Control and Prevention (CDC) and the National Cancer Institute (NCI), both parts of the Department of Health and Human Services; and the North American Association of Central Cancer Registries (NAACCR). The report includes a special section, which this year focuses on survival. It finds that several but not all cancer types showed a significant improvement over time for both early- and late-stage disease, and varied significantly by race/ethnicity and state.

 

Compared to cases diagnosed in 1975-1977, five-year survival for cancers diagnosed in 2006-2012 increased significantly for all but two types of cancer: cervix and uterus. The greatest absolute increases in survival (25% or greater) were seen in prostate and kidney cancers as well as non-Hodgkin lymphoma, myeloma, and leukemia. Cancers with the lowest five-year relative survival for cases diagnosed in 2006-2012 were pancreas (8.5%), liver (18.1%), lung (18.7%), esophagus (20.5%), stomach (31.1%) and brain (35%); those with the highest were prostate (99.3%), thyroid (98.3%), melanoma (93.2%) and female breast (90.8%).

 

According to the authors, while this report found that five-year survival for most types of cancer improved among both blacks and whites over the past several decades, racial disparities for many common cancers have persisted, and they may have increased for prostate cancer and female breast cancer. The authors added that we as a society still have a lot of work to do to understand the causes of these differences, but certainly differences in the kinds and timing of recommended treatments are likely to play a role.
This report also found that tobacco-related cancers have low survival rates, which underscores the importance of continuing to do what we know works to significantly reduce tobacco use. In addition, the authors stated that since every state in the nation has an adult obesity prevalence of 20% or more and with obesity as a known risk factor for cancer, there is a critical need to continue to support communities and families in prevention approaches that can help reverse the nation’s obesity epidemic. The authors also stated that more attention and resources are needed to identify major risk factors for common cancers, such as colorectal, breast, and prostate, as are concerted efforts to understand the increasing incidence trends in uterine, female breast, and pancreatic cancer.

First Direct-to-Consumer Tests that Provide Genetic Risk Information

 

The FDA has allowed marketing of 23andMe Personal Genome Service Genetic Health Risk (GHR) tests for 10 diseases or conditions. These are the first direct-to-consumer (DTC) tests authorized by the FDA that provide information on an individual’s genetic predisposition to certain medical diseases or conditions, which may help to make decisions about lifestyle choices or to inform discussions with a health care professional.

 

While consumers can now have direct access to certain genetic risk information, according to the FDA, it is important that people understand that genetic risk is just one piece of the bigger puzzle, and it does not mean that one will or won’t ultimately develop a disease.

 

The GHR tests are intended to provide genetic risk information to consumers, but the tests cannot determine a person’s overall risk of developing a disease or condition. In addition to the presence of certain genetic variants, there are many factors that contribute to the development of a health condition, including environmental and lifestyle factors.

 

The 23andMe GHR tests work by isolating DNA from a saliva sample, which is then tested for more than 500,000 genetic variants. The presence or absence of some of these variants is associated with an increased risk for developing any one of the following 10 diseases or conditions:

 

  1. Parkinson’s disease, a nervous system disorder impacting movement;
  2. Late-onset Alzheimer’s disease, a progressive brain disorder that destroys memory and thinking skills;
  3. Celiac disease, a disorder resulting in the inability to digest gluten;
  4. Alpha-1 antitrypsin deficiency, a disorder that raises the risk of lung and liver disease;
  5. Early-onset primary dystonia, a movement disorder involving involuntary muscle contractions/movements;
  6. Factor XI deficiency, a blood clotting disorder;
  7. Gaucher disease type 1, an organ and tissue disorder;
  8. Glucose-6-Phosphate Dehydrogenase deficiency, also known as G6PD, a red blood cell condition;
  9. Hereditary hemochromatosis, an iron overload disorder; and
  10. Hereditary thrombophilia, a blood clot disorder.

