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Doctor Debunks Common Health Myths | WIRED

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Misunderstood Microbes | National Geographic Society

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Recent scientific studies have revealed the importance of microbes. Despite common misconceptions, most microbes are more helpful than harmful to humans and the planet.

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User Submitted Science Misconception Subjects:  This resource contains a list of science misconceptions by subject.

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Science Teacher SUBMITTED SCIENCE MISCONCEPTIONS 

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Science Teacher SUBMITTED SCIENCE MISCONCEPTIONS 

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Select a science topic below to view some user submitted misconceptions about that topic. These were submitted by fellow science teachers. If you have a misconception you would like to add, please click here.

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User Submitted Science Misconception Subjects

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Select a science topic below to view some user submitted misconceptions about that topic. These were submitted by fellow science teachers. If you have a misconception you would like to add, please click here.

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Association for Psychological Science - APS

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This notion seems firmly rooted in popular culture despite many efforts to debunk it (Hughes, Lyddy, & Lamb, 2013). It was the basis of the movie Lucy (2014), which depicted what supposedly would happen if a person actually used all 100% of her brainpower. It has been used to justify belief in pseudoscientific psychic powers and is a tacit assumption in many self-help programs designed to "unleash" untapped human potential.

Hughes, et al. (2013) found that this misconception (hereafter called the 10% Myth) is one of the most prevalent misconceptions among the public. More concerning is the finding by Dekker et al. (2012) that about 50% of primary and secondary teachers across different cultures also endorse the 10% Myth.

There are a plethora of articles and videos debunking this myth both in popular media and from neuroscientists. What's more, neuroscientists now have tools for creating images and tracking the activity of living, functioning brains. The best known of these are PET (Positron Emission Tomography) scans and fMRI (functional Magnetic Resonance Imaging). These techniques, which have come into common use in the last 25 years or so, have revolutionized our understanding of brain function. In PET scans, a biologically active radioactive tracer is injected into the subject (for the brain, this is usually a form of glucose). The tracer is metabolized by the brain and in doing so, positrons are emitted. The more active the brain structure, the greater the positron emission. Sensors detect the positrons through gamma radiation and then a computer can construct a three dimensional representation of brain activity based on tracer concentrations.

If we only use 10% of our brain, then a PET scan should look like Slide 2 in the accompanying PowerPoint slides. The blue outline is the skull, and the circle of color indicates active brain structures. Most of the brain would be dark because of inactivity. (You are looking down on top of this person's head). But that isn't how the PET scan actually looks. Slide 3 shows an actual scan of a healthy person. The entire brain is constantly active, even in periods of sleep: regulating, monitoring, sensing, interpreting, reasoning, planning, and acting. Even people with degenerative neural disorders such as Alzheimer's and Parkinson's disease still use more than 10% of their brains.

For a good video clip of a neuroscientist debunking the myth, as well as a case study of a man who only has 10% of his brain, see McDonald (2016).
Tracing the Myth's Beginnings
The origin of the 10% Myth is unclear, but some people attribute it to a misunderstanding of a statement in an article by William James (1907). The quote is below:

Most of us feel as if we lived habitually with a sort of cloud weighing on us, below our highest notch of clearness in discernment, sureness in reasoning, or firmness in deciding. Compared with what we ought to be, we are only half awake. Our fires are damped, our drafts are checked. We [p. 323] are making use of only a small part of our possible mental and physical resources.

Note that James is saying we often don't feel fully energized, both physically and mentally. He in no way claims that we only use a small portion of our brain. In fact, he was observing how decorum, social norms, and routine fail to engage all of people's resources. His statement is actually consistent with what we now know about attention and flow states, but James clearly was not claiming that most people perpetually use only 10% of their brainpower.
Related Brain Myths
There are numerous other myths about the brain that you may want to address. These include the following:

People are either left-brained or right-brained

Amnesia involves forgetting who you are

Brain development is finished by puberty

When we sleep, the brain is dormant

Brain damage causes permanent loss of function, especially in elderly people

Brain training increases IQ and slows brain deterioration

Brain function declines significantly in old age

Listening to Mozart or to baroque music helps increase IQ or learning

References
Hughes, S., Lyddy, F., & Lambe, S. (2013). Misconceptions about psychological science: A review, Psychology Learning and Teaching, 12, 20-31. doi: http://dx.doi.org/10.2304/plat.2013.12.1.20

MacDonald, F. (2016). This man is missing 90% of his brain yet lives a normal, healthy life. Business Insider. Downloaded from http://www.businessinsider.com/missing-90-percent-of-brain-neuroscience-2016-7

William James (1907). The Energies of Men First published in Science, N.S. 25 (No. 635), 321-332. http://psychclassics.yorku.ca/James/energies.htm
DAY 1: Understanding the Relationship between Brain and Behavior
The starting point of the unit is the 10% Myth itself. Consider assigning Assignment 1 below before the first class and centering the class on discussion of that assignment. This will prepare students to understand how all parts of the brain contribute to behavior.

Begin by showing Slide 1 in the accompanying PowerPoint deck and asking who has heard of the 10% brain myth and what they have heard about its validity.

Show Slides 2 and 3 to show how brain scans reveal how all parts of the brain influence behavior. The online article by McDonald (2016) links to a nice accompanying video of a neuroscientist debunking the myth in more detail. This article also discusses a rare case where a man has only 10% of his brain and it's unknown how he manages to live a fairly normal life.

The stage is now set to discuss various brain structures and their contributions to behavior. Have each member of a group explain what their assigned brain structure does and their answers to the assignment. Have the group decide which brain part they would most and least be willing to lose. You can also go over the major brain structures or the gross features of the brain. Slide 4 contains a concept map of the nervous system that can be shared with students and used to organize the presentations.
DAY 2
The second class meeting can take several different directions. A concept map of the entire topic of brain and behavior is included in the PowerPoint slides. One option is to discuss the lobes of the brain and the function of each, then discuss the structure and function of neurons, including axonal and synaptic transmission. This is a chance to talk about important case studies in neuroscience (e.g. Phineas Gage, H.M., and Clive Wearing), single cell recording techniques as well as advancements in brain scans. A second option is to introduce the evolution of the brain across species and comparative psychology. A third option is to discuss how neuroscience relates to the question of whether or not human free will exists. Assignment 2 (below) is designed to spark this discussion. If something goes wrong in someone's brain, are they really responsible for their actions?
DAY 3
The third class meeting can be for special topics. Discussing the brain can easily segue into a variety of discussions including:

sleep and dreaming, a topic that is always of interest to students;

drug effects at the synapse and different kinds of psychoactive drugs (again, always of interest to students);

split brain research and how it is often misunderstood by the general public;

brain plasticity, especially with regard to children or elderly people, and recovery from injury or disease;

brain training programs to enhance brain function and slow intellectual decline, and the lack of evidence of its effectiveness;

recent research on exercise to maintain brain health;

recent developments on deep brain stimulation and other potential neuroscientific treatments for diseases and disorders; and

research on traumatic brain injury, including recent work on contact sports such as football and boxing and the prevalence of brain injury in war veterans.

