Category Archives: Uncategorized

15 Square Inches?? Not So Fast.

Let’s talk about the size of the foreskin. Anti-circumcision activists, called “intactivists,” like to say that the adult foreskin is about 15 square inches and so it makes up over 50% of the skin on the penis. This is really, frankly, irrelevant information if circumcision does not harm sexual or penile function, which it does not. If circumcision has no sexual or functional harms, then how much skin is removed is irrelevant. Nonetheless, it’s yet another claim that intactivists make, and so we’re going to look at it in some detail.

How Big is the Penis?

First off, what is the length of the penis? After all, if we want to know how much of the penis skin is foreskin, we need to know how long the penis is. A systematic review of all studies on the subject published in 2015 found that among 15,521 men across the planet, the average length of the penis is 9.16 cm flaccid and 13.12 cm erect (Veal et al, 2015).

Only less than 2.5% of men have a penis shorter than 10 cm erect and only 5% of men have a penis longer than 16 cm erect (Veal et al, 2015). This means that about 92.5% of men have a penis that ranges 3.9 to 6.3 inches, or about 4 to 6 inches long erect. There’s not much variation there, the shortest normal length varying only about 33% from the maximum normal length. The normal, non-prolapsed vagina is 10-12 cm (3.9-4.7 in) long (Matthes & Zucca-Matthes, 2016). So, in other words, the average erect penis is longer than the average vagina. This may be why the penis varies as much as it does but not more than that. Because the only evolutionary or created advantage to penis length would be a penis that is just long enough to deposit sperm near the cervix.

Flaccid, the difference in length is more pronounced. For example, only 2.5% of men have a flaccid penis shorter than 6 cm and almost 5% of men have a flaccid penis longer than 12 cm (Veal et al, 2015). This means for about 92.5% of men, the flaccid length is within 6-12 cm or 2.4-4.7 inches, almost 2.5 to 5 inches. In other words, the flaccid length differs much more than the erect length, as much as 50% of the maximum normal length. This should not come as a surprise, however, because the flaccid length is irrelevant to reproduction. Even though flaccid length varies significantly, erect length does not, and the erect length is what matters for reproduction.

The circumference of the penis, which is how big around it is, averages 9.31 cm flaccid and 11.66 cm erect. About 7.5% of men have a flaccid circumference less than 8 cm and about 2.5% have a flaccid circumference greater than 11 cm (Veal et al, 2015). So about 90% of men have a circumference that ranges 8-11 cm or 3.1-4.3 inches. Again, not a whole lot of variation there, only 28% from the max normal circumference.

How Big is the Foreskin?

In contrast, there is vast variation in the size of the foreskin. One study of almost 1,000 men (Kigozi et al, 2009) found that the inner and outer foreskin together averaged 35.0 cm2 (5.4 in2) and ranged in size from 7 cm2 (1.1 in2) to 99.8 cm2 (15.5 in2). If the average circumference, as we discussed already, is 9.3 cm, and the foreskin’s area measures 7-99.8 cm2, that means the foreskins were on average 3.8 cm (1.5 in) long and ranged anywhere from 0.75 cm (0.3 in) to 10.7 cm (4.2 in) long, including outer and inner foreskin. About 6.3% of men (the top 25% of the top 25%) had foreskins larger than 61.8 cm2 (9.6 in2) and about 6.3% (the bottom 25% of the bottom 25%) had foreskins smaller than 18.0 cm2 (2.8 in2) (Kigozi et al, 2009). So for almost 90% of men, the foreskin ranges in size from 2.8 in2 to 9.6 in2. Again, assuming the average circumference is 9.3 cm, this means the length (inner and outer foreskin combined) ranges 1.9 cm (0.76 in) to 6.6 cm (2.6 in), meaning the shortest normal length varies 71% from the longest normal length. This is a vast difference compared to the differences in penis length and penis circumference, which varies about 33% and 28%—i.e., less than half as much as the length of the foreskin.

What Proportion of the Skin is Foreskin?

If we just take the simple averages of the length of the penis (9.3 cm flaccid) and the length of the foreskin (3.8 cm), the foreskin makes up 29% of the skin of the penis. This is obviously much less than the intactivist claim of 50%.

If we assume that the shortest penises had the shortest foreskins and the longest penises had the longest foreskins:

  • The shortest normal size (6 cm flaccid penile length and 0.75 cm length of inner and outer foreskin) accounted for 11% of the skin of the penis.
  • The longest (12 cm flaccid penile length and 6.6 cm length of inner and outer foreskin) accounted for 35% of the skin of the penis.

If we assume the reverse, that the longest penises (12 cm flaccid) had the shortest foreskins (0.75 cm inner and outer), the foreskin would account for 6% of the skin of the penis. If we assume that the shortest penises (6 cm flaccid) had the longest foreskins (6.6 cm inner and outer), the foreskin would account for 52% of the skin of the penis.

