Category Archives: health

Chickenpox and Shingles Vaccines SHORT

This is the short version. For the long version with references, click here.

Varicella virus

What are chickenpox and shingles?

Chickenpox is a highly contagious rash caused by varicella zoster virus. Chickenpox infection generally confers lifelong immunity. You may develop an infection without symptoms, and this also generally confers immunity. It is normally a very mild rash illness and only very rarely causes serious complications; children with eczema are not at increased risk of complications. Death is very rare. However, in otherwise healthy adults, the chickenpox complication rate is 15-25 times higher and the death rate is 20 times higher.

After a chickenpox infection, the virus hibernates in a nerve. In times of stress or immune suppression, the virus may reawaken and cause shingles. (You cannot catch shingles. You can catch chickenpox, which might later develop into shingles if your immunity is low.) Shingles is associated with 4-5 times higher complication rate and medical costs than chickenpox.

Chickenpox vaccines are typically given twice in early childhood in North America, Germany, and Australia. The shingles vaccine is given to older adults. Most of the developed world does not use these vaccines.

How can I prevent or treat chickenpox and shingles in my child?

Because chickenpox is mild in childhood but potentially serious in adulthood, many people choose to intentionally expose their child and get it over with in childhood. If you choose to do this, avoid people with immune suppression, pregnant women, and infants during the contagious period. Do not mail infectious material and do not intentionally expose others without their knowledge and consent.

It takes about 10-21 days after exposure for the first spots to appear. Chickenpox is contagious from about 2 days before the spots appear to as much as 7 days later, when the spots are all crusted over. A fever often occurs for one or two days before the first spots appear. To prevent infection, avoid children with chickenpox, fever, or unidentified rash.

The vaccine contains a live virus. There have been several reports of people developing chickenpox with vaccine-strain virus shortly after a close contact was vaccinated. To prevent infection, avoid people who have recently been vaccinated against chickenpox or shingles.

Exposure to chickenpox acts as a natural “booster shot” to protect adults against shingles. If you or your child have had chickenpox or the vaccine, prevent shingles by seeking exposure to chickenpox.

You can treat chickenpox with calamine lotion and daily baths with soap and water. Do not use aspirin, Tylenol, or Benadryl (diphenhydramine), and do not use lotions that have diphenhydramine in them. Use ibuprofen to lower a fever only if the fever is over 106°F (41.1°C). You should generally not take steroids during a chickenpox infection; if your child is on steroids, talk to your doctor about whether to stop the steroids until he recovers. Use anti-infectives such as silver nitrate and essential oils on the spots to prevent bacterial infection. If he develops a secondary fever after the spots have appeared, seek immediate medical attention.

How effective are the vaccines at preventing asymptomatic carriage?

Vaccinated people can have asymptomatic infections with both vaccine-strain and wild-type varicella viruses, and have proven to be contagious during that time. However, whether the vaccine reduces, increases, or has no effect on the degree or duration of asymptomatic carriage is unknown.

How effective are the vaccines?

The chickenpox vaccine is more effective when fewer children receive it because natural exposure to chickenpox boosts immunity, so vaccinated children get a natural “booster shot” from their unvaccinated friends. However, in communities where chickenpox vaccination is widespread, effectiveness drops to very low levels within a few years. A few studies found it to be completely ineffective or even reverse-effective (increased the chickenpox rates). When the vaccine fails, people tend to get chickenpox at an older age, when it is more dangerous.

Since exposure to chickenpox boosts immunity and prevents shingles, researchers predicted that widespread chickenpox vaccination would increase shingles rates. They were proven right by numerous studies in many countries using the vaccine. Because shingles is much more dangerous than chickenpox, the vaccine results in overall increased complication rate and medical costs, so the vaccine is neither effective nor cost-effective. Furthermore, the addition of new booster shots and shingles vaccines to fix this problem is not cost-effective and is associated with a higher complication rate than if children had been permitted to get chickenpox naturally.

The shingles vaccine may be as much as 51% effective and last 1 month to 5 years, necessitating numerous booster shots. It is less effective in people over 70 and completely ineffective in people over 80. Exposure to a child with chickenpox would be much more effective and much safer.

Are there other infectious diseases related to chickenpox/shingles vaccination?

MMR vaccination indirectly resulted in increased severity of chickenpox. This increased severity is part of why the CDC recommends chickenpox vaccination. However, most of Europe still agrees that the risks of chickenpox vaccination far outweigh any possible benefit.

What are the risks of the vaccines?

Adverse reactions to the chickenpox vaccine are at least equal to, and some research shows is greater than, adverse reactions to chickenpox infection. The combination MMR and chickenpox vaccine causes a higher fever and more seizures than MMR and chickenpox vaccines given separately. Chickenpox vaccination increases the risks of shingles, multiple sclerosis, heart disease and heart attacks, and brain tumors.

The shingles vaccine is associated with a very high rate of adverse reactions, especially in the oldest groups. The vaccine also causes severe autoimmune reactions, including a doubled risk of arthritis and tripled risk of alopecia.

So what’s the bottom line?

Chickenpox is very mild in childhood and has some long-term health benefits (e.g., decreased risk of multiple sclerosis, heart disease/heart attack, brain tumors), but poses much greater risk and fewer benefits in adulthood. Vaccination may merely delay chickenpox infection until adulthood, when it has considerably more risk. Natural chickenpox infection and repeated exposure to chickenpox decreases the risk of shingles. Conversely, chickenpox vaccination has very low effectiveness against chickenpox, increases the risk of shingles, and results in more severe shingles occurring at younger ages. Shingles is much more dangerous than chickenpox. The shingles vaccine does not appear to be very effective, but research is very limited; it is not effective in the oldest groups and is not yet approved for people under 50. Both vaccines are associated with some serious adverse effects, especially the shingles vaccine.



Chickenpox and Shingles Vaccines

This is a continuation of a series I’ve been helping to write for an education forum. This is the LONG version. For the short version, click here.

Image result for chickenpox virus

Varicella virus

What is chickenpox? What is shingles?

Chickenpox (varicella) is a highly contagious illness caused by a virus known as varicella zoster virus. Cases tend to peak in winter and spring. You can also have chickenpox and develop immunity without ever developing symptoms. Generally speaking, chickenpox infection confers lifelong immunity. In children, chickenpox is generally very mild and only very rarely causes serious complications. However, in otherwise healthy adults, the complication rate is 15-25 times higher. Childhood chickenpox causes death in roughly 1 per 40,000 infections, so the risk of death from chickenpox in the U.S. is lower than the risk of death by lightning strike. However, the death rate from adulthood chickenpox infection is 20 times higher. In fact, even though children make up over 98% of chickenpox cases, adults make up almost half of chickenpox deaths [1-3]. Children with eczema are not at increased risk of complications [1].

After a chickenpox infection, the virus hibernates in a nerve. In times of stress and immune system dysfunction, the virus may reawaken and cause shingles. Shingles is associated with 4-5 times higher complication rate and medical costs than chickenpox [3].

In the U.S., the chickenpox vaccine is given at 12-15 months and again at 4-6 years [4]. The shingles vaccine is recommended for people over the age of 60 [5].

In Canada, the chickenpox vaccine is given alone or with the MMR at 12 mo, 15 mo, 18 mo, and/or 4-6 years, depending on the province [6]. The shingles vaccine is recommended for adults aged 50 and over [7].


How can I prevent chickenpox and shingles in my child?

A longstanding practice is to intentionally expose children to chickenpox because the infection is almost always harmless in children, but much more serious in adults. This practice is regarded as rarely harmful, but poses some risk of exposing immunocompromised people, with the exception that children with a planned exposure can have planned isolation during the potentially contagious period while children with an accidental exposure cannot. If you plan to intentionally infect your child, you should avoid immunocompromised people, pregnant women, and people with severe lung disease until you know for certain that your child is not contagious [1-2]. Also, if you choose to intentionally infect your child, be aware that mailing infectious material is highly illegal, in part because it is unknown how many people might be unknowingly exposed. Exposure is therefore best done in person.

It takes about 10-21 (usually 14-15) days after exposure to chickenpox before you develop the first spots; fever often occurs before the spots appear. The spots disappear within 7-10 days. Chickenpox is most contagious between 2 days before and 3 days after the start of the rash; but it is generally considered that children with chickenpox are contagious until at least 5 days after the onset of the rash or until all of the spots are dry and crusted. It is mainly contracted by direct contact with the spots, but it can be airborne as well. You can also catch chickenpox from direct contact with shingles lesions, but shingles is far less contagious. (You cannot catch shingles from shingles. But you can catch chickenpox from shingles. This is because the first time the virus causes an outbreak in you, it’s always chickenpox.) [1] To prevent chickenpox, avoid exposure to children with chickenpox, fever, or unidentified rash.

The chickenpox vaccine is a live virus vaccine, meaning the virus in the vaccine is capable of causing a chickenpox infection. There have been reported cases of people contracting the disease from a recently-vaccinated individual. For example, one pregnant woman contracted vaccine-strain chickenpox after her child was vaccinated [8]. In another case, an adult woman received the vaccine and both she and her children shortly afterward developed vaccine-strain chickenpox [9]. In yet another very alarming case, a woman who did not develop any symptoms, such as the characteristic rash, passed the vaccine-strain virus on to her newborn, who developed chickenpox [10]. The shingles vaccine is also a live virus [11] and so can be presumed to shed as well. To prevent chickenpox, you should also avoid individuals who have recently received the chickenpox or shingles vaccines, as they should be considered just as contagious as someone who has an asymptomatic chickenpox infection.

However, ironically, the exact opposite should be done to prevent shingles. Regular exposure to chickenpox acts as a natural “booster shot” to protect adults against shingles [12-15]. In fact, working in childcare reduces your chances of developing shingles by 94% [12]! (That’s FAR more effective than the vaccine, as you’ll see later.) If you have been infected with the chickenpox virus in the past, then to prevent shingles, you should seek exposure to chickenpox.


How can I treat chickenpox and shingles in my child?

Even though exposure to chickenpox boosts immunity, and exposing a child with an active infection to people who are already immune would boost their immunity and benefit them by reducing their risk of shingles, it is considered unethical to intentionally expose someone without their knowledge. Thus, you should isolate your child during the contagious period, except to people who are aware of your child’s contagiousness and willing to expose themselves. You should also keep your child away from people who are at higher risk of complications, such as infants, pregnant women, and immunocompromised people.

Generally speaking, you can give anti-fever medicine if your child develops fever. However, research has shown that Tylenol is not effective for chickenpox [1]. Other research has shown that anti-fever medicine degrades some of the immune response and makes the illness last longer, and so giving anti-fever medicine may be counterproductive [16, 17]. Do not give aspirin, which may cause a serious disorder called Reye’s syndrome in children with chickenpox. If you do give aspirin and your child develops vomiting, go to the emergency room, as this is a sign of Reye’s syndrome [1]. In short, Tylenol doesn’t work, ibuprofen might be counter-productive, and aspirin might be dangerous. In other words, it’s probably best not to use anti-fever medicine unless the fever is over 106°F (41.1°C) [18].

Do not give Benadryl, including any creams that have Benadryl in them, because Benadryl toxicity has often been reported in children with chickenpox [1]. Calamine lotion can give effective symptom relief, but make sure it doesn’t have Benadryl (diphenhydramine) in it. Daily baths with soap and water can also help destroy the virus and prevent bacterial infection [1].

Children with eczema are not at increased risk of complications. However, it’s important to note that a steroid cream should not be used during chickenpox, so if a child’s eczema is being treated with a steroid cream, you should stop using the cream while he has chickenpox [1].

An antiviral drug called acyclovir may shorten the length of the illness and reduce its severity, but does not reduce contagiousness. However, it does not reduce complications and has to be started no later than the first day of the rash because if it is started on or after the second day, it is ineffective [1]. Acyclovir also does not reduce complications in adults [2].

The most common complication, occurring in 1-4% of chickenpox infections, is a bacterial infection of the spots [1]. This should be prevented by keeping the spots clean, not breaking them open, and treating them with an anti-infective such as silver nitrate or certain essential oils. A brief fever before the spots appear is common. But if a second fever occurs several days after the spots appear, your child may have a serious bacterial infection and you should seek immediate medical attention [1].

Chickenpox may rarely cause pneumonia. You can prevent this by boosting your child’s immune system during the outbreak and having him breathe in an anti-infective such as certain essential oils. However, if your child develops difficulty breathing or starts looking sicker after he had started to get better (e.g., tired/lethargic, feverish, etc.), you should seek immediate medical attention [1].


How effective are the vaccines at preventing asymptomatic carriage?