Concept Checks
The following formative assessment questions allow both you and the students to gauge their level of understanding of the unit. When using these concept checks, be sure have students respond individually so both you and the students can see how well the class understands the concepts. Then they can discuss as pairs or as a class. There are a variety of high tech (clickers) and low tech (fingers) methods that can be used to administer these concept check questions.
I. Which of the following statements is true?
A. When we are sleeping we only use 10% of our brain, but we use more when we are awake

B. All parts of the brain contribute to our mental life and behavior, so we are always using more than 10% of our brain***

C. Babies are born with only 10% of their brain formed, and it grows rapidly until puberty

D. The average person lives a life of unstimulating routine and habit and only uses about 10% of his or her brain on a regular day.

II. Say a person has brain damage to one of the four lobes of the brain (frontal, parietal, occipital, and temporal). Fill in the blanks to show which lobe you suspect is damaged if the person:

A. sees bright flashes of light, even with their eyes closed ____

B. can no longer comprehend the meaning of what people say ____

C. moves his or her arms around without being aware of it until seeing it ____

D. has developed paralysis in their leg and has trouble standing ____
Answers: A., occipital; B, temporal; C., parietal; D, frontal III. Damage to the amygdala is mostly likely going to make a person
A. forgetful

B. fearless

C. hungry

D. deaf

E. paralyzed
IV. You meet a man who can no longer learn new facts. He has ____ amnesia which is probably caused by damage to his ____.
A. anterograde; amygdala

B. anterograde; hippocampus

C. retrograde; amygdala

D. retrograde; hippocampus
Assignment 1 Brain and Behavior
Everyone is susceptible to brain damage through head trauma, a cerebrovascular accident such or stroke, a brain tumor, or other conditions. In this assignment, you will consider the behavioral and mental consequences of damage to a major part of your brain.

You are to imagine that you have sustained a serious brain injury to a particular part of your brain. Then, based on your readings and other resources, you should write a short but complete answer to each of the following questions:

1. What behaviors are associated with that part of the brain, and what are the possible consequences of damage or loss of that part?

2. How would the brain damage affect your life - specifically, how would it alter your current life and your life ambitions?

3. How and to what extent could you compensate for the loss?

In summary, you should describe in detail the behavioral consequences that the damage would have for you.

You will be broken up into groups of six. Each of you will be assigned a brain part. Just count off and see which brain part you get to have damaged. Use the table below.

Read the textbook description of these structures and their function. For additional help, here are some video resources from the "2-minute Neuroscience" on the YouTube channel Neuroscientifically Challenged: You are welcome to use other resources, but you are responsible for the credibility of these sources. Be sure to cite any external sources you use.

amygdala

https://youtu.be/JVvMSwsOXPw

hippocampus

https://youtu.be/5EyaGR8GGhs

language areas (Broca's and Wernicke's area)

https://youtu.be/zIo_500V1LM
https://youtu.be/03Xtiz_ikw4

cerebellum

https://youtu.be/Fir-v6EoZNE

basal ganglia

https://youtu.be/OD2KPSGZ1No

hypothalamus

https://youtu.be/TVhm2rBGhB0

(Note to teachers: There is nothing sacred about this set of brain structures or this set of video resources. Feel free to alter either.)
Your written responses are due by class time. On that day, you will explain what you have found with the members of your group. Bring copies to share with them in addition to the copy you will turn in to me.

Your answers should be based on information from credible sources. A good answer will reflect a thorough understanding of concepts, critical reflection and clear, coherent, persuasive arguments. Clarity, organization, and writing style count as well as references and content.
Assignment 2 The Brain, Free Will and Personal Responsibility
The assignment consists of three parts. Read and answer each part in order without reading ahead
Part 1
Consider the following scenario:

Taylor is at a party. When distracted, someone puts a psychoactive drug in Taylor's drink. Although normally easy going, the drug causes Taylor to become loud, aggressive, and violent. Taylor gets into an argument with other partygoers and assaults a couple of them before being subdued. Taylor is arrested, but once the drug wears off Taylor is appalled by the violence and deeply remorseful about the incident.

Should Taylor be arrested and tried for the assault? Why or why not? If yes, would you vote to convict if you were on the jury? Would your feelings be different if you were one of Taylor's victims? If Taylor is convicted, should Taylor be incarcerated for the assault and for how long? Explain your reasoning at each step.

Complete Part 1 before moving on to Part 2.
Part 2
Consider this scenario:

Taylor is normally easy going but over a period of months, becomes progressively more violent and aggressive. Finally, Taylor gets into an argument with other people at a party and assaults a couple of them before being subdued. Taylor is arrested, but a brain scan at the hospital reveals a brain tumor pressing on Taylor's hypothalamus. Once this tumor is removed, Taylor's aggressiveness vanishes. Taylor is appalled by the violence and deeply remorseful about the incident.

Should Taylor be arrested and tried for the assault? Why or why not? If yes, would you vote to convict if you were on the jury? Would your feelings be different if you were one of Taylor's victims? If Taylor is convicted, should Taylor be incarcerated for the assault and for how long? Explain your reasoning at each step.
Part 3
Did you react differently to the two scenarios? How is the first scenario different from the second one, or are they fundamentally the same?

Your answers to these questions bear on key questions of human nature. Do people really have free will or are they bound by their brain activity? It bears on how we view the causes of crime and other kinds of antisocial behavior. It has important implications on the question of personal responsibility in society. Do we always hold people personally responsible for their actions? If not, under what conditions do we excuse them? Can society function in a lawful and orderly way if we do not hold people personal responsible for their behavior? Finally, it has implications for society as a whole. What if we could detect brain structures or genes that make it likely a person will develop destructive behaviors. How should we treat that person?

This scenario is not hypothetical. Brain tumors can cause significant changes in mood and behavior. See these two resources:

And here are case studies of how brain tumors can cause aggressive behaviors:

For Part 3, reflect on your answers to Parts 1 and 2. Did you find a difference between the two scenarios? What do these articles say about our free will and choice? If our brain tells us to do something, can we somehow disregard it? What does this mean for our personal responsibility for our actions? Should "My brain made me do it" be a legitimate reason for all our behavior? How can we decide when we have a choice and when we are victims of our brain?