In other words, it is only by making the most extreme comparison that we can finally get the number over 50% (or, on the other extreme, only 6%), in accordance with intactivist claims that the foreskin makes up 50% or more of the skin of the penis. (I’ve even seen the claim that it makes up 80%!) Most likely, the foreskin makes up less than a third of the skin of the penis. Until further research demonstrates this to be false, I think this is as accurate as it gets. Although once again, it’s irrelevant if circumcision does not harm sexual or penile function, and we know that it does not.

Conclusion

As a final note, recall that we found the length of the penis does not vary much in comparison to the length of the foreskin. An acquaintance of mine, writing previously on the topic of foreskin size, quoted Darwin (though I think it equally true of creation):

“An organ, when rendered useless, may well be variable, for its variations cannot be checked by natural selection.”

In short, the wildly variable length of the foreskin compared to the much less variable length and girth of the penis indicates that the foreskin is of little importance anymore. Presumably it was before the Flood radically changed the global environment (if you’re a creationist) or back when we were essentially apes (if you’re an evolutionist), but modern evidence indicates that it is of little importance now.

 

References

Kigozi, G., Wawer, M., Ssettuba, A., Kagaayi, J., Nalugoda, F., Watya, S., … & Serwadda, D. (2009). Foreskin surface area and HIV acquisition in Rakai, Uganda (size matters). AIDS (London, England)23(16), 2209. doi: 10.1097/QAD.0b013e328330eda8. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3125976/

Matthes, A. C. S., & Zucca-Matthes, G. (2016). Measurement of vaginal flexibility and its involvement in the sexual health of women. Journal of Women’s Health Care5(1), 1-4. doi: 10.4172/2167-0420.1000302. https://www.researchgate.net/profile/Angelo_Matthes/publication/298805584_Measurement_of_Vaginal_Flexibility_and_Its_Involvement_in_the_Sexual_Health_of_Women/links/5729e72b08ae2efbfdbbfbd5.pdf

Veal, D., Miles, S., Bramley, S., Muir, G., & Hodsoll, J. (2015). Am I normal? A systematic review and construction of nomograms for flaccid and erect penis length and circumference in up to 15,521 men. BJU International, 115(6), 978-986. doi: 10.1111/bju.13010. http://onlinelibrary.wiley.com/doi/10.1111/bju.13010/full

 

Chiropractors in a Fallen World

When I was 18, I woke up one morning with severe pain in my sacrum, the lowest part of my back. I found that I couldn’t walk, sit, crawl, kneel, or do anything comfortably except lie down. At the age of 18, you shouldn’t wake up one morning unable to walk.

Image result for chiropractor

I called a chiropractor I had recently met. She and I both specialized in maternity and newborns, so it was an eagerly-anticipated meeting, though honestly, it went nowhere because we had almost no professional need for each other. But now I found I had a personal need for her.

It took a few days to get in to see her, during which time I tried every recommended treatment she offered, from heat to cold, from massage to drugs. After the first adjustment, the pain almost completely vanished. After the second, it was entirely nonexistent. Initially, I saw her twice a week, then once a week, then once every other week, and finally once a month.

Having visits once a month was sufficient to control my pain. As long as I saw her once a month, the pain was gone. However, I struggled to square the idea that I, a healthy 18-year-old who had never experienced any injuries and didn’t have any musculoskeletal diseases, could be living in chronic pain. When the first chiropractor moved away, I tried another. After she moved away, I tried another and another. They all kept me out of pain, but I was frustrated by the need to seek chronic care. Would I need to use chiropractors for the rest of my life?

Image result for chiropractor

The second chiropractor introduced me to Foot Levelers. These eliminated my pain for a year at a time or more. However, they are expensive and only cover the pain. I thought surely there must be a permanent fix somewhere.

I haven’t found that permanent fix. And I’m having to accept the idea that I will simply live with chronic pain for the rest of my life. It seems like it shouldn’t be that way, but however you look at it, that’s sort of a fact of life. From the evolutionary perspective (specifically, the Laws of Thermodynamics), everything runs down over time. From the creationist perspective, sickness entered the world after the Fall. We live in a Fallen world, and my chronic pain is one of many symptoms of our world’s sickness.

It may seem hopeless when I phrase it like that. But let me put it this way…

With chiropractors, I experienced complete or nearly complete symptom relief with completely non-invasive and relatively inexpensive regular adjustments and/or Foot Levelers.

With mainstream medical doctors, I would possibly undergo surgery with the promise of more chronic pain (just a different kind) and no assurance of cure, and physical therapy to somewhat ameliorate the problems caused by the surgery. I would also receive pain medication, which would become less and less effective over time, a pharmacological fact known as “tolerance,” which would lead to more and more use of heavier and heavier drugs until I was popping tens of pills per day, many of them narcotics, and likely developing dependence and even addiction.