Some studies have found that children who were vaccinated may develop shingles with the wild-type virus [19-20]. In other words, even though they never had symptomatic chickenpox, they apparently had an asymptomatic infection with the wild-type virus. This means vaccinated individuals can have asymptomatic infections with the wild-type virus in spite of having been vaccinated. Furthermore, as mentioned earlier, there has been at least one recorded case of an asymptomatic individual passing on vaccine-strain virus to her newborn child [10].

So, in short, vaccinated people can have asymptomatic infections with both the wild-type and the vaccine-strain virus, and can be contagious during that time. However, whether the vaccine affects the degree or duration of asymptomatic contagiousness has not to my knowledge been studied with the chickenpox vaccine. (Other studies have found that some vaccines increase or decrease, but do not eliminate, the length of asymptomatic carriage, as discussed in my previous posts on pertussis, meningococcal, HiB, and pneumococcal.)

Until proven otherwise, vaccinees should be considered at equal risk of asymptomatic carriage.


How effective are the chickenpox and shingles vaccines?

The chickenpox vaccine has highly disputed effectiveness. Because natural exposure to children with the infection boosts immunity, the vaccine is more effective when fewer children receive it [12-15, 21]. We also know, for example, that vaccinees can get both chickenpox [8-9] and shingles [19-20, 22] from the vaccine virus.

A Japanese study reported that 34.2% of chickenpox-vaccinated children developed symptomatic chickenpox within 7 years after vaccination. The study did not continue after 7 years, but it can presumably affect more children who are further away from the date of their vaccine. The study also did not look for evidence of asymptomatic infection. The authors concluded that the vaccine may reduce the severity of the symptoms but is not strong enough to prevent infection [23]. A South Korean study found that chickenpox cases actually increased after the vaccine was introduced, and that symptoms were not milder in vaccinated children [24].

Since exposure to chickenpox boosts immunity and prevents shingles, researchers had long predicted that a decrease in chickenpox might cause an increase in shingles, estimating that it would result in an overall increased mortality rate (because shingles is more dangerous), with the increased disease and complications from shingles cancelling out any benefit from decreased chickenpox [12, 25-26]. In fact, this was the primary reason why nearly all European countries have chosen to forgo chickenpox vaccination. Some researchers even argued that it is unethical to vaccinate children against chickenpox, knowing that it will result in increased overall morbidity and mortality [27].

The researchers who predicted an increase in shingles were proven right when numerous studies in multiple countries using the chickenpox vaccine (including North America, Southeast Asia, and Australia) found that shingles cases increased and occurred in younger and younger ages, that cases of severe complications from shingles increased and occurred in ever younger ages, that chickenpox also occurred at younger and younger ages, and that chickenpox vaccination overall increased complications and medical costs—in other words, it was neither effective nor cost-effective [14-15, 21, 28-34].

Because the vaccines had very little effectiveness and also increased the incidence of shingles, it was necessary to add a booster shot [21] and later a shingles vaccine. The addition of these new vaccine doses is not cost-effective and is associated with a higher rate of complications than if vaccination had never been started [21].

According to CDC, the shingles vaccine lasts 5 years [5]. However, the research is less than inspiring. The study conducted by the shingles vaccine manufacturer, Merck, found that it was at best 51% effective, but many of the patients were only followed for 31 days [11], so all we know for certain is that it might cut your risk in half for the first month after receiving it. Furthermore, they found it to be less than 40% effective for those aged 70 and older, while in people over 80 years old, the vaccine was only as effective as placebo—in other words, completely ineffective [11, 35]. It is also not effective at preventing postherpetic neuralgia (i.e., shingles pain) [35].


Are there other infectious diseases related to chickenpox and shingles vaccination?

After the MMR (measles-mumps-rubella) vaccine was introduced, cases of encephalitis (serious brain inflammation) due to measles, mumps, and rubella essentially disappeared. However, it was replaced with an even greater number of encephalitis cases by other bacteria and viruses that both had and had not been previously associated with encephalitis, including chickenpox encephalitis. Furthermore, these new cases of encephalitis occurred in younger age groups, which post more serious risks [36]. In other words, MMR vaccination triggered more dangerous chickenpox infections, and one of the CDC’s cited reasons for chickenpox vaccination is the potential for severe complications like encephalitis [37]. In most of Europe, it is still argued that because chickenpox is very mild in childhood and very severe in adulthood, and the increased shingles risk offsets any potential benefit, there is no justification for routine childhood chickenpox vaccination [38].


What are the risks of the vaccines?


Some research suggests that adverse events from varicella vaccination are at least equal to the adverse events of chickenpox infection that the vaccine prevented—in other words, there is no net change in adverse events between nearly 100% natural infection rate and nearly 100% vaccination rate [14].

In one study, systemic adverse reactions occurred in 11.9% of the vaccinated children [24]. The manufacturer reports that the vaccine has caused some of the same serious side effects associated with the wild-type disease, such as pneumonitis [10]. There is a combination MMR and chickenpox vaccine called ProQuad which is associated with higher fever and seizure rates compared to children who get MMR and chickenpox vaccination separately [39].

Shingles. Non-immunocompromised individuals can also develop vaccine-strain shingles as shortly as 2 years after vaccination [19-20, 22].

Indirect risks include the following:

Multiple Sclerosis. There is an increased risk of MS in people who contract measles, mumps, rubella, or chickenpox at a later age [40]. Because the vaccines wear off and therefore put the individual at increased risk of infection at a later age, there is an indirectly increased risk of MS in children who receive the vaccine at a young age.

Heart Disease/Attacks. There is a decreased risk of heart disease such as coronary artery disease (CAD) and heart attacks in people who had chickenpox in childhood. Chickenpox reduces the risk of heart disease and heart attacks by 33% [41]. Thus, indirectly, chickenpox vaccination may increase the risk of heart disease and heart attacks.

Brain Tumors. People who have had chickenpox in childhood have a lower risk of certain aggressive brain tumors called gliomas [42-44]. Thus, indirectly, chickenpox vaccination may increase the risk of brain tumors.



One study by the manufacturer of the shingles vaccine, Merck, reported a relatively high adverse reaction and severe adverse reaction rate following shingles vaccination. The complication rate was especially high in those over 80 years old [11, 35].

The shingles vaccine has been noted to cause severe autoimmune reactions, including a doubled risk of arthritis and a tripled risk of alopecia [45]. The manufacturer study also found that people who received the shingles vaccine at the same time as the pneumonia vaccine had less of an immune response [11].

Another study of a newer shingles vaccine that is not currently available in the U.S. found that adverse reactions occurred in 84% of vaccine recipients within 7 days, and adverse reactions that were severe enough to prevent daily activities occurred in 17% of vaccinees [46].


What vaccines are offered against chickenpox and shingles?

(NOTE: These ingredients lists are not complete; they only list the most alarming ingredients.)

Chickenpox (Varicella)

  • ProQuad (U.S.). MMRV (measles-mumps-rubella-varicella) vaccine. Contains live measles, mumps, rubella, and varicella viruses. Ingredients include chick embryo, aborted human fetus lung cells (WI-38), aborted human fetus cells (MRC-5), cow serum, human albumin, monosodium L-glutamate (MSG), human albumin, and neomycin [39].
  • Varivax (U.S.). Varicella-only vaccine. Contains live varicella virus. Ingredients include human embryonic cells, aborted human fetus lung cells (WI-38), guinea pig cells, DNA and protein from aborted human fetus cells (MRC-5), monosodium L-glutamate (MSG), EDTA, and neomycin [10].
  • Varilrix (AU). Varicella-only vaccine. Contains live varicella virus. Ingredients include aborted human fetus cells (MRC-5), human albumin, lactose, cow products, and neomycin [47].


Shingles (Herpes Zoster)

  • Zostavax (U.S.). Contains live varicella virus. Ingredients include porcine (pig) gelatin, monosodium L-glutamate (MSG), residual DNA and protein from MRC-5 (aborted human fetus) cells, neomycin, and calf serum [11].


So what’s the bottom line?

Chickenpox is very mild in childhood and has some long-term health benefits (e.g., decreased risk of multiple sclerosis, heart disease/heart attack, brain tumors), but poses much greater risk and fewer benefits in adulthood. Vaccination may merely delay chickenpox infection until adulthood, when it has considerably more risk. Natural chickenpox infection and repeated exposure to chickenpox decreases the risk of shingles. Conversely, chickenpox vaccination has very low effectiveness against chickenpox, increases the risk of shingles, and results in more severe shingles occurring at younger ages. Shingles is much more dangerous than chickenpox. The shingles vaccine does not appear to be very effective, but research is very limited; it is not effective in the oldest groups and is not yet approved for people under 50. Both vaccines are associated with some serious adverse effects, especially the shingles vaccine.



















































Pneumococcal Vaccine (Pneumonia, Meningitis)

This is the LONG version. See also the SHORT version here.


S. pneumoniae

What are the “meningitis vaccines”?

There are two basic types of meningitis: viral and bacterial. There are no vaccines targeting viral meningitis. There are three vaccines targeting causes of bacterial meningitis: HiB, pneumococcal, and meningococcal. Meningococcal was Weekly Topic 03, HiB was Weekly Topic 05, and pneumococcal will be discussed here.

There are two types of pneumococcal vaccines: conjugated (PCV) and unconjugated (PPSV). PPSV were the first created and are thus the oldest, but were generally recommended only in adults until very recently. PCV are newer and recommended primarily in children. According to the CDC Vaccination Schedule (2015), pneumococcal vaccination (primarily with PCV, followed by one PPSV dose) occurs at 2, 4, 6, and 12-18 months; if the series begins at 12 months, only two doses are recommended, and if it begins at 24 months, only one dose is recommended [1, 2]. In Canada, depending on province/territory, pneumococcal vaccination occurs typically at 2, 4, and 12 months, with a few recommending an additional 6 month dose and/or moving the 12 month dose to 18 months [3].


What is pneumococcus?

Streptococcus pneumoniae, often referred to as pneumococcus, is a bacterium and “one of the most extensively studied microorganisms” [4, p. 591]. It was first isolated in 1881 by Louis Pasteur himself. Some strains have capsules while others do not, but when simultaneously infected with both a capsular strain and a noncapsular strain, the noncapsular bacteria steal the capsular bacteria’s DNA and thereby create a capsule and convert to the same strain as the capsular bacteria. It’s also possible for capsular bacteria to steal other capsular bacteria’s DNA and begin making a new capsule. Since the capsule is how the serotype (strain) is determined, this is termed “serotype switching” or “capsular switching.” Capsular bacteria are 105 times more virulent than noncapsular strains. Based on unique characteristics of their capsules, the bacteria can be divided into over 90 serotypes. The serotypes vary drastically by geographic area; for example, in the 1980s, researchers found that the same 20 serotypes that are responsible for ~90% of infections in the U.S. and Europe were responsible for less than 70% of infections in Asia. Antibiotic resistance or sensitivity also varies significantly by geographic region, though they are generally sensitive to penicillins. [4, 5]

S. pneumoniae is commonly carried asymptomatically by healthy people, though the rates vary by population. For example, carriers may make up 20-60% of school-aged children, 5-10% of adults without children, and 50-60% of military personnel [5]. A study that tested several hundred children for pneumococci approximately every four weeks for two years found that 54% became carriers at least once by age 6 months and 97% became carriers at least once by age 2 years [6]. Carriage seems to be more common after influenza infection [4] and is more likely when the patient has recently had sinusitis, has one or more older siblings, is enrolled in daycare, or lives in the city [7]. One study of penicillin-resistant pneumococcus found asymptomatic carriage ranged from 3 days to 267 days (median 19 days) [8] and one study in mice found that lower number of bacteria was associated with longer carriage while a higher number of bacteria was quickly cleared [9]. Different serotypes are carried for different lengths of time and one study found that the duration of carriage ranged from 5.9 weeks (serotype 15C) to 19.9 weeks (serotype 6B), and that longer duration of asymptomatic carriage correlated to a lower incidence of disease [6]. Pneumococcal disease mostly occurs after new infection with a new serotype rather than after a long period of asymptomatic carriage [4]. Because carriage is so common, disease is relatively very rare.

The incubation period for pneumococcal infections is only 1-3 days and the symptoms include a sudden onset of fever and chills or rigors, as well as pleuritic chest pain; cough with rusty, mucousy sputum; shortness of breath; rapid breathing; low oxygen levels; rapid heart rate; malaise (general feeling of sickness); and weakness. Less commonly, patients also experience nausea, vomiting, and headaches [5]. It is the most common cause of pneumonia in adults; and is one of the most common causes of bacterial meningitis in children and adults, alongside the HiB and meningococcal bacteria discussed previously [4]. S. pneumoniae is also a common cause of otitis media (middle ear infections) [5].