Write a short essay about these questions. Come prepared to discuss your views in class.
Discussion/Writing Assignment Sports, Concussions, and Brain Injury
Traumatic brain injury is a risk in many professions, and usually safety precautions - such as wearing helmets - are taken to minimize the risk. In some conditions, such as military combat, the risk of traumatic brain injury is high despite safety gear. Contact sports, such as American football and boxing, also carry the risk of head injury. In sports, however, participation often starts at an early age and people participate in it for enjoyment. Now questions are being raised about the cost of participating in contact sports in terms of concussions and long-term debilitating brain injury. Is the enjoyment worth the risk, especially for youth?

Complete one of these two assignments:

This is a PBS Frontline documentary on CTE, which is common among former professional football players and is now showing up in former collegiate and even some high school players.

Answer the following questions about the first part:

Mike Webster was the football player whose condition initiated the whole issue of concussions, repeated head trauma, and brain damage caused by football. Describe Mike Webster's life, his football career and the aftermath. Do you think he understood the risks and consequences of playing football for his brain health? Do you think the NFL acted appropriately and in the best interests of the players? Do you think the glory he experienced justified his later deterioration? If you had a child who wanted to play football or some similar contact sport, would you let him or her?

Answer the following questions about the first part:

Nick Buoniconti is an NFL Hall of Fame linebacker who played in the 1970's. This story and video describes his life now. Do you think he understood the risks and consequences of playing football for his brain health? Do you think the glory he experienced justified his later deterioration? He clearly has views on this now, but do you think young football players would think the same way? If you had a child who wanted to play football or some similar contact sport, would you let him or her?

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This notion seems firmly rooted in popular culture despite many efforts to debunk it (Hughes, Lyddy, & Lamb, 2013). It was the basis of the movie Lucy (2014), which depicted what supposedly would happen if a person actually used all 100% of her brainpower.

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ABSTRACT

Human papillomavirus (HPV) vaccine uptake consistently lags behind that of other adolescent vaccines. In 2017, uptake of a single HPV vaccine dose and HPV vaccine series completion was 66% and 49%, respectively, compared to uptake of tetanus, diphtheria, and acellular pertussis vaccine (89%) and quadrivalent meningococcal conjugate vaccine (85%). Reasons for not vaccinating adolescents again HPV are varied, and in many cases, are rooted in commonly spread myths and misperceptions about the vaccine. In this review, we address five key myths - HPV vaccination is not effective at preventing cancer; Pap smears are sufficient to prevent cervical cancer; HPV vaccination is not safe; HPV vaccination is not needed since most infections are naturally cleared by the immune system; 11-12 years of age is too young to vaccinate. For each myth, we summarize the scientific evidence refuting the myth and provide speaking prompts for healthcare professionals to communicate about HPV vaccination.

KEYWORDS: Human papillomavirus, HPV, vaccine hesitance, vaccine myths, vaccine misperceptions

Introduction

Human papillomavirus (HPV) vaccination was first recommended for use in the United States (US) for female adolescents and young adults in 20061 and male adolescents and young adults in 2009.2 Despite this, HPV vaccine coverage remains suboptimal, and lags behind that of other routinely recommended adolescent vaccines. In 2017, uptake of at least one dose each of tetanus, diphtheria, and acellular pertussis booster (Tdap) and quadrivalent meningococcal conjugate vaccine (MCV4) by United States (US) adolescents aged 13-17 was 89% and 85%, respectively. This stands in contrast to receipt of at least one dose of HPV vaccine (66%) and being up-to-date with the HPV vaccine series (49%).3 Vaccine hesitance has increasingly been identified as a key factor in suboptimal vaccine uptake, and this has been well-documented for HPV vaccination.

Previous research has identified multiple barriers to high acceptance and uptake of HPV vaccine, and earlier reviews have summarized the available evidence supporting HPV vaccination as a safe and effective cancer control method. Many of these reviews have focused on specific outcomes, such as reviewing and synthesizing available vaccine effectiveness data or broadly summarizing the current state of the knowledge about HPV vaccine. One review is notable in that it directly addressed a number of myths negatively impacting HPV vaccine perceptions and uptake.34 Since this review was published in 2013,34 there have been numerous advances in our knowledge of the safety and effectiveness of HPV vaccination.

This current review presents five common myths and misperceptions about HPV vaccination, followed by a summary of the evidence addressing each myth. This follow the same format as a series of presentations on this topic to healthcare providers in 2017-2018 (available for viewing for continuing medical education/continuing education credit at https://bit.ly/2RcoWnB).35 The material from these presentations has been summarized in this manuscript to provide healthcare providers and public health practitioners readily available access to evidence necessary to address specific concerns about HPV vaccine, while also providing speaking prompts for addressing these myths with patients. It is important to note that this review summarizes key findings in a manner designed to assist healthcare providers in speaking with parents about HPV vaccination, and is not a systematic review of all available evidence about the safety and effectiveness of HPV vaccination. In addition to the narrative review, Table 1 presents a series of speaking prompts to assist health care and public health practitioners communicate in response to these myths.

Table 1.

Myth

Speaking prompt to address the myth

"HPV vaccines were only tested against pre-cancers, and have not been shown to prevent cancer."

Because HPV-related cancers can take decades to develop, the initial clinical trials were conducted using pre-cancers as the endpoint. Continued monitoring over more than a decade of vaccine use has already found decreases in HPV cancer rates in those who have been able to get vaccinated.

"We have Pap smears, why do we need HPV vaccination?"

Pap smears have been very effective at reducing cervical cancer rates in the US. But, HPV vaccination can prevent more cancers than just cervical cancer, and can also prevent the pre-cancers that we look for when doing Pap smears, which can lead to less need for treatment for these pre-cancers.

"HPV vaccines have not been tested enough."

HPV vaccines were tested in clinical trials of tens of thousands of participants before they were approved for use in the US. And since 2006, when HPV vaccine was licensed and recommended, there have been many large studies, ranging from hundreds of thousands to over 3 million people evaluated, that continue to confirm the safety of HPV vaccination.

"HPV vaccines are very new, so shouldn't we wait to vaccinate?"

HPV vaccines were first recommended for use in the US in 2006, around the same time as two other common adolescent vaccines - the Tdap vaccine that prevents tetanus, diphtheria, and pertussis, and the meningitis vaccine. HPV vaccine is no newer than these vaccines.