Without either chiropractors or medical doctors, I would experience crippling pain every day of my life.

I choose the better option. And I am eternally grateful to my chiropractors for keeping me out of pain.

Is Circumcision Cosmetic?

A philosophical question sometimes raised is the following:

“Is circumcision cosmetic?”

The answer is YES and NO.

baby-boy

Definition of Cosmetic

The term “cosmetic” comes from the Greek kosmetikos, which comes from kosmein (“arrange” or “adorn”), which comes from kosmos (“order” or “adornment”). Thus, “cosmetic” would refer to anything that restores or improves the appearance of something. However, “cosmetic” is also very much subjective.

For example, a very decorative bridle has both the non-cosmetic function of controlling the horse and the cosmetic function of improving the horse’s appearance. However, to an animal rights activist who sees any form of animal bondage as ugly, the bridle would not serve a cosmetic purpose. Obviously, it also serves no cosmetic purpose to the horse himself, either. As in this situation, almost anything may be either cosmetic or non-cosmetic depending on the subjective feelings of the audience.

 

Cosmetic, Medical, or Both?

When something is referred to as “purely cosmetic” or “only cosmetic” or “solely cosmetic,” the implication is that it serves no purpose other than to improve the appearance.

For example, breast augmentation is purely cosmetic. However, breast reduction surgery may be cosmetic or it may be a combination of medical and cosmetic because reducing the size of the breasts reduces strain on the upper back, posing health benefits.

It is also possible for something to have medical purpose without being cosmetic, and this is, by far, the most common reason for a given surgery.

For example, a mastectomy for breast cancer serves medical purpose, but does not improve the woman’s appearance (in any culture) and thus is not cosmetic. If, however, the woman and her physician opted for a combination mastectomy and breast reconstruction surgery, it would be both medical and cosmetic since the mastectomy is purely medical and the breast reconstruction is purely cosmetic.

 

So What About Circumcision?

Even intactivists must admit that there are times when circumcision poses medical benefits. Anti-circumcision physicians around the globe admit that prophylactic (preventive; i.e., before there’s a problem) newborn circumcision poses medical benefits; the disagreement is whether the medical benefits outweigh the cultural, cosmetic drawbacks to circumcision in anti-circumcision cultures where the foreskin is highly valued. Nonetheless, it is undeniable that circumcision does have medical benefits, and so newborn circumcision cannot sincerely be labeled “purely” or “only” or “solely” cosmetic.

Furthermore, circumcision may not be cosmetic at all. If you consider a circumcised penis to be more attractive than an uncut penis, then circumcision would be cosmetic for you. If, however, you consider an uncut penis to be more attractive, then circumcision, like a mastectomy, would not be cosmetic. Thus, whether circumcision is cosmetic depends entirely on the subjective feelings of the people who would be affected by, and must make decisions regarding, that penis—e.g., the parents, the child, and his future partners. If the parents oppose circumcision for cultural reasons (e.g., most Western Europeans), then their choice is solely cosmetic. If the parents or the individual choose(s) circumcision for cultural reasons without regard for the proven health benefits (e.g., certain tribal circumcisions), then their choice is purely cosmetic, but the procedure itself is not purely cosmetic because the procedure still has health benefits.

Parents in developed nations rarely make the decision to circumcise based on a desire for their child’s penis to be “attractive.”* Rather, nearly all parents in developed nations choose circumcision at least in part due to a belief in the medical benefits. Thus, it cannot be argued that the choice is cosmetic in all, or even most, cases. In fact, because the medical benefits are cited even by those making a primarily religious choice, one would be hard-pressed to find a pro-circ parent (i.e., one who currently identifies as pro-circumcision, regardless of the choice they ended up making for financial or other reasons) whose reason was entirely cosmetic.

 

The Bottom Line

So in short, because it has health benefits, the circumcision procedure cannot be considered “purely” cosmetic. Furthermore, circumcision is almost never a cosmetic choice in the developed world because it is not made based on a belief in the greater attractiveness of the circumcised penis. However, the end-result may be cosmetic if the people involved generally consider it to be more attractive. Thus, circumcision is either: (1) purely medical and non-cosmetic, or (2) a combination of medical and cosmetic. However, circumcision cannot sincerely be labeled “purely cosmetic.”

 

Side Notes

*However, intactivists’ projection of this (the belief in the circumcised penis’s attractiveness) on pro-circ parents as their primary reason for choosing circumcision strongly implies that intactivists’ choice not to circumcise is largely based on a belief that the uncut penis is attractive—which, frankly, is quite disturbing—as demonstrated by their inability to conceive of people choosing circumcision for any other reason and projection of their own reasons onto others.