Vaccines targeting S. pneumoniae were first developed in the early 1900s but were not effective and had many adverse effects. A more effective vaccine was developed in the 1930s, but the interest in antibiotics led to the vaccine being largely ignored, rarely used, and ultimately removed from the market. New pneumococcal vaccines were developed in the 1970s and 1980s. [4]


How can I prevent or treat pneumococcal infection in my child?

Conditions that make an individual more susceptible to pneumococcal disease include recent viral infection, immune suppression, and a generally unhealthy lifestyle [4]. Infection and carriage cannot be prevented (discussed later), so the best prevention of disease is to boost the immune system, avoid people who are sick, and engage in a generally healthy lifestyle.

The destruction of S. pneumoniae releases the toxin pneumolysin, which causes inflammation, and this toxin-mediated inflammation is thought to be responsible for the symptoms of pneumococcal disease. Furthermore, the bacteria also produce hydrogen peroxide, an oxidant which causes further damage and is thus also responsible for some of the symptoms of pneumococcal disease. This peumolysin- and hydrogen peroxide-mediated damage is thought to be responsible for enabling the bacteria to migrate into the lungs or bloodstream, causing pneumonia or invasive disease; the bacteria may migrate to the meninges and cause meningitis either through the bloodstream or directly through the nasopharynx (nose and throat). Furthermore, the pneumolysin damages the cilia in the host’s throat, making it more difficult to move mucus up and out, similarly to pertussis. Also similarly to pertussis, antibiotics attack the bacteria but do not repair the damage and thus may shorten the contagious period or prevent disease if given before symptoms develop but do not improve the progression of the disease or the outcome if given after symptoms have already developed. In fact, by killing the bacteria and thus releasing more of the bacteria’s pneumolysin toxin, antibiotics may actually worsen the disease. [4] Furthermore, unfortunately, the most common strains are also the strains most commonly antibiotic-resistant [7]. Addressing this inflammation and oxidation directly by the use of a safe anti-inflammatory and anti-oxidant that is also effective in the treatment of pertussis—such as vitamin C [10]—may help alleviate some of the symptoms and prevent progression to pneumonia and invasive disease.


How effective are the vaccines at preventing asymptomatic carriage?

“These three factors—increased carriage of vaccine-targeted strains, increased carriage of dangerous strains, and increased carriage of other bacteria—suggest ironically that vaccinated (not unvaccinated) children pose significant risk to the vulnerable members of the population and that vaccination therefore should not be relied upon for herd immunity.”

Pneumococcal carriage occurs among vaccinated individuals in proportions similar to unvaccinated individuals. For example, the CDC states, “Studies comparing patterns of pneumococcal carriage before and after PPSV23 vaccination have not shown clinically significant decreases in carrier rates among vaccinees” [5] and a study on PCV7 found that the overall rate of carriage did not change because the decrease in vaccine-targeted serotype carriage occurred alongside an increase in non-vaccine serotypes [11]. The same study found that there was no change in the distribution of asymptomatically carried PPSV23-targeted serotypes, in agreement with the CDC [11]. The CDC goes on to say that carriage of the vaccine-targeted strains may be reduced in recipients of the PCV [5], though it says nothing of serotype replacement (i.e., whether those serotypes are simply replaced by different serotypes, having no net effect on carriage rates). However, studies have demonstrated that extensive serotype replacement occurs with the PCV, with increased carriage occurring in the vaccinated. One study found carriage of nonvaccine serotypes to be 79% in vaccinated children vs. 42.5% in unvaccinated children; another found 39% in vaccinated vs. 21% in unvaccinated; and similar findings have been recorded in other studies [12]. Another study found the overall carriage rate did not change due to simultaneous increases in non-vaccine serotypes and decreases in vaccine-targeted serotypes [13].

The rate of carriage of vaccine-targeted strains is higher among those more recently vaccinated. For example, one study of asymptomatic carriage in children found that 73.1% of the isolates in children <2 years old, 68.9% of the isolates in children 2-5 years old, and 51.2% of the isolates in children >5 years old were vaccine-targeted strains. [7] This indicates that the vaccine increases the risk of asymptomatic carriage of the vaccine-targeted strains. This same study found that all of the invasive strains found in these asymptomatic carrier children were vaccine-targeted strains [7], indicating that vaccinated children may be more likely to be infected with a dangerous strain (because they are less likely to develop disease from it). Another study that compared carriage rates in the same communities before and after widespread use of the PCV7 found that the rate of carriage increased in those younger than 6 months (those most recently vaccinated) and decreased in those older than 36 months (those least recently vaccinated) [11]. Interestingly, this study also found that carriage of H. influenzae B (HiB) slightly and Moraxella catarrhalis significantly increased in the same timespan [11]. Another study duplicated those results, finding no change in S. pneumoniae carriage and increase in M. catarrhalis carriage. It also found that the vaccinated children were more likely to be carriers of pathogenic (disease-causing) bacteria [14]. Yet another study found that decreased pneumococcal carriage is associated with increased Staphylococcus aureus carriage, suggesting that pneumococcal vaccination may result in increased Staph infections [15].

These three factors—increased carriage of vaccine-targeted strains, increased carriage of dangerous strains, and increased carriage of other bacteria—suggest ironically that vaccinated (not unvaccinated) children pose significant risk to the vulnerable members of the population and that vaccination therefore should not be relied upon for herd immunity.

As discussed previously, pneumococcal asymptomatic carriage is more common after influenza infection. [4] I’m unaware of any studies on the effect of the live virus intranasal FluMist influenza vaccination on pneumococcal carriage in humans, but it’s reasonable to believe that FluMist recipients may be more susceptible to pneumococcal carriage than those who received an injected influenza vaccination or no influenza vaccination. This theory holds up to a study in mice, which found that live influenza vaccination increases carriage of S. pneumoniae and Staphylococcus aureus [16].


How effective is the pneumococcal vaccine?

The pneumococcal vaccines are said to protect against otitis media (ear infections), pneumonia, meningitis, and sepsis. If the infection moves past the ears and/or lungs to infect the normally sterile linings of the lungs (empyema), meninges of the brain (meningitis), or the blood (sepsis), it’s referred to as invasive pneumococcal disease (IPD). To explain the effectiveness of the pneumococcal vaccines, we’ll consider:

  1. Special Populations (in whom the vaccines may have varying efficacy),
  2. Serotype Replacement and Capsular Switching (which helps the bacteria avoid the pressures of the vaccine),
  3. Otitis Media, and
  4. Invasive Pneumococcal Disease, which will encompass
    • Pneumonia,
    • Meningitis, and
    • Sepsis

1. Special Populations

Unfortunately, the vaccine is not very effective at producing an antibody response in the populations that might benefit from it most: immune-suppressed patients (those lacking a spleen, infected with HIV, etc.), patients with frequent respiratory infections, the elderly, and young children [4]. Furthermore, after the introduction of the vaccine, there was an increase in drug-resistant IPD in the most susceptible populations (those aged <5 and 65+), and a decrease in drug-resistant IPD in the least susceptible populations (those aged 5-64) [17]. Another study in Alaska confirmed these findings, with an increase in the IPD rate in children under 2 and adults over 45, particularly in Alaska Natives, following PCV7 vaccination of infants and toddlers [13]. This poses particular danger to “the herd,” since the vaccine is associated with an increased incidence of disease in the populations most vulnerable to disease complications.

2. Serotype Replacement and Capsular Switching

It was thought that vaccination would be very effective because the majority of cases were caused by only a few serotypes [4], but some researchers warned that other serotypes may quickly move in to replace them (called “strain replacement” or “serotype replacement”) and that the new serotypes may be more dangerous [12]—in colloquial terms, it was a discussion of whether to fight “the devil you know or the devil you don’t.” They also warned that the pneumococci’s ability to switch its capsule in order to change serotype (“serotype switching” or “capsular-switching”) would mean that after infecting a host that had been vaccinated, the bacteria would simply change its serotype in order to avoid the host’s vaccine-induced defenses, a phenomenon called “vaccine escape” [12, 18] (as is the case with meningococcal bacteria [19]). Unfortunately, these researchers’ predictions were correct.

The CDC states that no change in serotypes was noted following the use of PPSV23 in adults [5]. However, serotype-replacement has been observed with the PCV, the first of which (PCV7) was licensed in 2000. For example, one 2004 CDC study examined only serotype 19A, a serotype not included in the PCV7, and found that it almost tripled in incidence between 1999 and 2004 (another study using the same data found that it more than quadrupled [17]), and that it had become more genetically diverse and more drug resistant. Furthermore, their results indicated that many clones (genetic bases) targeted by the vaccine took up the genetic code for the capsule of serotype 19A—in other words, the vaccine-targeted strains changed into serotype 19A, a strain not targeted by the vaccine, an example of capsular-switching as vaccine escape [18]; unfortunately, other studies have shown serotype 19A to be more dangerous, so the decrease in vaccine-targeted serotypes has nonetheless occurred alongside an increase in at least one more dangerous non-vaccine serotype [20]. Other studies have provided further evidence to support capsular-switching and oppose antibiotic-directed evolution as the causes of increases in non-vaccine serotypes [20, 21], though some studies have found that while drug-resistant bacterial samples decreased, drug-resistant infections caused by non-vaccine serotypes increased [13]. In most populations, serotype replacement occurs within 3-4 years after introduction of the vaccine [13].

[22] Note that this occurred in Salt Lake City, Utah, and may not be representative of the general population.

[22] Note that this occurred in Salt Lake City, Utah, and may not be representative of the general population.

The pre-licensure vaccine trials showed no changes in serotypes in response to vaccination. However, this was likely due to the fact that relatively few children were vaccinated in the trials, whereas post-licensure, the vast majority of children have received the vaccine. When the vaccine is used on a large scale, it pushes the serotypes to switch. [11, 12, 20] Populations where PCV7 use was widespread (such as Alaska Natives) experienced significant serotype replacement while populations where pneumococcal vaccination was low or moderate (such as Navajo and Australian aboriginal children) did not experience serotype replacement. In fact, the proportion of Alaska children receiving the pneumococcal vaccine was significantly higher than either the national average or any other individual state [13]. Ironically, this means the pneumococcal vaccine would be most effective in recipients if fewer children received it—the opposite of what is usually asserted.

Another potential issue is that some studies had incomplete data and so chose to extrapolate from the data they did have, essentially guessing about the data they didn’t have and using those guesses in their final results. For example, the 2004 CDC study mentioned above did not have the serotype data for all of the samples and so estimated the actual number and proportions of serotypes by extrapolating from the data they did have [17, 18]. It’s unclear how this affected the results.

Finally, and most likely to have the greatest effect on the results, many studies are of low methodological quality. A meta-analysis of studies on the effect of pneumococcal vaccination against pneumonia in older adults found that when only high-quality studies were included, the results were very homogenous: they all agreed that the vaccine is ineffective. However, when studies of all quality were included, the results were very heterogeneous: the effectiveness of the vaccine was uncertain. [23] In this regard, pneumococcal vaccine effectiveness studies mirror influenza vaccine effectiveness studies [24].

3. Otitis Media

“the vaccine slightly reduces the incidence of [ear infections] in some children, but increases the incidence of [ear infection] that is difficult to treat or comes back again and again”

At least 60% of acute otitis media (AOM) is viral, pneumococcus makes up about 25% of all AOM causes, and over 80% of children with AOM recover without antibiotics. The vaccine was not licensed for prevention of otitis media, though it was nevertheless widely advertised for that use since its introduction. It has been suggested that the vaccine was advertised for this purpose because ear infections are very common among vaccinated children while the more serious concerns of pneumonia and meningitis are very rare [25]. Although the drug manufacturer and others found the vaccine to result in a 6-7% reduction in AOM (there was approximately a 34% reduction in S. pneumoniae ear infections, but S. pneumoniae only caused 25% of ear infections pre-vaccine, so the total effect on ear infections was minimal) with simultaneous decreases in vaccine-targeted serotype AOM and increases in non-vaccine serotype AOM [14, 26, 27], it is not effective at reducing the incidence of recurrent ear infections [28]. Another study found that while pneumococcal ear infections decreased from 48% of ear infections to 31% of ear infections in pneumococcal-vaccinated children, other bacterial causes of ear infection doubled, more than replacing the drop in pneumococcal ear infections. Interestingly, one of the bacteria that increased was nontypeable H. influenzae [29] (for more information on HiB, please refer to our previous publication on that topic here). Other studies found increases in carriage of M. catarrhalis (which is more difficult to treat) and HiB, and that vaccinated children were more likely to be infected with pathogenic (disease-causing) bacteria, increasing the risk of antibiotic treatment failure and recurrent AOM [11, 14]. Another study found not only that there was no reduction in AOM among pneumococcal-vaccinated children, but also that pneumococcal-vaccinated children were more likely to have ear infections caused by Staphylococcus aureus, which poses serious concerns about antibiotic resistant ear infections caused by methicillin-resistant Staphylococcus aureus (MRSA) [15, 30]. Another study found no decrease in AOM in children who received pneumococcal vaccines compared to children who received hepatitis A or B vaccines [31], which may be an odd choice for comparison, given that the hepatitis A vaccine may cause AOM [32]; this means they compared the AOM rate after pneumococcal vaccines to the AOM rate after another vaccine which can cause AOM; as there was no difference in AOM rate between the PCV-vaccinated and Hep A-vaccinated children, this seems to indicate that PCV increases AOM rates. At any rate, that last odd study aside, the vaccine slightly reduces the incidence of AOM in some children, but increases the incidence of AOM that is difficult to treat or comes back again and again.