"HPV vaccine is not safe - it can lead to death."

While there have been deaths reported to the CDC after HPV vaccination, these have been investigated and there is no evidence that the vaccine led to any of these deaths. In a large study of over 2 million adolescents and young adults who died within a year of receiving any vaccine, there was no consistent pattern of deaths after vaccination, and there was only one adolescent who died within a month of receiving HPV vaccine.

"HPV vaccine is not safe - it can cause autoimmune disease."

There have been multiple studies, ranging from hundreds of thousands to over 3 million people that have failed to find any consistent relationship between HPV vaccination and autoimmune diseases.

"HPV vaccine is not safe - it can cause ovarian failure."

This concern came out of a few small case reports that did not actually show a connection between HPV vaccination and ovarian failure. In fact, early ovarian insufficiency is more common than you might expect, affecting about 1 in 10,000 young women. In a study of almost 200,000 young women, 46 developed ovarian insufficiency, but none of those cases were associated with HPV or other routine adolescent vaccines.

"Our bodies do a good job of clearing HPV infections. 90% of them are taken care of by the immune system."

We are lucky that our immune systems can do such a good job of clearing HPV infections, and 90% of these infections are cleared this way. But HPV is such a common infection that even at this high level of clearance, there are still many women who cannot clear HPV on their own. Because we don't know who will or will not be able to clear HPV on their own, we want to vaccinate all adolescents to keep them protected.

"Isn't 11 or 12 years too young to vaccinate? Won't the vaccine wear off?"

HPV vaccination actually produces an immune response that is stronger than natural infection, and in follow-up from the large clinical trials, has been shown to persist steadily for at least 5 to 10 years. In fact, the vaccine works even better when given at younger ages, which is why we only need to give two doses before age 15 to get the same protection as three doses after 15.

"Isn't 11 or 12 years too young to vaccinate? Children aren't even sexually active, so they're not at risk for HPV."

We don't like to think about teenagers being sexually active, but we do know that about 16% of boys and 11% of girls have had sex by age 15, and about half have had sex by age 17. Vaccinating early gives us the best chance to protect them well in advance of any sexual activity. It's just like wearing a seatbelt - we put it on every time we get into the car, to make sure we are always protected.

"Isn't 11 or 12 years too young to vaccinate? Won't that send the message that they can be sexually active?"

This is a question that has been studied multiple times, and in every case, we have seen that adolescents who get HPV vaccine are no more likely to have sex or engage in high-risk behaviors than adolescents who do not get HPV vaccine.

Myth 1: HPV vaccine has not been shown to prevent cervical cancer

Because clinical trials supporting licensure of HPV vaccines used endpoints of HPV infection and pre-cancerous lesions or abnormal cytology, and not direct measurements of reduction in HPV-related cancers, it has been posited that it is incorrect to say that HPV vaccine can prevent cancer. Additionally, because the vaccine is considered to be a "new" vaccine that has not been tested long enough to show reductions in cancer, the effectiveness of the vaccine has been called into question.

Addressing myth 1

This misperception about HPV vaccine clinical trials does not account for the natural history of HPV infection and HPV-related disease development. While not all HPV infections or high-grade cytological lesions will lead to development of invasive cancer, these early outcomes are necessary steps in the causal pathway of cancer. It has been estimated that the proportion of cytological abnormalities regressing to lower grades or absence range from 57% for cervical intraepithelial neoplasia grade 1 (CIN1) to 32% for cervical intraepithelial neoplasia grade 3 (CIN3). However, that same review documented that whereas only 1% of CIN1 progress to invasion, 12% of CIN3 progress to invasion.57 Preventing these high grade lesions interrupts the natural history of HPV-related disease.58

Evidence for prevention of high-grade pre-cancers

The effectiveness of HPV vaccine continues to be studied in both continued follow-up of initial clinical trial participants and post-licensure studies. Initial clinical trials documented vaccine efficacy against vaccine-type cervical intraepithelial neoplasia grade 2 or higher (CIN2+) of 95% to 98%, and 100% against high grade vaginal and vulvar lesions. A recent evaluation of high-grade cervical pre-cancers in a surveillance site in Tennessee documented average annual decreases in CIN2+ of −24% in 18-20-year-olds and −10% in 21-24-year-olds in the HPV vaccine era.62

Evidence for prevention of cervical cancer

Early estimates of US national-level reduction in cervical cancer incidence were published in 2018 by Guo et al.63 That study compared cervical cancer rates between 2003-6 and 2011-14 for age groups for whom HPV vaccine has been recommended (15-24 years and 25-34 years of age). Relative to 2003-2006, cervical cancer rates were 29% lower in 2011-14 for 15-24-year-olds and 13% lower for 25-34 year-olds, with no differences observed in women aged 35 and older.63 In a long-term (up to 12 years post-vaccination) per-protocol follow-up of 2,084 women from the FUTURE II HPV vaccine clinical trial, only one breakthrough cytological abnormality (cervical intraepithelial neoplasia [CIN] grade 1 [CIN1]) was detected among those vaccinated, with no cases of invasive cancer identified.64

Effectiveness in preventing genital warts

As genital warts typically develop more quickly following incidence HPV infections than anogenital cancers, they provide a good model for early effectiveness studies. Genital wart incidence within 36 months of a new HPV-6 or HPV-11 infection is 64%.65 This rapid development of external lesions offers a mechanism for studying population-based HPV vaccine effectiveness in genital wart prevention. In clinical trials, HPV vaccination efficacy against genital warts ranged from 89 to 98%. Numerous post-licensure surveillance studies and reviews have also identified decreases in genital wart development among vaccinated populations, both through assessment of population-level differences relative to HPV vaccine uptake and through direct comparison of vaccinated and unvaccinated individuals.

One of the earliest studies to show decreases in genital warts after achieving high HPV vaccination was conducted in Australia, where HPV vaccine series completion rates for adolescent females reached 73% by 2010.73 The proportion of clinic visits for new genital warts cases declined from the period pre-2007 (before vaccine introduction) and 2011 (when surveillance for this study was completed) for women under 21 years (11.5% in 2007 to 0.9% in 2011), women 21-30 years (11% in 2007 to 3% in 2011), men under 21 years (12% in 2007 to 2% in 2011), men 21-30 years (18% in 2007 to 9% in 2011).66 This is notable because females younger than 21 years were the priority group for vaccination, and decreases in genital warts in other related populations provides evidence of breaks in the chain of transmission through community protection, otherwise commonly known as herd immunity.