Pneumococcal Vaccine (Pneumonia, Meningitis) SHORT

This is the short version. See the long version with references here.

streptococcus_pneumoniae_2

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 (Weekly Topic 05), pneumococcal, and meningococcal (Weekly Topic 03).

There are two types of pneumococcal vaccines: conjugated (PCV) and unconjugated (PPSV).

What is pneumococcus?

Streptococcus pneumoniae, often referred to as pneumococcus, is a bacterium. It may have a capsule or not have a capsule. The structures on the capsule determine its serotype. It can adopt or change its capsule, thus changing its serotype. This is called “serotype switching.” There are over 90 serotypes. Which serotypes are most common and how many are resistant to drugs varies significantly by geographic location.

S. pneumoniae is normally carried by healthy people with no symptoms (asymptomatic carriers). Depending on the population, 5-60% may be carriers. About half of babies become carriers by age 6 months and almost 100% become carriers by age 2 years. Carriage is more common after viral infection (especially influenza). Asymptomatic carriage typically lasts months. Because carriage is so common, disease is relatively rare.

S. pneumoniae is a common cause of otitis media (middle ear infection). If disease develops, complications are uncommon but include pneumonia, meningitis, and sepsis.

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. The best prevention is to boost the immune system, avoid people who are sick, and engage in a generally healthy lifestyle. The vitamin C protocol for pertussis may help treat pneumococcal infection.

How effective are the vaccines at preventing asymptomatic carriage?

Neither PPSV nor PCV decrease asymptomatic carriage. Some studies find that asymptomatic carriage increases with PCV. After PCV, vaccine-targeted pneumococcal serotypes decrease but non-vaccine serotypes increase (called “serotype replacement”), and carriage of other species of bacteria (including HiB, M. catarrhalis, and Staphylococcus aureus) increase. FluMist vaccination also increases carriage of S. pneumoniae and Staph.

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.

1. Special Populations. The vaccine is less effective in the populations who are most susceptible to complications from pneumococcus: immunosuppressed patients, patients with frequent respiratory infections, the elderly, and young children. Some studies found that vaccination of children with PCV was followed by an increase in drug-resistant pneumococcal infections in young children and/or the elderly.

2. Serotype Replacement. S. pneumoniae can change its serotype after infecting someone. When one serotype is targeted by a vaccine, the bacteria can simply infect the vaccinated child and then switch its serotype in order to bypass the child’s defenses. This is called “vaccine escape.” The newest PCV targets 13 serotypes, but there are over 90 pneumococcal serotypes. After vaccination, researchers noted significant serotype replacement, which has often resulted in no change or an increase in the total number of IPD cases. Some studies have also shown an increase in antibiotic resistance.

3. Otitis Media (Ear Infection). 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. Studies have found either a 6-7% decrease or no change in AOM; no change in recurrent AOM; and an increase in other serotypes (serotype replacement) and other species of bacteria which are more likely to be antibiotic resistant and harder to treat. In other words, the vaccine may or may not affect the rate of AOM but increases the likelihood that AOM will be difficult to treat.

4. Invasive Pneumococcal Disease (IPD). Studies vary significantly, with results ranging from a decrease to no change to an increase in IPD; however, serotype replacement is common. Disease caused by non-vaccine serotypes is more severe and some studies report it is also more likely to be antibiotic-resistant and more difficult to treat. The worst effects occur in the very young, the very old, and those who’ve received the most doses of the vaccine.

a. Pneumonia. In children, studies find slight decrease, no change, or significant increase in overall pneumonia cases; extensive serotype replacement; and an increase in empyema (severe pneumonia). In other words, the vaccine may or may not affect the rate of pneumonia in children, but it increases the rate of severe pneumonia that is difficult to treat. In older adults, pneumococcal vaccination is ineffective.

b. Meningitis. Studies seem to agree that meningitis rates decrease, but this drop in meningitis occurs alongside an increase in pneumonia and sepsis.

c. Sepsis. Studies have found decrease, increase, or no change in sepsis rate; extensive serotype replacement; and increases in severe disease, drug-resistant cases, and cases caused by other bacteria (notably E. coli). In other words, the vaccine may or may not affect the sepsis rate, but makes it more difficult to treat.

What are the risks of the vaccine?

A short list of the most concerning risks includes:
• seizures
• asthma
• thrombocytopenia
• autoimmune diseases
• local reactions that will be mistaken for infection and result in unnecessary hospitalization and antibiotic use

So what’s the bottom line?

S. pneumoniae is so common that almost 100% of the population carries it and develops some degree of immunity by age 2. There are over 90 serotypes, and the bacteria easily change their serotype to avoid the host’s vaccine-induced defenses. The vaccine may increase asymptomatic carriage not only of S. pneumoniae but also of other bacteria and so cannot contribute to herd immunity and may actually 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.