4. Invasive Pneumococcal Disease (IPD)

It’s difficult to say what impact the vaccine has on IPD because studies examining all serotypes have observed both a decrease [22] and an increase [21] in IPD. A study in Spain found the proportion of IPD cases caused by non-vaccine serotypes increased from 38% in the prevaccine period to 72% in the



postvaccine period with an increase in the total number of IPD cases [21]. Although about half of the children in the Spain study had received the PCV7, and this is suggested as a possible reason for the increase, the same phenomenon of sharply increased IPD (specifically due to non-vaccine serotype increases significantly outweighing the vaccine-targeted serotype decreases) was observed in Alaska as well, where the vast majority of the children had received the PCV7 (the proportion who had received at least 3 doses of PCV7 ranged from 88% in 2003 to 96% in 2006). Particularly interesting is that the proportion of IPD cases designated serious and requiring hospitalization also increased (i.e., IPD cases increased in number and became proportionately more dangerous) [13]. However, another 2004 study that looked at all serotypes found a simultaneous decrease in vaccine-targeted serogroups and increase in non-vaccine serogroups such that the total number of IPD cases did not change, though the proportion of cases caused by drug-resistant bacteria and the proportion of cases identified as serious or life-threatening increased. Especially important to note was that the cases caused by non-vaccine serotypes were the most severe [22], suggesting that the vaccine-targeted serotypes were replaced with more dangerous serotypes, which, as discussed above, researchers had previously warned might occur. It is interesting to note that the increase in drug resistance was noted in PCV7-targeted serotypes in one study [22] but in non-vaccine serotypes in another study [11], while another study found a decrease in drug resistance [21]. Another study found a decrease in drug-resistant bacteria overall but a total increase in drug-resistant IPD in young children and the elderly; and an increase in drug-resistant IPD caused by vaccine-targeted serotypes with the greatest increase in drug resistance in serotype 19A (the nonvaccine serotype which increased the most in overall number and proportion of cases) [17]. Other more recent studies have found further increases in both 19A and other non-vaccine serotypes as well as a further increase in drug-resistant pneumococcal infections among the vaccinated but not among the unvaccinated, with the risk highest among those who’d received the most doses of vaccine [20].

Why are the results so variable between studies? It’s probably mostly an issue of which populations are included in the study. For example, the CDC study mentioned above, which found a drop in total IPD cases and apparently no change in the seriousness of IPD cases [17, 18], did not include the population reported by another study, where there was no change in total IPD cases and an increase in serious and life-threatening cases [22]. As discussed previously, the proportions of each serotype vary significantly from population to population, so the vaccine may be very effective in one population and very ineffective in another. If a study of the entire nation, which necessarily must sample various populations rather than including every single case across the country, selectively studies the populations where the vaccine is most effective, as the CDC apparently did (probably unintentionally, since they examined data from the designated CDC surveillance sites), this will skew the results. For this reason, I’m afraid all that can really be said is some studies found the vaccine to be productive and others found the vaccine to be counter-productive, and unfortunately we can’t really know which is true for the general population, nor can we accurately predict which populations will be most benefitted by the vaccine or most harmed by it. (And I know that statement will be unpopular with both pro-vaxxers and anti-vaxxers. Sorry, not sorry.)

A. Pneumonia

“…in children, the vaccine may increase or slightly reduce the incidence of pneumonia but increases the incidence of severe pneumonia that is more dangerous and more difficult to treat. [….] …pneumococcal vaccination does not prevent pneumonia in older adults… but was associated with an increase in severe pneumonia requiring hospitalization.”

In 2004, just four years after the PCV7 was licensed, researchers noted an increase in parapneumonic empyema (a very severe form of pneumonia where the lining of the lungs becomes infected, with mortality as high as 30% in non-immunocompromised patients) caused by pneumococci in spite of decreases in pneumococcal disease and pneumococcal pneumonia, data which confirmed previous studies [22]. A Cochrane Review from 2004 found no effect of PCV7 on clinical pneumonia rate [33] while the Cochrane Review from 2009 found that PCV7 slightly decreases the clinical pneumonia rate [34]. However, a more recent study from 2010 found that PCV7 vaccination was associated with an increase in drug-resistant pneumonia among the PCV7-vaccinated but not among the PCV7-unvaccinated [20]. As discussed above, serotype prevalence differs significantly from population to population and so the vaccine may be very effective in one population and very counter-productive in another. This was exemplified in Britain, where the PCV7 was introduced in 2006, and by 2008, health authorities noted that the incidence of empyema (very severe pneumonia) had risen significantly, due in part to the 10-fold rise in serotype 1 (not included in the vaccine). Though the rise in serotype 1 began before introduction of the vaccine and thus cannot be blamed solely on the vaccine, serotype-replacement surely contributed [35]. Spain also saw an overall increase in IPD in children under 2 after introduction of the PCV7, including a more than fourfold increase in pneumonia [21]. Alaska saw the same pattern, with an overall increase in pneumonia cases and an increase in the proportion of pneumonia cases that involved empyema [13]. In other words, in children, the vaccine may increase or slightly reduce the incidence of pneumonia but increases the incidence of severe pneumonia that is more dangerous and more difficult to treat.

A rigorous meta-analysis published in 2009 found that pneumococcal vaccination does not prevent pneumonia in older adults [23]. As in studies of children discussed above, the use of the PPSV in elderly adults was not associated with a decrease in pneumonia, but was associated with an increase in severe pneumonia requiring hospitalization [36].

B. Meningitis

A study in Spain found that though the rates of sepsis and pneumonia increased after introduction of the PCV7, the rate of meningitis decreased. Nevertheless, the decrease in meningitis cases was not great enough to offset the large increases in pneumonia and sepsis [21].

C. Sepsis

Also called septicemia or bacteremia and “blood poisoning,” this refers to a bacterial infection of the blood. A study in elderly adults found a decrease in pneumococcal sepsis following pneumococcal vaccination, but did not examine other potential causes of sepsis [36]. However, as early as 2004, researchers noted that the number of invasive pneumococcal disease cases did not change due to simultaneous decreases in vaccine-targeted serogroups and increases in non-vaccine serogroups, and there was an increase in cases of severe disease (those classified as “serious” or “life-threatening”) [22]. In 2005, researchers noted that though the overall pneumococcal IPD rate decreased, the proportion of IPD cases caused by non-vaccine serogroups increased (a form of serotype replacement), and the proportion of cases caused by drug-resistant bacteria increased [18]. Studies in other countries, such as Spain, confirmed some of these results. Oddly, the Spain study found that sepsis rates overall increased (from a per 100,000 population rate of 14.5 to 21.4 in children <2 and 1.5 to 5.8 in children 2-4) and the specific causes of sepsis that increased in incidence were S. pneumoniae, the species targeted by the vaccine, and E. coli [21]. A study in Alaska also found an increase in bacteremia [13].


So if it’s not effective, why did it get licensed and put on the CDC vaccine schedule?

Of the 12 committee members at the FDA responsible for determining whether to approve Prevnar for licensing, four had financial ties to the drug company making Prevnar. Of those four, three were granted waivers so that they could still vote. [37] For this reason, some believe the committee’s approval of the pneumococcal vaccine was largely a matter of bias. For a long time, Prevnar was the most expensive vaccine on the market. At one time, Prevnar alone accounted for 40% of the cost of vaccination according to the CDC schedule. Financially speaking, Prevnar performed exceptionally well compared to other vaccines.


Are there other infectious diseases related to pneumococcal vaccination?

The use of other bacterial vaccines, particularly pertussis, seems to have contributed to the sudden increase in HiB infections in the 1970s and 1980s. [38] This led to the creation of the HiB vaccine. However, the introduction of the HiB vaccine also seems to have caused the sudden increase in pneumococcal infections, which are more dangerous and less treatable than HiB. This led to the introduction of the pneumococcal vaccine. However, the introduction of the pneumococcal vaccine seems to have caused the sudden increase in meningococcal infections, which are more dangerous and less treatable than pneumococcal infections. This led to the introduction of the meningococcal vaccine. There is concern that meningococcal vaccination will also be followed by the sudden increase of another more dangerous and less treatable bacterial disease. [39, 40]


What are the risks of the vaccine?

Prevnar has a troubled history. As mentioned above, there were significant financial conflicts of interest in the licensing process. Furthermore, a whistleblower came forward in 2004 with allegations that the company was violating certain FDA rules regarding quality control [41]. Many in developing nations such as Argentina were apparently coerced into participating in the Prevnar vaccine trials under threat of having their children taken from them if they refused [42]. It was also halted or outright banned in many countries shortly after introduction due to severe adverse reactions, particularly death, including, but not limited to, the Netherlands [43], Portugal [44, 45], Japan [46], and India [47].

The drug company making Prevnar performed short-term safety studies in which Prevnar was compared to an experimental vaccine. Prevnar was found to cause more seizures and rashes, and higher fevers than the experimental vaccine. Prevnar was not compared to a placebo. [25, 37]

Please note that having had the vaccine once without any serious reactions does not mean serious reactions will not happen with future vaccination. For example, this article reported a case where a patient with previous pneumococcal vaccination nevertheless had a serious local reaction (severe pain and swelling that extended beyond the area of the injection) upon repeat vaccination [48] and, in fact, reactions are more common in those who have had the vaccine before than in those receiving the vaccine for the first time [49].

Seizures. One study conducted by the vaccine manufacturer found seizures to occur four times as often in children receiving the pneumococcal vaccine than in children receiving another experimental vaccine (it was not compared to a saline placebo) [25].

Asthma. One study found the incidence of asthma in pneumococcal-vaccinated children (2.96/1000) was nearly double the incidence in pneumococcal-unvaccinated children (1.66/1000). The authors postulated that this was related to “the hygiene hypothesis of decreased childhood infections” [50]. The hygiene hypothesis notes that children who have fewer childhood infections (including measles and hepatitis A) have a higher incidence of allergies and asthma, and hypothesizes that induction of a Th1 response early in life prevents or even reverses the imbalanced Th1/Th2 ratio in people who are prone to asthma [51].

Thrombocytopenia. The vaccine has been noted to cause relapses of immune thrombocytopenia [52].

Autoimmune Diseases. Pneumococcal vaccination has been shown to cause onset or rebound of the following autoimmune conditions: idiopathic thrombycytopenic purpura, peripheral and central demyelinating disease, Henoch-Schönlein Purpura (a form of leukocytoclastic vasculitis), Guillain-Barre Syndrome, minimal-change nephritic syndrome, neuromyelitis optica (a.k.a., optic neuritis), Sweet’s syndrome, autoimmune hemolytic anemia, systemic lupus erythematosus, migrating arthralgia, angioimmunoblastic lymphadenopathy with dysproteinemia (a type of lymphoma), and chronic fatigue syndrome. It has been involved in at least two cases of bullous phemigoid, myositis, but other vaccines were given simultaneously, so causation with pneumococcal vaccination cannot be demonstrated. These conditions have largely occurred following PPV rather than PCV, as the PCV is too new for most autoimmune conditions to have presented themselves and is given primarily in children, in whom many autoimmune reactions are missed due to age-related difficulty expressing or recognizing symptoms [53]

Local Reactions. Local reactions, such as severe pain and swelling that extends far beyond the area of the injection, have been reported to occur even in those who have previously received pneumococcal vaccination or had extensive laboratory contact with pneumococci with no previous reaction [48]. These local reactions may mimic cellulitis and have high white blood cell counts, leading to unnecessary hospitalization and antibiotic treatment if the treating physician is unaware that this is a typical, noninfectious reaction to the vaccine. A local reaction occurs in as many as 50% of vaccine recipients, with the highest rate in those who have previously had pneumococcal vaccination [49].