HPV is not a "new" vaccine. At the time of this review (2018), HPV vaccination has been recommended for over 12 years in the US. HPV vaccine was first recommended1 within a year of two other routinely recommended adolescent vaccines - tetanus, diphtheria, and acellular pertussis vaccine (Tdap)74 and quadrivalent meningococcal conjugate vaccine (MCV4)75 - all of which are recommended for administration at ages 11-12 years.

Myth 2: pap smears are sufficient to prevent cervical cancer

Because Pap smears are an effective means of identifying cervical pre-cancers to trigger treatment, some have argued that they offer a better means for cervical cancer prevention than vaccination.50,52,79

Addressing myth 2

The impact of Pap smears on reducing cervical cancer incidence and mortality cannot be overstated. In every country where Pap smear testing has been implemented, the incidence rate of cervical cancer has significantly decreased. However, Pap smear testing can only identify cervical pre-cancers, and does not address other HPV-related anogenital cancers (vaginal, vulvar, penile, and anal cancer) or oropharyngeal cancers. Globally, cervical cancer is the most common HPV-related cancer, with over 527,000 new cases per year.82 While there are 12,000 new cervical cancer cases per year in the United States, there are also approximately 12,000 new cases of vaginal, vulvar, anal, and oropharyngeal cancers in women in the US each year, and nearly 19,000 new cases of anal, penile, and oropharyngeal cancers in men in the US each year,83 highlighting the non-cervical cancer burden of HPV

It is also notable that the same high-grade lesions (CIN grades 2/3 [CIN2/3]) that typically trigger initiation of treatment when discovered as part of Pap smears are the same high-grade lesions that were used as endpoints in many of the clinical trials. To accept the logic that these endpoints are not adequate to support HPV vaccination as a cancer prevention method would be akin to indicating that Pap smears have not prevented any cases of cervical cancer, but merely served as a mechanism to treat high-grade lesions without impact on cancer development.58

Myth 3: HPV vaccines are not safe nor have they be sufficiently tested

Concerns over the safety of HPV vaccine have been widely cited as a major parental barrier to HPV vaccine acceptance and adolescent and young adult HPV vaccine uptake.23,24,84-87 Additionally, concerns about vaccine safety have been widely disseminated through online channels, reaching wide audiences. This has included high-profile coverage of individuals who died after HPV vaccination. The main concerns raised about the safety of HPV vaccination have focused on death following vaccination, autoimmune and neurological conditions, and premature ovarian insufficiency (POI) or ovarian failure.

Addressing myth 3

Multiple clinical trial and post-licensure studies have identified a positive safety profile for HPV vaccination, with no associations identified for serious adverse events, and triggering appropriate updates to vaccination practices for other less severe adverse events following immunization.

Vaccine safety data from clinical trials

As summarized in the published recommendations of the Advisory Committee on Immunization Practices and the vaccine package inserts, HPV vaccine recipients in multiple pre-licensure clinical trials comprised of tens of thousands of participants were more likely to experience acute injection-site reactions (i.e. pain, swelling, redness at the injection site) than placebo recipients, but experienced systemic adverse events (e.g. headache, nausea) at similar levels to those seen in placebo recipients. Additionally, autoimmune disease incidence during the clinical trials did not differ between vaccine and placebo recipients.

Post-licensure general safety assessments

Routine post-licensure surveillance through both the Vaccine Adverse Events Reporting System (VAERS) and Vaccine Safety Datalink (VSD) have consistently found no safety signals or elevated risks of specified adverse events, with the exception of syncope. One large study (over 600,000 HPV vaccine dose administrations) identified a significantly elevated risk of syncope following HPV vaccination.107 This is in-line with VAERS-based surveillance that found higher reporting of syncope after adolescent vaccines in general.108 These findings supported recommendations that adolescents remain seated or laying down for 15 minutes after vaccination to prevent falls and fall-related injuries.108

Post-vaccination deaths

Post-licensure surveillance of deaths after HPV vaccination through VAERS identified no consistent association between HPV vaccine receipt and death, in terms of dose, timing, or cause of death. These findings have been supported through a VSD analysis of deaths in the 30 days after vaccination among 9-26-year-olds. That study found no association between vaccination and death within that 30-day window, for any vaccines evaluated.110

No evidence of increased autoimmune and neurological conditions

Numerous large studies have been conducted to evaluate the potential for increased risk of autoimmune disease after HPV vaccination. These include evaluations of nearly 350,000 HPV vaccine dose administrations,111 270,000 girls,112 568,000 boys,113 nearly 1,000,000 adolescent females aged 10-17 years114 and 3,100,000 adult females aged 18-44 years115. While a few significantly elevated relative risks for autoimmune disease development were identified in some studies (Bechet's syndrome, Reynaud's disease, Type 1 diabetes in one study116; celiac disease in one study115; vitiligo and narcolepsy in one study113), there were no consistencies in the outcomes for which elevated risks were identified, the time period after vaccination in which the outcomes developed, or the vaccine dose proximal to the outcome, and no causal association could be identified for any of these condition. One explanation for these elevated risks in administrative data analysis is the potential of unmasking, whereby the medical encounter at which vaccination was administered also triggered other examinations that led to diagnosis with the autoimmune condition after vaccination.117

No evidence of POI

Concerns about POI have been promulgated primarily through animal models, case reports, or ecological analyses evaluating pregnancy rates as a function of the proportion of the population vaccinated against HPV, but not through large epidemiologic studies. In 2018, a large managed care organization-based study of nearly 200,000 females aged 11-34 years found no association between adolescent vaccination and POI. In this study, there were 120 diagnoses adjudicated, with 46 confirmed POI diagnoses. No significantly elevated risks for POI were estimated for receipt of any of four vaccines, including HPV vaccine. Notably, only 1 case received HPV vaccine prior to symptom onset.

Myth 4: HPV vaccines are unnecessary because most people clear HPV infections naturally

Because estimates from HPV natural history research have identified that approximately 90% of new HPV infections are cleared by the immune system within two years, the need for HPV vaccination has been erroneously called into question, in favor of natural immunity.