HiB Vaccine (Meningitis)

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

H. influenzae type B, (c) NHS

H. influenzae type B, (c) NHS

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 will be discussed here, and pneumococcal will be discussed in a future Weekly Topic.

According to the CDC Vaccination Schedule (2015), HiB vaccination occurs at 2 mo, 4 mo, 6 mo, and 12/15 mo. No further doses are recommended after the 15 mo dose, even if it was the only dose ever received. It is not recommended after age 5 years in healthy children. It is only available as a combination vaccine, not alone [1, 2]. In Canada, depending on province/territory, a HiB combination vaccine is typically recommended at 2 mo, 4 mo, 6 mo, and 18 mo [3].

 

What is HiB?

Haemohpilus influenzae type B is a bacterium that normally lives in the respiratory tracts of healthy people without causing disease. Up to 5% of the population is infected at a given time, and most children become infected by H. influenzae bacteria by the age of 5, whereby they develop immunity. Infection is more common in crowded housing and settings such as daycare; in fact, in daycare, the infection rate is approximately 15%, 3-15 times the proportion of the general population. Asymptomatic carriers remain infected and contagious for months at a time and the bacteria may easily pass from one person with disease through a long line of asymptomatic carriers before causing disease in another. It is present in the nose and throat and thus is passed by coughing or contact with mucus. However, cribs and toys of daycare children known to be asymptomatic carriers test negative for the bacteria, so contact with contagious children’s belongings is not believed to be a route of transmission. [4]

Because H. influenzae bacteria are a normal part of our respiratory tracts, probably 100% of the population becomes infected at some point, and most infections are asymptomatic, HiB disease is relatively very rare. However, when it does occur, HiB disease may result in sepsis, meningitis, and even death. Among those with HiB disease, approximately 3-6% die and 15-35% suffer permanent neurological sequelae (the most common being partial hearing loss). The most common symptoms of HiB disease include fever, decreased mental status, and stiff neck. [4, 5, 6]

 

How can I prevent or treat HiB in my child?

Conditions that make an individual more susceptible to HiB disease include recent viral infection, smoking or other respiratory irritants, immune suppression (e.g., sickle-cell anemia, absence of a spleen, antibody deficiency disorders, cancer, chemotherapy, etc.), and crowded housing or environment. [4] Avoid exposing your child to these triggers as much as possible by smoking cessation, avoiding crowded living spaces if possible, boosting the immune system, etc., and engaging in a generally healthy lifestyle. If your child has a known exposure to HiB, prompt evaluation by a physician for prophylactic antibiotics may be prudent.

Breastfeeding offers significant protection against HiB, lasting years after weaning [4, 7]. If breastfeeding is not possible due to adoption or other issues, look into relactation, pumping, or donor milk.

Note as discussed later in this post that there is an increased risk of HiB disease in the first week following vaccination. Therefore, if you choose to vaccinate and your child develops symptoms of HiB following vaccination, take it seriously.

 

How effective are the vaccines at preventing asymptomatic carriage?

Several studies have found HiB carriage to be reduced (but not eliminated) by vaccination. [4] Other studies have shown that when HiB vaccination was introduced to a population, HiB disease rates in both vaccinated and unvaccinated infants decreased, but were not eliminated in spite of very high vaccination rates [4]. Because it does not eliminate asymptomatic carriage, and the bacteria can jump from asymptomatic carrier to asymptomatic carrier regardless of the carrier’s vaccine status before causing disease in a susceptible individual, the vaccine cannot be relied upon for herd immunity, as evidenced by continued HiB disease in highly vaccinated populations.

 

How effective is the HiB vaccine?

Prior to the introduction of the vaccine, HiB caused over 80% of all invasive H. influenzae disease among children [8]. The incidence of HiB began to drop before the introduction of the vaccine [9, 10] and continued to drop after vaccination.

The HiB vaccine is of questionable efficacy, with some studies finding it not to be protective in children younger than 18 months, others finding variable efficacy in children over the age of 2, and others finding an increased risk of meningitis immediately following vaccination, with efficacy ranging from 88% to -69%. [6, 11] Newer conjugate vaccines have widely ranging efficacy depending on the population in which it they are tested. For example, the diphtheria-HiB (PRP-D) vaccine ranged from 35% efficacy (in producing an antibody response) in Alaskan Natives and <40% in Finnish children to 87% in another group of Finnish children [12]. Even across a single country, the same vaccine may be associated with vastly varying efficacy, as in one study that found a HiB vaccine that was effective in other areas of the U.S. was not associated with increased antibody response or decreased disease rate in Minnesota [13]. Another study found that HiB-vaccinated children with HiB disease had significantly lower HiB antibody levels than unvaccinated children with HiB disease. This was in spite of appropriate antibody response to other vaccines they had received. It’s thought to be partly due to a genetic defect that affects their ability to produce antibodies specifically to HiB [14].