Apnea in Preemies. Apnea (temporary suspension of breathing) has been observed in premature infants who receive Prevnar. [54]

Bronchiolitis, Gastroenteritis, Pneumonia. Ironically, one of the most common serious adverse events following this pneumonia vaccine is pneumonia. [54]

Hypotonic-Hyporesponsive Episodes. This is similar to fainting; the child may be awake but have altered consciousness. This is one of the most common serious adverse reactions reported. [54]


What vaccines are offered against pneumococcal?

In the U.S., there are two pneumococcal vaccines, the PCV13 (the replacement for PCV7), which targets 13 strains and is recommended for children under 5 and adults over 64 (and those aged 6+ who are at high risk), and the PPSV23, which targets 23 strains and is recommended for adults over 64 (and those aged 2-64 who are at high risk). (NOTE: These ingredients lists are not complete; they only list the most alarming ingredients.)

  • Prevnar 13: diphtheria-pneumococcal (diphtheria CRM197 protein, pneumococcal 13 serotypes, soy, yeast, ammonium sulfate, polysorbate 80, aluminum) [54]
  • Pneumovax 23: pneumococcal (pneumococcal 23 serotypes, phenol) [55]


So what’s the bottom line?

The bottom line is that S. pneumoniae is so common that almost 100% of the population carries it at some point and develops some degree of immunity by age 2. There are over 90 serotypes, and the bacteria easily change their serotype (serotype switching) to avoid the host’s vaccine-induced defenses. The vaccine does not prevent asymptomatic carriage—in fact, it may increase asymptomatic carriage not only of S. pneumoniae but also of other bacteria—and so cannot contribute to herd immunity and may, in fact, pose greater risk to the herd. The vaccine is said to protect against ear infections, pneumonia, meningitis, and sepsis, but may actually be ineffective for all of these purposes due partly to serotype switching and serotype replacement, and partly to increases in other bacteria. The serotypes not covered by the vaccines are more dangerous, and so the proportion of serious infections is higher in vaccinated children than in unvaccinated children. Because it is mostly ineffective, the risks, no matter how mild, outweigh the benefit.





















[19] See the previous Meningococcal Weekly Topic located here:





[24] Per Cochrane Collaboration: “An earlier review of 274 influenza vaccine studies in all age groups (including most of the studies in this review) showed an inverse relationship between risk of bias and the direction of study conclusions. Conclusions favourable to the use of influenza vaccines were associated with a higher risk of bias. In these studies, the authors made claims and drew conclusions that were unsupported by the data they presented. In addition, industry-funded studies are more likely to have favourable conclusions, to be published in significantly higher-impact factor journals and to have higher citation rates than non-industry-funded studies. This difference is not explained by either their size or methodological quality (Jefferson 2009a). Any interpretation of the body of evidence in this review should be made with these findings in mind.”









[33] NOTE: The link provided goes to the abstract; however, the information about clinical pneumonia is in the full text of the article, not in the abstract.






[39] “Several factors indicate that mass immunisation with pertussis and other non-Hib vaccines may have been responsible for the unprecedented epidemics of invasive bacterial infections such as Hib, during the 1970’s and 1980’s.” (p. 315) Miller, N.Z. (2008). Vaccine Safety Manual.














[53] Shoenfeld, Y., Agmon-Levin, N., & Tomljenovic, L. (2015). Vaccines and Autoimmunity (pp. 193-195, 227, 323, 340, 346, 354). Hoboke, NJ: Wiley Blackwell.



Pertussis (Whooping Cough)

In another forum, I shared some very basic information on whooping cough. Recently, I was asked to post it in a place where it can be widely shared. So here it is!

Weekly Topic 02: Pertussis (Whooping Cough)

Thanks to the recent viral video of a baby with whooping cough, we’re doing pertussis this week.

In the United States, pertussis is currently the least well-controlled vaccine-preventable disease despite excellent vaccination coverage and 6 vaccine doses recommended between 2 months of age and adolescence. [E2]

What is whooping cough?

Whooping cough or “pertussis” is a coughing illness that usually lasts many weeks (“the 100-day cough”); when the child has the typical whooping cough symptoms, it’s called “classic pertussis.” Many pertussis infections are asymptomatic or present as the flu. For example, this study [1] found that among unvaccinated 10 year olds who had not had classic whooping cough, 64% had antibodies against pertussis toxin and 100% had antibodies against other pertussis antigens, indicating that 100% of unvaccinated children without history of whooping cough nevertheless had an infection but fought it off without symptoms. In this same study, they found that 61% of unvaccinated 10 year olds had had whooping cough, indicating that in a given population, about 60% will have classic pertussis and 40% will develop immunity by an asymptomatic or mild flu-like infection. Natural infection confers about 30 years of immunity [2], whereas the vaccine lasts at least one year for only 73% of recipients, and at least 2-4 years for only 34% [3]. When symptoms do appear (i.e., when the child actually gets classic pertussis), it is most severe in newborns.

Whooping cough or pertussis is caused by one of several bacteria:

  • Bordetella pertussis
  • Bordetella parapertussis
  • Bordetella holmesii

What is B. pertussis?

B. pertussis is the first bacteria we discovered that causes whooping cough. It was discovered in 1900 and is the only bacteria used for the whooping cough vaccine. Thanks to the vaccine, the bacteria has evolved and there are now two important strains to know about:

  • Pertactin-deficient or “Non-PRN” B. pertussis is a new strain that makes up 85% of B. pertussis in the U.S. today [4]. (EDIT: A later American study found 91.7% of tested B. pertussis isolates to be Non-PRN [E1]. However, this apparently varies by country and even by region within a country.) According to the CDC, those who are vaccinated are at higher risk of contracting this strain and the risk increases with more vaccine doses given [4]. EDIT: This was later confirmed by other research in humans [E2] and experiments in mice [E3].
  • PtxP3 B. pertussis is a new strain that produces more pertussis toxin and is therefore believed to be more dangerous. It was responsible for recent Australian outbreaks [5]. It is believed that the vaccinated are at higher risk of contracting this strain [6]. EDIT: This is supported by other recent research [E4]. Like Non-PRN B. pertussis, PtxP3 B. pertussis evolved in response to the vaccine. Since this strain first appeared right when whooping cough rates began increasing, it is thought to be the primary reason for the increased incidence of whooping cough [E5].
  • EDIT: The prevailing theory seems to be that the increase in pertussis rates in spite of higher-than-ever pertussis vaccination rates is due to a combination of the vaccine wearing off and vaccine resistance due to Non-PRN and PtxP3 strains [E5].

What is B. parapertussis?

B. parapertussis is another species that causes whooping cough. It was discovered in the 1930s. The vaccine may increase the risk of infection with this species 40-fold [7].

What is B. holmesii?

B. holmesii is a new species that causes whooping cough. It was discovered in 1985. The pertussis vaccine may increase the risk of B. holmesii (DTP) or have no effect on the risk of B. holmesii (DTaP) [8].

What is the popularity of these species and strains?

Knowing how common the different species and strains are can help us predict vaccine-induced risk. A study in Ohio in 2010 [9] found the proportions to be:

  • 42.3% B. pertussis (or mix)
    • estimated 36.0% Non-PRN
    • estimated 6.3% PRN+
  • 42.5% B. parapertussis
  • 15.3% B. holmesii

The only species and strain against which the vaccine protects is PRN+ B. pertussis, which makes up approximately 6.3% of all whooping cough bacteria in circulation (if we take the CDC’s report that 15% of B. pertussis is PRN+). However, the vaccine has no effect on 15.3% of all whooping cough bacteria (B. holmesii) and increases your risk of 78.5% of all whooping cough bacteria (non-PRN B. pertussis and B. parapertussis).

Look up any recent news articles about whooping cough outbreaks. Although they frequently blame the unvaccinated, if they admit how many were vaccinated, it usually disproportionately affects the vaccinated.

EDIT: In fact, the CDC itself says that the unvaccinated are not responsible for the increase in whooping cough cases over the past few decades [E9].

What about herd immunity?

Because the vaccine is so ridiculously ineffective at preventing whooping cough—in fact, it increases your risk of whooping cough, as described above—there’s no such thing as herd immunity for whooping cough. However, even if the vaccine actually prevented whooping cough, it would not contribute to herd immunity because it does not prevent a person from becoming contagious.

A 2013 FDA study [10] found that after being exposed to an animal with classic whooping cough, vaccinated baboons got infected but did not have symptoms and were contagious. In other words, vaccinated people may be protected from developing classic whooping cough caused by PRN+ B. pertussis (which was the strain used in the study and the only strain against which the vaccine protects), but they are not protected against becoming infected and contagious. In this respect, the vaccinated may pose a greater risk to vulnerable people like infants and immunocompromised individuals because they are more likely to get whooping cough caused by newer species/strains and more likely to develop a contagious asymptomatic infection caused by the vaccine-targeted strain. If they have no symptoms, they do not know they are contagious.

ETA: The lead author of the FDA baboon study also gave the New York Times an interview in which he explained that the vaccinated still develop infection when they are exposed and grow the bacteria in the backs of their throats, and thereby are contagious. He described this as “good for you, but not for the population” [E8].

What about getting the vaccine during pregnancy?

Women who get the vaccine during pregnancy develop some antibodies and pass them on to their babies–about 68.8 U/mL [E6]. However, the level of antibodies required to prevent pertussis is 246 U/mL [E7]. Not surprisingly, it has not yet been demonstrated that infants who received the Tdap vaccine during pregnancy have reduced risk of pertussis.

What’s the bottom line?

Many pertussis infections are so mild that they are not recognized as pertussis. Furthermore, the pertussis vaccine offers no real protection. It increases your risk of almost 80% of whooping cough bacteria and protects against only 6%. It also makes you susceptible to becoming a contagious asymptomatic carrier. There is no evidence that getting it during pregnancy protects your baby.





[4] see page 6:


[6] see slide 18:



UPDATE 9/16/16: Looks like the above link no longer works. Here’s an archived version of the link:















Please note that the exact proportions of species and strains differs from country to country, so the vaccine-targeted strain may make up less or more of the total in your region. The U.S. studies mentioned above should be used only as a rough estimate.

Look Below: Another Conspiracy Theory Sinks

There’s a quote often attributed to comic John Cleese that always makes me laugh: “The Spanish are all excited to see their new submarines ready to deploy. These beautifully designed subs have glass bottoms so the new Spanish navy can get a really good look at the old Spanish navy.” This hilarious imagery exactly describes how anyone taking any conspiracy theory “ship” under consideration should constantly look below, acutely aware of the possibility that it actually sank in a magnificent battle long ago.

Many of you may be aware of a new conspiracy theory making the rounds of social media. The most updated version of the theory is that the recent alleged rash of deaths and disappearances of physicians who practice alternative medicine and died or disappeared in Florida is a sign of something more sinister. The implication is that it has something to do with the FDA and, ostensibly, Big Pharma.


The Free Thought Project reported, “Another Florida Doctor Murdered, Bringing Total to 8 Dead & 5 Missing in Just the Last Month”

From the first article I read on the topic, I was put in mind of the recent alleged rash of black church burnings. That conspiracy theory referred to seven predominately African American churches that had been burned within a week, claiming these alleged hate crimes as evidence of racism in America. However, this article explained that two of those churches were struck by lightning (one of which was a predominately Caucasian church), one was due to an electrical failure, and in one case, it was actually the church van that burned, not the church itself, leaving only three black church burnings considered to be deliberate—i.e., arson. Furthermore, it goes on to explain that there are an average of 1,600 church fires per year in the U.S., which averages out to 31 fires per week. Therefore, the “rash” of 7 church burnings is in no way unusual. In fact, it comes out to less than a quarter of what is expected for any given week. I’m sure there were other church fires that went unreported, but the point is that this was not an unusual circumstance.

The logical fallacy that would apply to this is the fallacy of incomplete evidence, a.k.a. cherry-picking, where one selects and reports only those facts which support his/her theory, ignoring those which do not support his/her theory.