Addressing myth 4

HPV acquisition, particularly after the onset of sexual activity, is often rapid. Notably, in a cohort of university women, 39% had at least one new incident HPV infection within 2 years of study enrollment, and more than 60% had a new incident infection after 5 years.120 In continued follow-up of this population, approximately 90% of incident HPV infections were cleared by the immune system within two years of detection. These estimates of HPV acquisition and clearance were similar to those identified in a separate cohort of newly sexually active females.119 However, for HPV infections that do not clear, there is also often a rapid development of HPV-related cytological changes and genital wart development. While more than half of low-grade (CIN1) and one-third of high-grade (CIN3) will regress even if untreated, more than half of CIN3 will persist, and approximately 12% will progress to invasion.57

While the 90% clearance estimate represents a substantial proportion of HPV infections, it needs to be put into context of the number of HPV infections that occur. Assuming approximately 32,568,000 females aged 15-29 years in the United States in 2017,123 with a 24-month incidence of vaccine-type HPV of 32.3% in the absence of vaccination,118 we would expect over 10.5 million new cases of HPV infection over a two-year period. Even if 90% of these are cleared by the immune system, there will still be more than one million women with persistent infections that could progress to cytological abnormalities.

Myth 5: 11-12 years of age is too young to vaccinate

Multiple concerns have been raised about recommending and administering HPV vaccine at ages 11-12 years. First, there are concerns about whether vaccination at 11-12 years of age will last long enough to protect individuals when they may be exposed to HPV in later adolescence and adulthood.124 Second, because HPV is most commonly spread through sexual activity, opposition has been raised to vaccinating pre-teenagers because of a perception that they do not need to be vaccinated if they are not sexually active. Notably, this perception is held by both parents ("It's like blaming a kid before they even get a chance to do anything") and healthcare providers ("I rarely give it at 11 or 12. I most commonly give it in the like 8th, 8th to 10th grade range when sexual activity would put them at risk, rather than just an age. This is what I tell parents: it's very different than other vaccines because you can quantify your risk by what you're doing.").125 Third, concerns have been raised that early vaccination sends a message that adolescents now have permission to become sexually active.

Addressing myth 5

There are many reasons why HPV vaccination is recommended at ages 11-12 years of age, including the strength of the immune response at younger ages, inclusion in the broader adolescent vaccine platform, and vaccination prior to onset of sexual activity when individuals could be exposed to HPV infection.

High HPV vaccine immune response at earlier ages

Clinical trial data has documented that, for both males and females, receipt of HPV vaccine prior to 15 years of age results in HPV antibody titers approximately twofold higher than when vaccination is provided at 15 years of age or older.61 These findings, along with clinical trials showing sustained high antibody titers following two doses of HPV vaccine given at younger ages, led to the 2016 recommendation change for two vaccine doses for adolescents younger than 15 years of age.77

Sustained immune response and protection

HPV antibody titers have been documented to persist a minimum of five130 to eight131 years, based on available follow-up data, with statistical modeling estimating at least 20 years of antibody persistence.130 Antibody titers do decline from their peak, with a plateau approximately 18 months after the vaccine series is complete. Notably, even with this decline, vaccine-induced antibody concentrations are approximately an order of magnitude higher than antibody titers following natural HPV infection.132 In a per-protocol analysis of 2,084 women from the FUTURE II HPV vaccine clinical trial, sustained effectiveness was noted for up to 12 years post-vaccination, with only one breakthrough cytological abnormality (CIN1) detected among those vaccinated.64

The 11-12-year-old vaccine platform

Three vaccines - HPV vaccine; tetanus, diphtheria, and acellular pertussis vaccine (Tdap)74; quadrivalent meningococcal conjugate vaccine (MCV4)75 - are recommended for administration at ages 11-12 years. High coverage of both Tdap and MCV43 indicate that adolescents are seeking medical care where vaccines are administered, highlighting the potential for increasing HPV vaccine through reduction of missed opportunities. Concomitant administration of these vaccines can reduce missed opportunities, and lead to higher coverage of all adolescent vaccines.133

Vaccination prior to onset of sexual activity

HPV vaccine is most effective when given prior to the onset of sexual activity, when exposure to HPV may occur. Data from the National Survey of Family Growth estimates that 11% of females and 16% of males had sexual debut by 15 years of age, with the average age at first sexual intercourse of 17 years.134 Vaccination before age 13 is important, as the Youth Risk Behavior Surveillance System estimates that 2% of female and 5% of male adolescents had sexual debut before age 13.135

These statistics highlight the importance of early vaccination. The notion that because a child is not sexually active, they do not need to be vaccinated against HPV ignores the goal of vaccination - to stimulate an immune response prior to exposure to reduce the likelihood of disease development. The idea that 11-12 years of age is too young to vaccinate because a child is not at risk of sexual activity is akin to the idea that because the likelihood of a motor vehicle crash is low, it is unnecessary to wear a seat belt prior to being involved in a car crash.

HPV, while being the most common sexually transmitted infection,136 is not exclusively sexually transmitted. HPV is an epithelial virus, and can be spread by skin-to-skin contact, not requiring sexual intercourse or fluid transfer.137 A recent systematic review highlighted non-sexual and non-penetrative sexual modes of transmission of HPV, including digital-genital contact, fomites (including sex toys, ultrasound wands, and reusable specula), and shared clothing. While rare, these findings do highlight the ability of HPV to spread without sexual activity.138

HPV vaccine does not increase sexual promiscuity

Numerous studies, including parental and adolescent/young adult surveys about post-vaccination behaviors, evaluations of age at sexual debut and number of sexual partners among HPV vaccinated and unvaccinated individuals, and evaluations of clinical outcomes (e.g. sexually transmitted infection incidence, pregnancy) related to sexual activity among HPV vaccinated and unvaccinated individuals, provide consistently reproducible evidence that HPV vaccination is not associated with increased sexual activity. Prior systematic reviews have summarized these data to support the lack of association between HPV vaccination and promiscuity.

Conclusions

There are numerous reasons why parents may be hesitant to vaccinate their children against HPV, and why healthcare providers may be hesitant to strongly and consistently recommend HPV vaccination. Five of the most common and impactful myths related to HPV vaccination (HPV vaccine has not been shown to prevent cervical cancer; Pap smears are sufficient to prevent cervical cancer; HPV vaccines are not safe nor have they be sufficiently tested; HPV vaccines are unnecessary because most people clear HPV infections naturally; 11-12 years of age is too young to vaccinate) have been summarized here, with links to examples of how these myths can be spread through social media or other platforms. For each of these myths, we have presented the key findings that refute these myths, to give healthcare providers readily available access to these key findings to facilitate communication within the clinical practice.

Improving the ability of providers to communicate about vaccines, including assessments of optimal timing for vaccine discussions, can lead to an increase in parental vaccine confidence. Notably, this fits in with recently developed multi-level theoretical models addressing a broader systems perspective for promoting preventive behaviors, by addressing barriers as the healthcare practice-, provider-, and patient-levels concurrently.151

One method for improving provider communication - taking a presumptive announcement approach to vaccine recommendations (e.g. "Your child is due for three vaccines - meningitis, HPV, and Tdap - and we are going to vaccinate them today") - has been shown to improve vaccine uptake relative to a more conversational approach.152 However, parents may still have questions based on myths and misperceptions they have been exposed to. Key evidence to address these myths has been summarized above, and speaking prompts - designed to not contain detailed statistics or medical jargon - have been presented to assist in these communications.