All of the above estimates of efficacy depend on assumptions regarding what antibody level will be effective at preventing HiB disease, though the CDC states, “the precise level of antibody required for protection against invasive disease is not clearly established.” [15] However, the change in HiB incidence following vaccination can give us an idea of the vaccine’s efficacy.

The introduction of the HiB vaccine was followed by a shift in the dominant strains of H. influenzae from type B (HiB) to predominately nontypeable and type F (HiF)—that is to say, the incidence of infections and invasive disease caused by type B dropped while the incidence of infections and invasive disease caused by other strains increased. The overall incidence of H. influenzae invasive disease and death increased after the introduction of the vaccine. In other words, the introduction of the vaccine was followed by a net increase in H. influenzae-related morbidity and mortality in spite of the decrease in type B disease and death. [8]

This suggests that the HiB vaccine increases the overall risk of H. influenzae morbidity and mortality by increasing one’s risk particularly to non-B H. influenzae. This goes back to the theory of original antigenic sin. In short, people who are vaccinated against one strain are able to produce antibodies only to the antigens included in the vaccine, which handicaps them in fighting other viruses or bacteria that are similar enough to trigger their body’s antibody response but different enough that they don’t have antibodies against the primary antigens. In the case of pertussis, we see how vaccination against PRN-positive B. pertussis increases the risk of PRN-negative B. pertussis, B. parapertussis, and sometimes B. holmesii [16]. In the case of N. meningitidis, we see how the meningococcal vaccine increases the risk of infection with serogroups not included in the vaccine [17]. And here we see that the HiB vaccine increases the risk of H. influenzae strains not included in the vaccine, as discussed above.

The majority of H. influenzae invasive disease occurs in those aged 65 years or older. Furthermore, the introduction of the vaccine in children was followed by a rise in H. influenzae invasive disease and death in adults, especially the vulnerable elderly, demonstrating a negative herd effect. The introduction of the vaccine in children was followed by a net increase in H. influenzae-related morbidity and mortality in those too old to be vaccinated and in the vulnerable. In other words, the vaccine seems to have the opposite effect on the herd—a harmful rather than a helpful effect. [8]

 

Are there other infectious diseases related to HiB 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. [18] 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. [5, 19]

 

What are the risks of the vaccine?

Type 1 Diabetes. The HiB vaccine is associated with a 25% increased incidence of type 1 diabetes as compared to vaccinated children who did not receive the HiB vaccine [5, 20, 21, 22; 23, p. 872; 24]. The risk increases with just one dose of HiB vaccine, but is highest in children who received all four doses [25]. In fact, the long-term complications from HiB-vaccine-induced type 1 diabetes alone outweigh the long-term complications from HiB disease if no children were vaccinated against HiB [26].

H. influenzae non-B Invasive Disease. As discussed above, the vaccine is associated with an overall increased incidence in H. influenzae infections and deaths. This is because the increase in non-B infections is more than the decrease in type B infections. The increase in non-B H. influenzae disease and death alone outweighs the drop in type B disease and death.

HiB Invasive Disease. Many studies have found an increased incidence of HiB invasive disease in the first week following vaccination with some types of HiB vaccine. “The evidence favors acceptance of a causal relation between unconjugated PRP vaccine and early-onset Hib disease.” [11] It’s said that this risk is only present with unconjugated vaccines (which we no longer use in the U.S.) [11], but it’s actually more common with conjugated vaccines (which we currently use in the U.S.) [27]. At times, this has occurred as early as 3 hours after HiB vaccination [28] and after a second HiB vaccine when there was no reaction to the first [29]. It’s important to note that this is not due to injection with live bacteria—that is, the contents of the vaccine do not directly cause the infection. Rather, it may be due to two related issues. One is that a dramatic decrease in antibody levels occurs in the first few days after vaccination due to the antibodies already present in the child pre-vaccination being quickly used up in fighting the antigens found in the vaccine, leaving the child susceptible to HiB in the environment due to inadequate antibody levels [28]. Another is the vaccine causing a briefly suppressed immune system, which makes the recipient more susceptible to disease. This is called “provocation disease” and was first recorded in medical literature in the 1960s in relation to polio, tuberculosis, and a few other diseases occurring secondary to vaccination [30, pp. 179-188].

Transverse Myelitis. There may be an association between the vaccine and transverse myelitis. This association is based on VAERS reports, not on medical literature. “The evidence is inadequate to accept or reject a causal relation between Hib vaccines and transverse myelitis.” [11]

Guillain-Barré Syndrome (GBS). There may be an association between the vaccine and transverse myelitis. This association is based on a published case series and VAERS reports. “The evidence is inadequate to accept or reject a causal relation between Hib vaccines and GBS.” [11]

Thrombocytopenia. This possible association is based on data from a HiB vaccine trial conducted in adults, as well as VAERS reports. “The evidence is inadequate to accept or reject a causal relation between Hib vaccines and thrombocytopenia.” [11]

SIDS. There are VAERS reports of SIDS cases occurring in close temporal association to HiB vaccination. [31] The association does not seem to have been studied in depth.