However, in my opinion, this is more likely an example of the availability heuristic (at least, as regards its spread on social media). This cognitive shortcut applied to media takes the form of the viewer/reader believing something to be more common, more likely, or increasing in incidence because he/she is seeing/hearing more news stories about the topic. For example, I read a story about how the media reported several assaults on elderly women in New York, which led to a rash of starvation deaths among elderly women because they were afraid to leave their homes, thinking assaults on elderly women were becoming more common. A hypothetical example would be that when the media reports several shark attack deaths, people consider dying of a shark attack to be more common than dying from being hit by falling airplane parts, when in reality the reverse is true. Another hypothetical would be that, during the Disneyland measles outbreak, people heard far more about measles on the media than they did about lightning strikes and came to believe that death is a significantly high risk factor for measles; however, in reality, Americans are more likely to die of a lightning strike than from the measles. Similarly, people heard a series of news reports on black black church burningchurch burnings and came to believe that these represented an unusually high incidence and, therefore, sinister intent—specifically, racism—when in reality, the majority of the fires were accidental, not all of them were directed against black churches, and the number was well within the expected range for a given week.

I wondered whether the same was true of these alternative medicine doctors–i.e., whether it’s a combination of (A) people hearing of the death of one conspicuous alternative medicine physician and then subconsciously taking greater note of all following physician deaths, and (B) clickbaiters consciously cherry-picking the data to convince their readers that there is an epidemic of alternative physician deaths by homicide. But, typically, I was too occupied with other things to look it up.

Finally, as the tally kept rising and people were sharing these stories more and more on Facebook, I eventually got sick of it and decided to look it up. By then, Snopes had published an article about it. It was a thoroughly-researched article and answered all of my questions, and all of the links they provided checked out. (In fact, even the conspiracy theorists conceded some of Snopes’ points.) The only issue I take with it is the random snide comment that mainstream doctors are “science-based,” implying that anyone who practices alternative medicine is not science-based. Perhaps I’m more accepting of alternative medicine because I’m a midwife, which is considered alternative in the U.S. but mainstream just about everywhere else. Furthermore, I live in Japan, where the vast majority (probably close to 100%) of the physicians believe in the power of acupuncture, traditional Chinese medicine, and other practices deemed “alternative” in the U.S., yet in spite of this “anti-science” opinion, Japan has a lower infant mortality rate, longer life expectancy, and overall better health than does the U.S. The spiteful comment about alternative health practitioners smacks of bigotry and ethnocentrism.

At any rate, back to the topic on hand. The short of it is that (1) they weren’t all murders, (2) they weren’t all alternative medicine doctors who died in Florida, and (3) the number of murders is within the expected range for a given month.

  1. First, like the “black church burnings” which turned out to be mostly accidental fires, the “murdered” physicians were not all murdered. In the last alternative media article I found on the topic, the tally stood at 8 “murders” and 5 disappearances. Of the five disappearances, three were Mexican doctors who lived and practiced in Mexico and were found dead in Mexico; only two of the disappearances were American doctors living and practicing in America. Of those two, one, Dr. Whiteside, has been found dead, so we’ll add him to the eight “murdered” physicians. Of the eight—now nine—“murdered” physicians, four are known to be a homicide, one was ruled a suicide but is being further investigated by private detectives hired by the family, two died of natural causes, two have pending autopsies and are therefore unknown at this time, and one is unknown as the cause does not appear to have been reported anywhere.
  2. Second, like the “black church burnings” which turned out not to be all black churches, not all of the physicians were alternative medicine doctors living or working in Florida. Of the eleven doctors, five were alternative medicine doctors and six were mainstream (or, at least, there is no evidence that they practiced alternatively, or even that they espoused alternative beliefs); significantly, of the four homicides, three were mainstream physicians. Furthermore, five died in Florida while six died elsewhere; and only one of those who died outside of Florida lived and worked in Florida, but he also lived and worked in two other states.
  3. Third, like the “black church burnings” which turned out to be within the expected range, the number of murders is also completely within the expected range. As Snopes reports, statistically speaking, approximately 6,500-8,200 physicians die every year, adding up to approximately 700 in one month—so these 11 are WELL within the range of expected physician deaths. However, I’d like to further address the argument that these physicians all had connections to Florida. In reality, as discussed above, about half of them did not. Nevertheless, based on the differences in population of various states, we could expect approximately 13 of those 700 monthly physician deaths to occur in Florida. Therefore, even the five who specifically died in Florida (or six with Florida connections) fall within the expected number for any given month.

Here’s a tabulated breakdown:

Name Cause of Death Type of Physician State
Bradstreet, M.D. suicide or homicide [1] alternative NC (died);FL, GA, AZ (worked)
Hedendal, D.C. natural causes alternative FL
Holt, D.C. unknown—autopsy pending alternative FL
Fitzpatrick, M.D. (missing) mainstream ND
Sievers, M.D. homicide alternative FL
Whiteside, M.D. unknown—autopsy pending mainstream WI
Riley, D.O. homicide mainstream [2] GA
Schwartz, M.D. homicide mainstream FL
Crews, M.D. homicide mainstream CA
Castellano, D.D. unknown—not reported mainstream FL
Gonzalez, M.D. natural causes alternative NY

M.D. = Medical Doctor. D.C. = Doctor of Chiropractic. D.O. = Doctor of Osteopathic Medicine. D.D. = Doctor of Dentistry [3].

(I want to note here that D.O.’s can be very mainstream—in fact, in the ER, I worked with several—but are more likely than M.D.’s to be alternative. D.O.’s learn both mainstream medicine and chiropractic medicine, but may or may not practice chiropractic medicine.)

  1. Dr. Bradstreet was found with a gunshot wound to the chest. Local authorities ruled it a suicide. His family has hired several private detectives to investigate the possibility of homicide.
  2. Dr. Riley was a D.O., and many D.O.’s are alternative practitioners. However, they are also very often mainstream. Dr. Riley was an ER doctor, and there’s no evidence that she was an alternative practitioner or even that she held any “controversial” views, so it’s generally believed she was a mainstream physician.
  3. There are several abbreviations for dentists; I’m not sure which one applies to Dr. Castellano.


Conspiracy theories do occasionally turn out to be true, so it’s prudent to give thought to the facts of any given case. For example, although racist killings of minority individuals by white cops are exceptionally rare, it’s prudent to look into the possible motives of any such killing just to be sure. Of course, in the same way that we should give up any theory of bias on the part of the cop when a preponderance of evidence demonstrates that the crime was not related to racism, we should also give up any conspiracy theory when evidence pokes so many holes in its hull that it can no longer stay afloat. And this particular conspiracy theory is one that seems to have sunk long ago. It’s time to stop looking for it on the horizon and realize that it’s below us.



A Brief History of Pertussis Vaccines

Previously, I wrote about the dangers of attempting to protect an infant by cocooning (vaccinating all of his adult contacts against whooping cough), demonstrating how doing so actually increases the risk to the infant rather than decreasing it. I discussed how I’ve never been a fan of influenza or HPV vaccination, but how, due to research published primarily in the last couple years, I’ve come to feel similarly about pertussis vaccination.

Whooping cough deaths and cases dropped dramatically prior to introduction of the vaccine. They continued to drop after the introduction of the vaccine, decreasing by about 99% between the mid-1940s and 1970. Vaccination rates fell in concert with rising concerns about the safety of the DTP vaccine in the 1970s-1990s. However, vaccination rates have steadily risen since then and are now at an all-time high. Nevertheless, since the 1980s, the incidence has steadily increased in spite of simultaneously increasing rates of pertussis vaccination.

As I was reading studies and articles about the many possible explanations for this paradoxical increase, I came across what was to me a fascinating and detailed (and apparently award-winning) article authored by Dr. Geier, a former researcher at the National Institutes of Health (NIH) and advisor to the Centers for Disease Control and Prevention (CDC), about the history of pertussis vaccines. After reading it, I’m amazed at how much disinformation abounds on the internet about this topic! You may not be as fascinated by the topic as am I—in which case, you can skip this one and wait for my next blog post—but I found it so interesting that I summarized the article and filled in the few blanks from a few other sources. So without further ado, I present to you a brief history of pertussis vaccination.


And So It Starts

In 1906, researchers Bordet and Gengou developed a technique to grow B. pertussis in a laboratory, which paved the way for the creation of a pertussis vaccine. The first whole cell pertussis (wP) vaccine was produced by Bordet and Gengou in 1912 and by 1914, there were six U.S. manufacturers of pertussis vaccines. Pertussis vaccines sans formal testing were used sporadically between 1914 and 1925. The first clinical trials of wP vaccines were published in 1925 and 1933, with the 1933 study reporting serious adverse effects for the first time in its listing of two deaths that occurred within 48 hours of vaccination. The first modern wP vaccine, which was combined with diphtheria and tetanus toxoids, was created in 1942 by Dr. Pearl Kendrick. Because the wP vaccine does not inactivate endotoxin or pertussis toxin, it may be associated with some or all the side effects of pertussis infection from fever to seizures, shock, and death. Evidence of the dangerous side effects of the wP vaccine as compared to the aP vaccine were reported as early as the 1930s and considered conclusive by the 1950s, with the first deaths reported in 1933 and the first published reports of irreversible brain damage appearing in 1947 and 1948. By 1948, there were a dozen manufacturers of DPT. The “mouse toxicity test,” which essentially determined the toxicity of the vaccine by seeing how many mice died from it, was introduced to ensure licensure of safer vaccines; however, researchers concluded in 1963 that there was no correlation between mouse safety and human safety. From the late 1940s to the early 1960s, physicians continued to use wP vaccines because they had no other choice on the market and because manufacturers hid the presence of endotoxin in the vaccine and its associated risk. Vaccine manufacturers began a successful lobbying campaign of pediatric societies and state legislators in the 1940s, ultimately resulting in legislation requiring DTP vaccination prior to school entry in most states by the mid-1960s. However, with such widespread vaccination came the first published reports of irreversible brain damage and deaths resulting from the vaccine, with these reports being published almost every year from the early 1950s through the early 2000s, with additional published reports coming out of other countries. This causal relationship was deemed definite by a report from the National Institutes of Health (NIH) in 1963. Criticism of the wP vaccine due to its high rate of adverse effects, cited at 93% in a 1984 study, increased through the 1970s and peaked in the 1980s.


A Better Option?

The first aP vaccine was created in the 1920s and it was obvious from at least the 1930s that it was associated with fewer adverse events than the wP vaccine. Lederle Laboratories patented a new aP vaccine in 1937, which was shown clinically to be 94% protective against disease, making it significantly more effective than the wP vaccine, and was used widely in the 1940s. However, new federal laws were passed which would require expensive and labor-intensive efficacy testing of aP vaccines, and so Lederle ceased production of its more expensive but more effective and less reactogenic aP vaccine in 1948 and began producing a wP vaccine instead. Another aP vaccine was produced in 1954 but never licensed or marketed in the U.S. due to the higher cost of production and increased clinical trial requirements. Eli Lilly Company created an aP vaccine and named it Tri-Solgen. Tri-Solgen was associated with significantly fewer adverse reactions compared to wP vaccines and was sold widely from 1962-1977, at one point capturing up to 65% of the U.S. market for pertussis vaccines. Merck Sharp & Dohme produced another aP vaccine in 1960 which was found to be both safer and more effective than the wP vaccines, but ceased production by 1963 due to the cost. The following year, 1964, Merck also removed all wP vaccines from the market citing a fear of lawsuits due to damages caused by its wP vaccine because they had a safer and more effective aP product that didn’t sell. Many other aP vaccines were produced but never marketed due to their cost and to similar concerns about legal liability due to having a safer and more effective product (the aP vaccine) but continuing to sell the more dangerous and less effective product (the wP vaccine). Due to these concerns, the market severely contracted and only four manufacturers were still producing DTP vaccines by the 1970s. Lilly ceased production of all biologic products in 1975 and sold the rights to its high quality aP vaccine Tri-Solgen to Wyeth. However, the yield was low and when Wyeth reformulated it to increase its yield, the government required new safety and efficacy trials. Wyeth determined the cost, both financial and legally, wasn’t worth it and ceased production of Tri-Solgen; specifically, Wyeth’s concerns were the same as Merck’s had been—that the studies would show the aP Tri-Solgen to be safer and more effective than Wyeth’s wP vaccine, making them legally liable for continuing to market an inferior product. Hence, the only aP vaccine on the market became unavailable after 1977. By 1984, Wyeth also completely stopped production of pertussis vaccines, again due to concerns of legal liability from its failure to produce its safer product. The end result was that only two pertussis vaccine manufacturers remained in the U.S., and both produced only the wP vaccine.