 

The FDA reviewed data for the 23andMe GHR tests through the de novo premarket review pathway, a regulatory pathway for novel, low-to-moderate-risk devices that are not substantially equivalent to an already legally marketed device. Along with this authorization, the FDA is establishing criteria, called special controls, which clarify the agency’s expectations in assuring the tests’ accuracy, reliability and clinical relevance. These special controls, when met along with general controls, provide reasonable assurance of safety and effectiveness for these and similar GHR tests.

 

In addition, the FDA intends to exempt additional 23andMe GHR tests from the FDA’s premarket review, and GHR tests from other makers may be exempt after submitting their first premarket notification. A proposed exemption of this kind would allow other, similar tests to enter the market as quickly as possible and in the least burdensome way, after a one-time FDA review.

 

Excluded from today’s marketing authorization and any future, related exemption are GHR tests that function as diagnostic tests. Diagnostic tests are often used as the sole basis for major treatment decisions, such as a genetic test for BRCA, for which a positive result may lead to prophylactic (preventative) surgical removal of breasts or ovaries.

 

Authorization of the 23andMe GHR tests was supported by data from peer-reviewed, scientific literature that demonstrated a link between specific genetic variants and each of the 10 health conditions. The published data originated from studies that compared genetic variants present in people with a specific condition to those without that condition. The FDA also reviewed studies, which demonstrated that 23andMe GHR tests correctly and consistently identified variants associated with the 10 indicated conditions or diseases from a saliva sample.

 

The FDA requires the results of all DTC tests used for medical purposes be communicated in a way that consumers can understand and use. A user study showed that the 23andMe GHR tests’ instructions and reports were easy to follow and understand. The study indicated that people using the tests understood more than 90% of the information presented in the reports.

 

Risks associated with use of the 23andMe GHR tests include false positive findings, which can occur when a person receives a result indicating incorrectly that he or she has a certain genetic variant, and false negative findings that can occur when a user receives a result indicating incorrectly that he or she does not have a certain genetic variant. Results obtained from the tests should not be used for diagnosis or to inform treatment decisions. Users should consult a health care professional with questions or concerns about results. 
The FDA granted market authorization of the Personal Genome Service GHR tests to 23andMe, Inc.

Holiday Sweet Sticky Nut Bars

 

Jules gives this dessert five stars. ©Joyce Hays, Target Health Inc.

 

Ingredients

 

Crust

 

  • 2 cups almond flour
  • 1/4 cup coconut oil, melted
  • 2 Tablespoons honey

 

Filling

 

  • 3 eggs
  • 1/2 cup walnut or pecan halves, or chop in pieces, you decide
  • 1/2 cup coconut sugar
  • 1/2 cup maple syrup
  • 2 tsp vanilla extract
  • 3 Tablespoons butter or butter substitute
  • pinch of Kosher salt

 

Just a few ingredients. I like to use vanilla extract with bourbon infused into the extract. There’s no bourbon flavor in the dessert, but somehow this addition, enhances the vanilla. ©Joyce Hays, Target Health Inc.

 

Directions

 

  1. Preheat oven to 350°F.
  2. If you want the nuts chopped, do that now and set aside.

 

Chop your nuts or keep them in whole pieces, you decide. I’ve done my recipe with chopped nuts and whole halves. It doesn’t matter. ©Joyce Hays, Target Health Inc.
3. Mix the crust ingredients in a medium-sized bowl until combined. Press mixture evenly into an 8” or 9” square baking dish, covering the bottom and sides.

 

Mix well, the three crust ingredients. ©Joyce Hays, Target Health Inc.

 

Press the crust mixture down with the type of spatula I have above, or the back of a wooden spoon. Keep pressing until the mixture takes on a solid look and feel and it no longer looks like crumbs. After you’ve gotten a solid dough-like crust, then try to push it, up the sides of the baking dish or pan, just a little. Push it up the sides all around the baking dish. ©Joyce Hays, Target Health Inc.