Asthma and Allergies. A Swiss study found HiB-vaccinated children to have a higher incidence of asthma and allergies as compared to HiB-unvaccinated children [32]. Studies in guinea pigs found asthmatic reactions to begin as early as four days following HiB vaccination [33].

Epiglottitis. The same Swiss study referenced above [32] found that an increase in epiglottitis was associated with the HiB-vaccine-associated increase in asthma and allergies.

Autism. The autism rate did not change significantly after the introduction of the MMR and DTP vaccines. However, it began to rise significantly after the introduction of the HiB and Hep B vaccines. Many parents have noted autistic regression following the MMR, which used to be given at the same time as the HiB vaccine. [34] Correlation does not equal causation, but a study comparing the autism rates in children who did and children who did not receive the HiB vaccine would be interesting. To my knowledge, such a study has not been conducted.

Encephalitis. There is at least one report of encephalitis occurring after HiB vaccination, but the child was simultaneously vaccinated against DPT (known to be associated with encephalitis) and OPV, so it’s uncertain whether the HiB vaccine can be blamed in this case. [35]

Others. Convulsions (seizures) and allergic reactions to the vaccine (including anaphylaxis) have also been reported. [36]

 

What vaccines are offered against HiB?

In the U.S. and Canada, there are no HiB-only vaccines. All HiB vaccines are combo shots. (NOTE: These ingredients lists are not complete; they only list the most alarming ingredients.)

  • ActHIB: tetanus-HiB (tetanus and HiB antigens, ammonium sulfate, formaldehyde, casein [milk protein]) [37]
  • Pentacel: DTaP-IPV-HiB (contains ActHIB; diphtheria, tetanus, acellular pertussis, 3 strains of inactivated poliovirus, and HiB antigens, aluminum, polysorbate 80, formaldehyde, cow serum, 2-phenoxyethanol, neomycin, polymyxin B, ammonium sulfate, casein [milk protein], and MRC-5 [aborted fetus cells]) [38]
  • MenHibrix: Men C/Y-tetanus-HiB (meningococcal C/Y, HiB, and tetanus antigens, formaldehyde) [39]
  • PedvaxHiB: Men B-HiB (meningococcal B and HiB antigens, aluminum) [40]
  • Hiberix: tetanus-HiB (tetanus toxoid and HiB antigens, formaldehyde, lactose) [41]
  • Comvax: Hep B-Men B-HiB (contains PedvaxHiB; hepatitis B, meningococcal B, and HiB antigens, yeast cells, soy, aluminum, and formaldehyde) [42]

 

So what’s the bottom line?

The bottom line is that HiB is so common that 100% of the population carries it at some point and virtually 100% of the population is immune to it by age 5. The vaccine does not prevent asymptomatic carriage and so cannot be relied upon for herd immunity. The vaccine simultaneously decreases the risk of H. influenzae type B, which makes up a minority of strains today, and increases the risk of all other H. influenzae strains. Vaccination of children is associated with an overall increased risk of H. influenzae invasive disease and death in both children and adults, especially the elderly. HiB vaccination is also associated with increased incidence of other more dangerous and less treatable bacterial infections. The vaccine is associated with type 1 diabetes, and the complications of vaccine-induced type 1 diabetes when vaccinated alone outweighs the risk of HiB disease when not vaccinated. The vaccine is also associated with other adverse events such as asthma, allergies, epiglottitis, an increased incidence of HiB disease in the first week after vaccination, and more. The bottom line is the risk of death is higher with the vaccine than without.

 

References

[1] http://www.cdc.gov/vaccines/schedules/downloads/child/0-18yrs-child-combined-schedule.pdf

[2] http://www.cdc.gov/vaccines/vpd-vac/hib/vac-faqs-hcp.htm

[3] http://healthycanadians.gc.ca/healthy-living-vie-saine/immunization-immunisation/children-enfants/schedule-calendrier-table-1-eng.php

[4] Evans, A.S. & Brachman, P.S. (2013). Bacterial Infections of Humans: Epidemiology and Control (Fifth Ed.). (pp. 315-316) New York: Springer-Verlag New York Inc.