Trouble in Paradise

In 1975, two babies in Japan died from DPT vaccination, and these were two of 37 SIDS deaths linked to vaccination; in response, the Japanese government initially banned the DTP vaccine, but later in the year resumed vaccination in children over age 2. The following year, 1976, the government sent Dr. Sato to the NIH to study aP vaccine production. His aP vaccine was tested between 1978 and 1981 and found to be nearly 100% effective and significantly less reactogenic, and so the Japanese government mandated switching to aP vaccination in 1981. During this period, infant deaths plummeted, bringing Japan from a high 17th place in world comparison of infant mortality rates to 1st place with the lowest infant mortality rate in the world. (Coincidentally, when they reintroduced vaccinations in children as young as 3 months of age in 1988, their SIDS rate quadrupled.)

Also in the 1970s, rising awareness of vaccine adverse effects led to a reduction in the pertussis vaccine compliance rate. Pertussis is an epidemic disease–i.e., there are periodic outbreaks every 3.3 years with low disease rates in the interepidemic periods–but the interepidemic period that correlated to the lowest pertussis vaccine compliance rates was an unusually long interepidemic period with the lowest whooping cough incidence on record. In the 1970s, the U.K. determined that the benefits of continued use of wP vaccination outweighed its risks, while Sweden determined the opposite, pointing out that no one had died from pertussis since 1970 and that the causal relationship between wP vaccines and encephalopathies was too great to ignore, and banned the wP vaccine. Most studies of efficacy look only at the ability of the vaccine to produce an antibody response—termed by some “research efficacy.” However, because the presence of antibodies does not necessarily correlate to immunity, a study of actual disease rates may be used to determine the ability of the vaccine to prevent disease—termed by some “clinical efficacy.” The wP vaccines were determined to be 45-48% clinically effective while the Japanese aP vaccines when tested in Sweden were found to be 55-69% clinically effective. Even when the Swedish scientists compared a two-dose regimen of aP vaccines to a five-dose regimen of wP vaccines, the aP vaccines were found to be more effective.

In the 1970s and 1980s in the U.S., several factors contributed to consideration of abandoning wP vaccination, including: the relative absence of whooping cough in the population; improvements in medical treatment of whooping cough; the serious adverse effects of the wP vaccine, which led to health clinics requiring parents to sign an informed consent prior to receiving a wP vaccine; several SIDS deaths in 1979 which the CDC deemed to be caused by a particular lot of the wP vaccine, causing the FDA to order a recall of the defective lot, followed by a reversal of the recall and efforts by manufacturers to prevent future recalls (e.g., Wyeth began spreading lots out across the country rather than sending an entire lot to one area so that adverse effects of any one lot would not be noticed as quickly in the future); and numerous lawsuits beginning in 1981 which were ironically successful because it was argued that the manufacturers had known how to produce a safer aP product but chose not to. (Unsuccessful lawsuits had been filed previously.) In 1982, a television program about the adverse effects of DPT vaccination raised parental awareness so much that attorneys trying the cases were flooded with hundreds of requests for representation. The vaccine manufacturers attempted to stop the cases by harassing the expert witnesses, leading at least one to file a suit against them. Nevertheless, by 1985, 219 such lawsuits had been filed. Pressure from parents and especially from a group formed in 1982 called Dissatisfied Parents Together led the American Academy of Pediatrics (AAP) to conduct over 8 months of hearings to develop recommendations for the creation of a federal compensation program for vaccine-injured children. Due to the AAP’s recommendations and to the large-scale civil litigation against vaccine manufacturers, Congress introduced the National Compensation Act in 1983, which sought to limit liability for vaccine injuries. One manufacturer agreed to settle out of court for $26 million and then cite its case as an example of why the act was needed. In 1986, the U.S. Congress passed the National Vaccine Injury Act, which established, among other things, the National Vaccine Injury Compensation Program (NVICP) and essentially ended litigation against vaccine manufacturers. However, with the threat of litigation gone, manufacturers were no longer under pressure to produce a safer aP vaccine. Foreseeing that this would happen, the Congress also stipulated in the Act that the IOM hold hearings and make recommendations for improving vaccines in general and the pertussis vaccine specifically.


Safety Wins

As previously stated, the causal link between DPT and neurological sequelae was deemed definite by the NIH in 1963. However, after receiving several generous donations from vaccine manufacturers and being staffed and/or headed by former and current employees of vaccine manufacturers, the AAP and the Pediatric Neurology Society “mysteriously” reported in 1992 that there was no such link. This was followed by several heavily manufacturer-funded researchers publishing articles that also attempted to deny the link. Backing up a few years, we’ll examine what the government saw. In 1985, the Institute of Medicine (IOM) published a report stating, among other things, that in spite of its initially higher costs, the aP vaccine saves on overall medical costs as compared to the wP vaccine, and the United States would save millions of dollars if the wP vaccine was replaced by the aP vaccine due to the high rate of adverse reactions; it advised that the highest priority should be given to making the switch. However, this recommendation was put on the back shelf and when another IOM committee convened in 1990, only five years later, they were surprised to learn that data presented in the meeting came from their own archives. Nevertheless, the evidence against the wP vaccine was so overwhelming that, regardless of the opinions of those bought by the manufacturers, the IOM determined that the causal link between wP vaccination and encephalitis was definite. The IOM convened a third time in 1993 to again discuss the DTP vaccine and determined that it definitely causes permanent brain damage. Even the AAP failed to argue the point, instead merely notifying its members of the IOM’s position. In 1992, the FDA approved the use of aP for the boosters given at 18 months and 6 years of age. In 1996, the FDA approved the use of aP for the entire schedule. Finally, by the beginning of 2001, the wP vaccine had been removed from the U.S. market, though American manufacturers continue to produce the cheaper (in every sense of the word) wP vaccines for sale in the third world.


“The development and acceptance of acellular pertussis vaccine in the United States demonstrates that scientific evidence alone is not always enough to change harmful medical practices. Given the powerful resistance to change demonstrated by the pharmaceutical industry, it took years of litigation, consumer advocacy, international scientific development, and congressional action to create a new norm for childhood immunization. It would seem that open discussion of vaccine problems in the scientific and medical communities, along with policies that preclude those with a conflict of interest from determining vaccine policy, might help to prevent similar difficulties in the future in the rapidly expanding vaccination field.” (Geier & Geier, 2002, p. 284]




Centers for Disease Control and Prevention (1997). “Vaccination: Use of acellular pertussis vaccines among infants and young children recommendations of the Advisory Committee on Immunization Practices (ACIP).” Morbidity and Mortality Weekly Report, 46(RR-7):1-25. Retrieved from < >.

Fine, P.E.M., & Clarkson, J.A. (1982). “The recurrence of whooping cough: Possible implications for assessment of vaccine efficacy.” The Lancet, 319(8273):666-669. doi: 10.1016/S0140-6736(82)92214-0.

Geier, D., & Geier, M. (2002). “The true story of pertussis vaccination: A sordid legacy?” Journal of the History of Medicine, 57:249-284. Retrieved from < >.

Hieb, L. (2015). “How vaccine hysteria could spark totalitarian nightmare.” WND. Retrieved from < >.

Howson, C.P., Howe, C.J., Fineberg, H.V., eds. (1991). “B pertussis and rubella vaccines: A brief chronology.” In Adverse Effects of Pertussis and Rubella Vaccines: A Report of the Committee to Review the Adverse Consequences of Pertussis and Rubella Vaccines. Institute of Medicine Committee to Review the Adverse Consequences of Pertussis and Rubella Vaccines. Retrieved from < >.


EOs and Bad Advice

DISCLAIMER: I am an ER nurse, but I’m also a midwife. As such, I straddle both “conventional” and “alternative” medicine. I use and recommend alternative pharmaceuticals (e.g., herbs, essential oils, homeopathic remedies, etc.), but I’m not above using conventional pharmaceuticals (e.g., antibiotics, lidocaine for stitches, etc.). I treat all pharmaceuticals, be they conventional or alternative, with the same pause, consideration, and concern. Please note this is not aimed at anyone in particular but rather at everyone who uses or is considering using essential oils. I do not pretend to be an expert on essential oils; I am just beginning my research. I merely hope to open some eyes to potential dangers with improper use and encourage people to begin doing their own research independently of any rep’s advice.

COMMENTS: People tend to get a little… uptight… dare I say defensive?… when discussing essential oils. Please see my About page for my comments policy.

Long story short, I’ve recently come to learn some specific things about proper use of essential oils (EOs) that most people don’t seem to know and the bad advice flying around has always bothered me, but it’s gotten much more bothersome lately. Maybe it’s because I’ve learned more about EO safety over the past couple months. Maybe it’s because I was recently given bad advice for treatment of my mastitis that could have harmed my newborn if I didn’t know better, which really brought home to me the risks people undergo just by having friends they trust who use EOs. I’ve also always been deeply irritated by people who claim or pretend to know more than they do and use their fake expertise or credentials to influence people who don’t know better. For example, during the Ebola “epidemic” in America, a couple of acquaintances of a friend were using their position in a hospital (which, coincidentally, did not involve any medical training whatsoever, but rather health insurance training, and zero patient contact, facts which no one who works outside of a hospital would know unless they specifically looked it up) tothis is why doves cry convince people that they knew what they were talking about when they said Ebola was more contagious than the flu or measles. (#facepalm #thisiswhydovescry) Similarly, many MLM EO reps who have little to no training (and what they do have is provided by others with little or no training or experience) use their fake credentials to convince clients that they know what they’re talking about when they say X use of X oil is safe in X person for X ailment, but they’re often wrong, putting others at risk with their bad advice, and never seem to be willing to admit they’re wrong, even arguing with aromatherapists (those who actually have undergone in-depth, unbiased training on essential oil use). There is also a much larger subset of people who have taken bad advice from others and, through no fault of their own, pass on that bad advice simply because they don’t know better and because they trust the person who gave it to them. It’s been said that the most dangerous place to be is where you have just enough knowledge to give you confidence in your practice but not enough to recognize when your practice is dangerous. So maybe I’m writing this because I resent it when those with little or no education use their dangerous level of knowledge to influence others to do dangerous things—and then argue with those who actually have the education to know the truth. At any rate, whatever my reason for writing this blog post, consider this a PSA.

(As a side note, this risk of bad advice and potential harm is true of virtually any alternative medicine. I’ve had pregnant clients receive recommendations for herbs that I knew to be abortifacient. Luckily, being a midwife and having taught classes on birth control, which includes abortifacients, I knew better and could advise against it, but many people wouldn’t know better and would blindly take those herbs while pregnant and potentially miscarry.)

I know this post is going to tick off a bunch of people (mostly MLM EO reps), but I’m an ER nurse and, as such, am not afraid to tell someone, “You’re being unwise with certain aspects of your healthcare and may seriously harm yourself or your child with some of these uninformed decisions.” (Of course, in the ER, it was often more along the lines of, “Dear God, you’re such an incomparable moron. How are you still living?” Slightly different situation. But the point is that I learned a little bit about bravery in regards to telling people the truth about their health.) Some of this may seem overly cautious, but if you don’t know all the cautions, then you can’t make a truly informed decision. It may seem overly cautious to tell someone who has been taking narcotics daily for decades that they’re not supposed to drive while on narcotics, but if I as an ER nurse didn’t offer that education, that would be considered bad practice, and if that person then got into a car accident, I would be liable in a malpractice suit. Ditto the failure to educate a patient taking an antifungal pill regarding potential liver damage from drinking alcohol while taking the drug, or any other number of potential risks with conventional medicine. What you do with the education provided here is up to you. But at least my conscience will be clear and your eyes, hopefully, will be opened to the potential dangers of the extremely potent alternative medicine known as essential oils and you will gain a new respect for this potentially harmful and potentially beneficial “wonder drug.”


What is It?

EOs have been used for thousands of years in humans to treat a variety of conditions. As such, it’s difficult to patent and therefore difficult to obtain research grants because of the risk of no return on investment. It also means many of the EO remedies have been tested by time. On the other hand, it has sometimes taken thousands of years to abandon bad medical practices from the past, so just because a practice is very old doesn’t mean it’s good.
antibiotic-history-58-728Nevertheless, in this case, there’s plenty of scientific evidence indicating that EOs are beneficial for the treatment of various conditions when used correctly (however, remember to take all studies on any topic by any author with a grain of salt, understanding that it’s extremely easy to publish fraudulent studies and that most published research is false [1]). For example, the University of Minnesota has an article [2] on EO research wherein it asserts that EOs have shown “positive effects for a variety of health concerns including infections, pain, anxiety, depression, tumors, premenstrual syndrome, nausea, and many others” and then lists 75 published research studies for a brief glance at the literature on the topic. The book Essential Oil Safety by Robert Tisserand reportedly lists over 4,000 studies.