 

Next put into oven to bake. As I continued to perfect this recipe and, therefore, made it a number of times, it didn’t seem to matter how thick this crust was. In this photo, for example, on the right side of the baking dish, the crust is thicker than in the middle. I thought this would not taste good. However, it was wonderful. Because the crust is so flexible, I am assuming that you could use any shape baking pan or dish, and even the size could vary. ©Joyce Hays, Target Health Inc.

 

Coming out of the oven, nice warm browned crust. (smells wonderful). ©Joyce Hays, Target Health Inc.

 

  1. Bake for 10 minutes or until the crust starts to brown. Remove from the oven and allow to cool.
  2. Using an electric mixer, whisk the eggs with the coconut sugar until you get a pale brown foam. Add the vanilla extract. Transfer the mixture to a saucepan. Add the butter and maple sugar. Cook over medium-low heat for about 8 minutes, stirring constantly, until the mixture thickens. Turn off the heat. Allow to cool for 5-10 minutes.

 

Best to crack your eggs into a separate, small dish, in case a tiny piece of shell falls in. Easier to pick shell out of a small dish than the big mixing bowl. ©Joyce Hays, Target Health Inc.

 

To the eggs, add the coconut sugar and vanilla extract. Beat until well combined and you see, (above) some light brown foam. ©Joyce Hays, Target Health Inc.

 

Transfer the egg mixture to a saucepan, and add the butter and maple syrup and medium-low heat, cook for 8 to 10 minutes, stirring constantly so it doesn’t stick, but does thicken. After this mixture has reached a nice thick consistency, remove from heat and allow it to cool for five to ten minutes.
6. Fill the crust with the warm, thick filling. Arrange walnut or pecan halves (or chopped nut pieces) over the filling.

 

After filling, has cooled down a little, pour it into the baking dish over the browned crust. ©Joyce Hays, Target Health Inc.

 

Over the warm filling, add all the nuts (either chopped or whole halves or both).

Then put into oven. ©Joyce Hays, Target Health Inc.
7. Bake for 20-25 minutes at 350°F.

 

Going into oven. ©Joyce Hays, Target Health Inc.

 

  1. Let cool to room temperature and refrigerate for at least 4-6 hours before serving.
  2. Serve the pie with cool whip or your favorite garnish.

 

Just out of the oven. Let it cool just a bit before you cut the bars. Cut the bars as large or as small as you wish. But wait until this delicious dessert has cooled down. ©Joyce Hays, Target Health Inc.

 

Warm and gooey and irresistible! ©Joyce Hays, Target Health Inc.

 

Serve on dessert dishes, plain or with whipped cream or ice cream or Cool Whip, which is what we opt for. ©Joyce Hays, Target Health Inc.

 

 

This is one of the first times I experimented with this recipe. I didn’t wait long enough for the crust to cool. I poured the filling over a warm crust. Just so you know, it didn’t change the flavor at all. Some of the filling seeped into the crust, as you can see here, and it didn’t matter. Wanted to let you know this, so you can see how flexible the recipe is. Great flexibility. ©Joyce Hays, Target Health Inc.

 

Every bite is delectable! :) ©Joyce Hays, Target Health Inc.

 

Cheers to Spring, which is beautiful here in Manhattan. ©Joyce Hays, Target Health Inc.

 

This weekend we’re going to see the new Broadway production of Tennessee Williams’ Glass Menagerie. We saw a Broadway revival of this play 3 years ago and didn’t like it. We’re going again because NY has a new young, extremely talented director, Sam Gold, whose ascent has been remarkable. Sam Gold is directing Menagerie, and we want to see how he deals with the challenges of this great play. Already, he has eliminated all intermissions, in order for the acting to go smoothly without interruption.

 

He always has some creative surprise in each play he directs. Sam Gold won a Best Director Tony recently for Broadway’s Fun House. His interpretation for off-Broadway, Look Back in Anger, a few years ago was awesome.

 

One way or another, we’ll have a good time.

 

Hope your weekend is restful and filled with the beauty of Springtime!

 

From Our Table to Yours !

Bon Appetit!