This review has some limitations. It is a narrative review, designed to provide direct access to key parts of the vast, and ever-growing evidence base supporting HPV vaccination. It was not designed as a systematic review, but rather as a summary of current evidence that healthcare providers can use as a readily available source of information to help support their conversations with patients and parents. Future avenues of research should include more targeted systematic reviews of the data addressing each of the myths presented in this manuscript, to allow a more rigorous accounting of the extensive evidence supporting the safety and effectiveness of HPV vaccination. Additionally, this manuscript does not include an exhaustive list of all myths and misperceptions that may be encountered regarding HPV vaccination, but presents the most common. While recent research has identified patterns in reasons for parental refusal over time,153 research such as this is still based on identifying the top reason why parents refuse, and may miss the spectrum of related reasons that exist concomitantly. Surveillance of reasons for HPV non-vaccination, accounting for the breadth of reasons for refusal, needs to continue, to ensure that these reasons are well understood, to allow for development of appropriate responses and communication strategies to help healthcare providers speak with parents about these concerns.

Time and time again, the safety and effectiveness of HPV vaccination has been confirmed through well-conducted research. However, the spread of misinformation through social media channels can overwhelm efforts by public health and medical practitioners to address those misperceptions. With recommendations existing to develop better communications tools, social engagement, and mass media utilization to address vaccine hesitance,159 we have sought to distill the large amount of HPV-related information available into usable speaking prompts, with supporting references to provide additional information and context. This is in-line with recommendations for addressing misinformation that call for clear and easy to process communications, to avoid cognitive overload.160

Funding Statement

This work was supported by the Centers for Disease Control and Prevention [NH23IP000960]; National Institute of Allergy and Infectious Diseases [K01 AI106961].

Acknowledgments

Dr. Bednarczyk is supported by a grant (K01AI106961) from the National Institute for Allergy and Infectious Diseases, National Institutes of Health. Funding for the development and initial dissemination of the presentation from which this manuscript is based was provided by the Centers for Disease Control and Prevention, cooperative agreement number, NH23IP000960. The views expressed in this manuscript and related presentations do not necessarily reflect the official policies of the Department of Health and Human Services, nor does the mention of trade names, commercial practices or organizations imply endorsement by the US Government.

Portions of the content related to this manuscript have been presented at the American Society for Colposcopy and Cervical Pathology annual meeting, the University of Calgary Pediatric Infectious Disease Conference, meetings of the Georgia and Florida Chapters of the American Academy of Pediatrics, the Georgia Association of Family Physicians, grand rounds at Emory University and Midtown Medical Center (Columbus, GA), as well as the Texas Immunization Conference, Finger Lakes (NY) Immunization Conference, Western New York Immunization Conference, New Jersey Immunization Conference, and the Immunize Georgia annual conference.

Disclosure of potential conflicts of interest

Dr. Bednarczyk has no conflicts of interest to report.

References

22. Palmeri S, Costantino C, D'Angelo C, Casuccio N, Ventura G, Vitale F, Pojero F, Casuccio A. HPV vaccine hesitancy among parents of female adolescents: a pre-post interventional study. Public Health. 2017;150:84-86. doi: 10.1016/j.puhe.2017.05.009. [[ PubMed] [ CrossRef] Google Scholar]

66. Ali H, Donovan B, Wand H, Read TR, Regan DG, Grulich AE, Fairley CK, Guy RJ. Genital warts in young Australians five years into national human papillomavirus vaccination programme: national surveillance data. BMJ. 2013;346:f2032. doi: 10.1136/bmj.f1164. [[ PubMed] [ CrossRef] Google Scholar]

82. Bruni L, Albero G, Serrano B, Mena M, Gómez D, Muñoz J, Bosch FX, de Sanjosé S ICO/IARC Information Centre on HPV and Cancer (HPV Information Centre). Human papillomavirus and related diseases in the world. Summary Report. 2018. [accessed 2018 September 27]. http://hpvcentre.net/statistics/reports/XWX.pdf.

134. Abma JC, Martinez GM. [ Sexual activity and contraceptive use among teenagers in the United States, 2011-2015. Hyattsville (MD): National Center for Health Statistics; 2017. [ Google Scholar] PubMed]

Articles from Human Vaccines & Immunotherapeutics are provided here courtesy of Taylor & Francis

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Addressing HPV vaccine myths: practical information for healthcare providers

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Human papillomavirus (HPV) vaccine uptake consistently lags behind that of other adolescent vaccines. In 2017, uptake of a single HPV vaccine dose and HPV vaccine series completion was 66% and 49%, respectively, compared to uptake of tetanus, diphtheria, and acellular pertussis vaccine (89%) and quadrivalent meningococcal conjugate vaccine (85%).

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When Is Too Much Information Dangerous for your Health?

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When Is Too Much Information Dangerous for your Health?

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Plastic Straws vs. Paper Straws and the Carbon Footprint

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Plastic Straws vs. Paper Straws and the Carbon Footprint

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The server comes up to you, pours a glass of water and lays a straw down. You take the straw out of its wrapper and come to the unfortunate revelation that it is made out of paper. The paper straw is no one's first choice but we need to save the sea turtles, right? Paper straws are way better for the environment... right?

Turns out, paper straws might not be as eco-friendly as you might think.

Straws don't just magically appear on our tables or in our drinks. There is a lot that goes into the creation of a single straw. Materials need to be harvested, refined, and transported. Processes require energy, chemicals, and workers. So, let's see how our straws stack up.

Paper straws, as the name suggests, are made out of paper. Paper comes from trees, but we need to chop them down first to make paper. The transporting of lumber requires large diesel trucks to haul the logs to the paper processing plant. There the logs are transformed into craft paper that can be shipped off to a straw production company. Finally, the paper is cut and glued together, and you have a finished straw. This process requires a surprising amount of energy. Each paper straw made requires about 96 kilojoules of energy and emits 4.1 grams of carbon pollutants. However, these numbers mean nothing without something to compare them to.

The process of making plastic straws is no better than that of their paper counterpart. Instead of starting in a forest, this time we begin our journey in an oil field. While the process of turning oil into plastic is far more damaging to the environment, the distance the raw materials need to travel is significantly shorter, cutting out a large amount of transportation related pollutants. With all this in mind, what are the numbers? Each plastic straw produced will need around 39 kilojoules of energy and output 1.5 grams of carbon emissions.