Ok… But what **are** they? Basically, EOs are super-concentrated herbs in oil form. EOs are far more potent than dried herbs. In fact, one ounce of EO may have literal tons of plant matter and be over 100x the strength of its herbal version. EOs are extremely potent, then, and pose a high risk of chemical reactions if used incorrectly or unwisely. Which brings us to the next topic…


EO Dangers and Sensitization

EOs pose similar risks to those you’d expect from any highly concentrated substance. For example, dermatologists sometimes recommend a bath with half a capful of bleach to treat childhood eczema, but touching undiluted bleach can give you a chemical burn. As another example, vitamin C is relatively harmless, but it’s still an acid—in fact, I once burned the roof of my mouth by sucking on a low-dose (500 mg) vitamin C tablet. EOs are similar. A given EO may be harmless at a certain dilution but cause serious harm if undiluted.

Sensitization-is-described-as-“aPerhaps the most commonly discussed risk with EOs is “sensitization.” The West Coast Institute of Aromatherapy [3] and aromatherapist Lea Harris of [4] explain what this is. Basically, many EOs can cause skin irritation, and this typically occurs on the first use. However, sensitization is basically an allergic reaction. Like all allergic reactions, it’s typically *not* the first use that causes a visible reaction (in fact, I had taken Vicodin off and on for years for various ailments before I first developed an allergic reaction to it; sometimes it takes one use, but other times it takes years to develop an allergic response). Sensitization is more likely in those with sensitive skin (e.g., eczema, infants, etc.) and is typically associated with undiluted (“neat”) use or overuse (e.g., lavender is considered one of the safest EOs, but aromatherapists most often become sensitized to lavender because they use it with their clients so frequently). This is why undiluted use is rarely recommended, and why it’s recommended you don’t use the same EO daily for a long period of time. Furthermore, if you are in a profession or have a career or side job that involves frequently handling essential oils (e.g., aromatherapist, massage therapist, seller of essential oil-infused soaps or lotions or other care products, etc.), you should strongly consider wearing gloves when handling oils so as to prevent sensitization to any oils, which may hamper or prematurely end your career, as it has for others (e.g., 14). Sensitization may occur with any EO and brand is irrelevant in the same way that if you’re allergic to peanuts, you’ll be allergic to all brands of peanut butter.

There are also some side effects associated with each EO that should be taken into consideration. For example, “thieves”-type blends typically contain cinnamon bark and clove, both of which are blood thinners; rosemary and eucalyptus, both of which can inhibit the respiratory drive in children (Footnote 1); and lemon and bitter orange, both of which are phototoxic (note that sweet orange, sometimes used instead of bitter orange, is not phototoxic) [5]. Therefore, these additive—or even synergistic—effects make thieves blends unsuitable for people prone to bleeding (e.g., people taking blood-thinners), children under age 10, and people at risk of sunburn (e.g., fair-skinned people planning to be out in the sun for a significant length of time). Knowing about these side effects can help people avoid using an EO that might be fine for most but harmful for them.

What I’m trying to say is that EOs, like any medicine, must be treated with the respect they deserve. They are powerful medicinals and may indeed be that magic cure you’ve sought, but when used unwisely, they may do you serious harm.


General Guidelines

There are some general guidelines for proper, safe use of EOs. You certainly have the right and ability to violate these guidelines, but you do so at your own (or your child’s) risk. My hope is only that you would be informed so that, at the least, you’re aware of the guidelines and know that what you’re doing is potentially dangerous—basically, that if something goes wrong, it won’t be because you were uninformed and your response won’t be that ever-heartbreaking “I didn’t know.”

Dilution and Mixing

EOs are most often diffused into the air and inhaled, but may be used topically (put directly on the skin). Some people also ingest EOs.

Diffusion is the safest way to use EOs, so it’s generally the first recommendation. However, topical application is generally safe when done correctly.

dilute dilute diluteWhat is the correct way to use EOs topically? Generally speaking, the correct way to use them topically is to dilute them first in a carrier oil such as coconut oil. The term “neat” refers to undiluted topical application—i.e., putting the oil directly on your skin without first diluting it by mixing it in a carrier oil. Directly applying any undiluted, concentrated substance is rarely recommended, regardless of whether you’re cooking, cleaning, or formulating/administering medications as a nurse working in a hospital setting, and the same is true of EOs. Neat application is a particularly predictive risk factor for sensitization, as mentioned above, so should be avoided if at all possible. properly dilutingNeat application is NEVER recommended for children, whose skin is far more sensitive and absorbent than that of adults and who therefore are at significantly increased risk of having reactions to topical EOs, including sensitization. Neat application is almost never indicated for adults, either. Furthermore, EOs are actually spread and absorbed better when diluted in a carrier oil, and many carrier oils have additive or synergistic effects due to their own therapeutic properties (for example, coconut oil is antiinflammatory). Therefore, EOs are generally more effective when diluted prior to topical application and are more likely to cause problems if not diluted before topical use [6,7,8,10].

lowest dilution possibleHow much should they be diluted? That depends on the age of the patient and the purpose of the treatment, but the concentration of the oil ranges from 0.25% (1 drop EO to 4 tsp carrier oil) to 2% (2 drops per tsp). For very short-term use in adults, 3% concentration or even 25% concentration may be used. Exceptionally rarely, an EO may be used neat in adults. Check out Lea Harris’s article for more information on dilution [8].

ingestioncautionNow, as for ingestion… The mucous membranes of your mouth, throat, etc., allow absorption much more readily and are much more sensitive to bad side effects of EOs. When used topically, you absorb about 10% of the dose, but when swallowed, you absorb about 95%, which goes straight to (and can accumulate in) your liver, so there’s also a risk of what amounts to overdose with ingestion. Remember that essential oils are extremely potent. Swallowing a drop of EO is NOT the same as swallowing an herbal pill or two. One drop of EO is FAR more potent than a couple pills of herbs.

Aromatherapist Lea Harris warns, “Physical contact of essential oils on the mucous membranes can cause immediate irritation, or even burns. Long-term consequences of allowing essential oils to physically touch this delicate skin can lead to permanent damage, including scarring and ulcers, as well as liver and/or kidney damage, and the potential for cancer.”

EO and waterAromatherapists will very rarely agree that ingestion is safe or preferable. If you wish to ingest it, though, you should do so only under the guidance of a certified aromatherapist and you should first dilute it in a carrier oil and put it in a capsule so that when you swallow the pill, the EO bypasses your most sensitive tissues and will be diluted when it does contact your mucous membranes.

oil and waterEOs should NEVER be added to water and drunk. Oil and water does not mix. In other words, the oil is being placed directly against your sensitive mucous membranes—you might as well have swallowed the EO directly without adding it to your water because it has the same undiluted effect. An EO added to water is NOT diluted because oil and water do not mix.

Again, brand doesn’t matter—ALL EOs are highly concentrated and therefore pose a risk of chemical irritation and sensitization. [9]

Age Restrictions

3 mo

There are also lots of oils that should not be used in children of certain ages. As a general rule:

  • Under 3 months: NO EO use in any form (Footnote 2)
  • Under 2 years: preferably no EO use, with hydrosols and herbs preferred over EOs due to greater risks with EOs; generally only diffusion permitted (if used at all), though the extremely rare topical use may be recommended (e.g., for treatment of bug bites)
  • Under 6 years: very limited EO use; diffusion and topical permitted
  • Under 10 years: diffusion and topical permitted

EO poisoningThere are many EOs that are not safe for use in any form in children of certain ages. For a list of EOs not recommended for each age, here’s a quick, reader-friendly cheat sheet.

As with drugs, children are more sensitive to the effects of EOs, are at higher risk of overdose, metabolize EOs differently, and absorb more of a topically applied dose as compared to adults. Their skin is also more sensitive (consider, for example, how many infants react to various laundry detergents as compared to older children and adults), and so are at higher risk of skin irritation and reactions—including sensitization—than adults, even if the EO is used correctly, which demonstrates the importance of very judicious use of EOs in children, especially young children and infants. You wouldn’t give a 2-year-old 800 mg of ibuprofen. Similarly, I hope you would think twice about using EOs on your small child—and preferably choose the less concentrated and therefore safer hydrosols or herbs instead. [10,11]

Pregnancy/Breastfeeding Restrictions

Some EOs, like the herbs from which they come, may cause birth defects or miscarriage, and some may enter the breastmilk. Like drugs, most EOs have unknown safety profiles in pregnancy or breastfeeding and so should generally be avoided in pregnancy unless absolutely necessary and used with caution while breastfeeding. Neat (undiluted) and internal (swallowed) use in pregnancy and breastfeeding is never recommended. [12]

pregnancy lactationJust because it’s “natural” doesn’t mean it’s safe. Remember that some herbs can cause miscarriages and birth defects and that EOs are super-concentrated herbs that are over 100x more powerful. Therefore, the risk for untoward effects on the unborn baby is great.

Furthermore, something most people don’t seem to talk about is that an EO may be safe for an adult but not safe for an infant, and so a woman who is breastfeeding shouldn’t use such an EO topically in an area where her nursing infant might breathe or touch. For example, a friend recommended I use two EOs topically on my armpits when I had mastitis. However, my baby was only a couple weeks old at that point—far younger than the minimum age for EO inhalation of 3 months and EO topical use of 2 years—and if I did as recommended, there was a risk that my newborn would both inhale and potentially touch the EOs on my skin. Luckily, I knew enough to seek advice from an aromatherapist before following my friend’s advice, but most people wouldn’t know better and would put their newborns at risk. The same friend recommended putting a blend on my feet to treat the mastitis. Though the effectiveness of such a use is in question, my newborn wouldn’t be smelling or touching my feet, so that would be a safe use as regards my baby (assuming all the oils in the blend are otherwise considered safe when breastfeeding—which, coincidentally, they were not).

For a list of EOs not recommended in pregnancy and breastfeeding, there’s another quick, reader-friendly cheat sheet on the same page as the children’s cheat sheet.



If you’re the type of person to blindly swallow whatever pills any doctor prescribes you, no one (well, very few people, anyway) would think you a hypocrite for blindly following the advice of friends more knowledgeable than yourself as regards EO use. However, if you are the kind of person to avoid overuse of conventional medicine (e.g., antibiotics for every infection, antipyretics for fevers, etc.), to use natural or alternative medicine due to a belief that it is safer, to think twice before adding a new prescription to your list, to research drug reactions before agreeing to a new drug, or at the very least to hesitate when given a pharmaceutical recommendation from a healthcare professional, but you don’t hesitate when given an essential oil recommendation by a friend, even a very knowledgeable friend, then you are practicing alternative medicine dangerously. As with all alternative medicine, educate yourself prior to use, generally avoid use if not needed, and don’t blindly follow ANY advice. I always recommend that you err on the side of caution. YOU (or your child) are the one who will have to live with the consequences of bad advice followed blindly.





Footnote 1: Eucalyptus and Rosemary Inhibit Respiratory Drive in Children. This is widely agreed upon among aromatherapists and written in basically every aromatherapy textbook. However, there are some who disagree with this. See here for more information if interested.

Footnote 2: No EO Use in Infants Under 3 Months of Age. It’s unknown what age is actually safe for EO use. However, Robert Tisserand talks about how infants reach a developmental milestone as regards skin permeability and sensitivity to EOs around 3 months of age. For this reason, many don’t recommend use under age 3 months, but consider 3+ months to be “probably safe” for very limited, properly diluted use (e.g., 13).



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  3. West Coast Institute of Aromatherapy (N.d.) “Essential Oil Safety–Skin Sensitization.” Retrieved from <>
  4. Harris, L. (2014). “A Word on Sensitization.” Retrieved from <>
  5. Harris, L. (2014). “Thieves & OnGuard essential oil blends – what you must know before using thieves-type blends.” Retrieved from <>
  6. Harris, L. (N.d.). “Undiluted Essential Oils For Babies: Busted Essential Oil Myth #3.” Food Renegade. Retrieved from <>
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  8. Harris, L. (2013). “Properly Diluting Essential Oils.” Retrieved from <>
  9. Harris, L. (2013). “Ingesting Essential Oils.” Retrieved from <>
  10. Harris, L. (2014). “Safely Using Essential Oils for Children.” Herbal Academy of New England. Retrieved from <>
  11. Harris, L. (2014). “Essential Oils and Children.” Retrieved from <>
  12. Harris, L. (2013). “Essential Oil Safety During Pregnancy.” Retrieved from <>
  13. Anthis, C. (2014). “Safe Essential Oil Use with Babies & Children.” The Hippy Homemaker. Retrieved from <>
  14. The Untamed Alchemist (2015). “Put Essential Oils in ALL the Things! (Yeah, NO.)” Retrieved from <>