You read that right, paper straws produce almost three times the amount of carbon dioxide. (In , we've shared sources ((2020)) that say it is more like 5.4 times as much.)

At double the energy usage and nearly 3X ~ 5X the emissions, paper straws seem to be a far worse choice when it comes to eco-friendly straws. However, there is another trait to consider: biodegradability.

Plastic is as bad as it gets when we talk about waste decomposing. It floats around our oceans and sits in landfills practically forever, but what about paper straws?

While most paper straw producers advertise their products as "biodegradable", this is only partially true. The materials that most paper straws are made out of will decompose under very specific conditions, but all bets are off once the straw makes it to a landfill. If a paper straw is mixed in with other trash and shipped to a landfill, the protective chemical treatment needed to maintain the quality of the straw results in emissions from disposal being greater than that of plastic.

Do we have our answer? Are plastic straws better for the environment than paper straws? Is there anything paper straws are better at? Well, yes. The very thing so many of us complain about when using a paper straw. They disintegrate in water. This means that if a paper straw were to end up in an ocean, it would turn into mushy pulp instead of sticking

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Paper vs. Plastic: The (brief) Surprising Truth About Paper Straws.

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You walk into a restaurant and sit down at the table. The server comes up to you, pours a glass of water and lays a straw down. You take the straw out of its wrapper and come to the unfortunate revelation that it is made out of paper.

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Most people have heard about genetic testing when it comes to cancer risk, but there is a lot of misinformation. Today, gynecologic oncologist Casandra Liggins, MD joins us to bust the myths about genetic testing and share the facts.
MYTH #1: Most Cancers are Genetic
FALSE. The majority of patients who develop cancer do not have a genetic predisposition. "Genetic inheritance plays a role in approximately five to ten percent of cancers," Dr. Liggins explains. When it comes to breast cancer in particular, five to ten percent of breast cancer patients have an identified gene, although another ten to 15 percent of patients will have a familial correlation, even though the gene is not present.
MYTH #2: Everyone Should Get Genetic Testing for Cancer
FALSE. Given the limits of genetic testing, it does not make sense for the general population to get tested. "It's not always beneficial, nor informative," Dr. Liggins explains. Genetic testing recommendations are established by the National Comprehensive Cancer Network (NCCN) and other organizations that look at the data and adjust guidelines on a yearly basis.

Dr. Liggins adds that the risk of cancer is more influenced by environmental factors and lifestyle choices (the largest threats being obesity and smoking) than it is by genetics. For that reason, the focus for the majority of the population should be on those preventable factors.
MYTH #3: BRCA gene mutations only relate to breast cancer
FALSE. Mutations in the BRCA 1 and 2 genes are linked to various cancers, including breast, ovary, prostate, pancreatic, and melanoma. People who inherit harmful variants of a BRCA gene have increased risks of developing one of these cancers, and also tend to develop cancer at younger ages than people who do not have a variant.
MYTH #4: If I have a BRCA1 or BRCA2 gene mutation, I will get cancer (and if I do not, I will not)
FALSE. "Genetic inheritance is just a piece of the puzzle," Dr. Liggins says. "Having an inherited genetic mutation in any gene can increase an individual's lifetime risk of cancer, but does not guarantee an individual will get cancer."

The National Cancer Institute provides an example: "About 13% of women in the general population will develop breast cancer sometime during their lives. By contrast, 55%-72% of women who inherit a harmful BRCA1 variant and 45%-69% of women who inherit a harmful BRCA2 variant will develop breast cancer by 70-80 years of age."
MYTH #5: Only women need genetic testing
FALSE. Many common cancers in men are genetically linked, specifically pancreatic, prostate, and colon cancer. By finding out their genetic profile, both men and women can take steps to reduce their risk in other areas and start cancer screening earlier, if needed, which could save their life. "Cancer is not gender specific," Dr. Liggins reminds us.

MYTH #6: Genetic testing is not accurate

FALSE. The companies performing genetic testing for cancer have standardized and accurate testing. "No test is 100% accurate," says Dr. Liggins, "But we have come a long way in our ability to identify inherited genetic mutations, and the field will continue to develop."

Genetic testing at its current stage has helped many people identify inherited gene mutations and take actionable steps to reduce their cancer risk and catch cancer early, if it does develop. The fact remains that genetic testing saves lives.
MYTH #7: I do not need a genetic counselor; I can order my own genetic test online
MOSTLY FALSE. It's true that you can order direct-to-consumer genetic tests. However, without consulting a genetic counselor, you won't know what information to take away from your results. "Genetic counselors are crucial in helping to understand the results of genetic testing," Dr. Liggins says. "They also provide recommendations about what to do if a mutation is identified, as well as how and what to communicate to other family members." A genetic counselor can also help you better understand your cancer risk if an inherited mutation is not identified through testing.
MYTH #8: Genetic testing is expensive
FALSE. With next-generation sequencing technology, the cost has dropped dramatically. "Genetic testing is much more affordable today than it used to be," Dr. Liggins says. Insurance covers testing for most patients who meet the criteria. If not, most companies offer a cash pay price of only around $250.
MYTH #9: If my results show a gene mutation, I will be uninsurable
FALSE. "The Genetic Information Nondiscrimination Act (GINA), passed in 2008, prevents health insurance companies from using genetic information to make coverage or rate decisions," Dr. Liggins explains. A genetic counselor can provide additional information prior to genetic testing.
MYTH #10: Genetic testing and genomic testing are the same thing
FALSE. Genetic testing helps to assess a person's cancer risk. It consists of looking for a germline mutation, which is a gene mutation passed down from a parent to a child, and would be contained in just about every cell.

Genomic testing tests tumor tissue to look for genetic mutations that will determine a cancer's likely behavior. It is used to help doctors choose which treatments will be most effective against that tumor.

Do you still have questions about genetic testing? Visit our genetic testing FAQs or contact us to see if genetic testing for cancer might benefit you.

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Most people have heard about genetic testing when it comes to cancer risk, but there is a lot of misinformation. Today, gynecologic oncologist Casandra Liggins, MD joins us to bust the myths about genetic testing and share the facts. MYTH #1: Most Cancers are Genetic FALSE.

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Widespread Misinformation About Infertility Continues to Create COVID-19 Vaccine Hesitancy

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This Medical News article discusses ongoing misinformation that COVID-19 vaccines affect fertility and pregnancy outcomes.