[5] https://www.youtube.com/watch?v=QVE2l2RJ8lY

[6] http://www.cdc.gov/vaccines/pubs/pinkbook/downloads/hib.pdf

[7] http://www.ncbi.nlm.nih.gov/pubmed/10569222

[8] http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3322072/

[9] http://www.ncbi.nlm.nih.gov/pubmed/8417239

[10] http://www.unboundmedicine.com/medline/citation/8143010/Eradication_of_Haemophilus_influenzae_type_b_disease_in_southern_California__Kaiser_UCLA_Vaccine_Study_Group_

[11] http://www.ncbi.nlm.nih.gov/books/NBK236299/

[12] http://www.cdc.gov/mmwr/preview/mmwrhtml/00041736.htm

[13] http://www.ncbi.nlm.nih.gov/pubmed/2785147

[14] http://www.ncbi.nlm.nih.gov/pubmed/3491315

[15] http://www.cdc.gov/mmwr/preview/mmwrhtml/00023705.htm

[16] https://schaabling.wordpress.com/2015/12/18/pertussis-whooping-cough/

[17] Weekly Topic 03: Meningococcal Vaccine (Meningitis)

[18] “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.

[19] http://www.wellwithin1.com/HibPneuButler1993to2006letters.pdf

[20] http://www.ncbi.nlm.nih.gov/pubmed/14679101

[21] http://www.ncbi.nlm.nih.gov/pubmed/12482192

[22] http://www.ncbi.nlm.nih.gov/pubmed/12793601

[23] http://care.diabetesjournals.org/content/23/6/872.long

[24] Shoenfeld, Y., Agmon-Levin, N., & Tomljenovic, L. (2015). Vaccines and Autoimmunity (pp. 185-190). Hoboke, NJ: Wiley Blackwell.

[25] http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1116914/

[26] http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1114674/

[27] http://www.ncbi.nlm.nih.gov/pubmed/1669664

[28] http://www.ncbi.nlm.nih.gov/pubmed/8762955

[29] http://www.ncbi.nlm.nih.gov/pubmed/9133234

[30] http://soilandhealth.org/wp-content/uploads/02/0201hyglibcat/020152.vac.haz/vac.haz.pdf

[31] http://www.ncbi.nlm.nih.gov/books/NBK236284/

[32] http://www.ncbi.nlm.nih.gov/pubmed/9027536

[33] http://www.ncbi.nlm.nih.gov/pubmed/6335351

[34] https://web.archive.org/web/20041029232155/http://mothering.com/articles/growing_child/vaccines/biochemistry.html

[35] http://www.ncbi.nlm.nih.gov/pubmed/8103131

[36] http://www.ncbi.nlm.nih.gov/pubmed/3497381

[37] http://www.fda.gov/downloads/BiologicsBloodVaccines/Vaccines/ApprovedProducts/UCM109841.pdf

[38] http://www.fda.gov/downloads/BiologicsBloodVaccines/Vaccines/ApprovedProducts/UCM109810.pdf

[39] http://www.fda.gov/downloads/BiologicsBloodVaccines/Vaccines/ApprovedProducts/UCM308577.pdf

[40] http://www.fda.gov/downloads/BiologicsBloodVaccines/Vaccines/ApprovedProducts/UCM253652.pdf

[41] http://www.fda.gov/downloads/BiologicsBloodVaccines/Vaccines/ApprovedProducts/UCM179530.pdf

[42] http://www.fda.gov/downloads/BiologicsBloodVaccines/Vaccines/ApprovedProducts/UCM109869.pdf

HiB Vaccine (Meningitis) SHORT

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

H. influenzae type B, (c) NHS

H. influenzae type B, (c) NHS

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 will be discussed here, and pneumococcal will be discussed in a future Weekly Topic.

The HiB vaccine is generally given at 2, 4, 6, and 12-18 months (though it varies by country and province).

 

What is HiB?

Haemohpilus influenzae type B (HiB) is a bacterium that normally lives in the respiratory tracts of healthy people without causing disease. Up to 5% of the population is infected at a given time, and most children become infected by H. influenzae bacteria by the age of 5, whereby they become immune. Infection is more common in crowded housing and settings such as daycare; in fact, in daycare, the infection rate is approximately 15%. Asymptomatic carriers remain infected and contagious for months at a time and the bacteria easily pass through a long line of asymptomatic carriers before causing disease in someone. It is present in the nose and throat and thus is passed by coughing or contact with mucus.

Because (a) H. influenzae bacteria are a normal part of our respiratory tracts, (b) 100% of the population becomes infected at some point, and (c) most infections are asymptomatic, HiB disease is relatively very rare. However, when it does occur, HiB disease may result in sepsis, meningitis, and even death. Among those with HiB disease, approximately 3-6% die and 15-35% suffer permanent neurological sequelae (the most common being partial hearing loss). The most common symptoms of HiB disease include fever, decreased mental status, and stiff neck.

 

How can I prevent or treat HiB in my child?

Conditions that make an individual more susceptible to HiB disease include recent viral infection, smoking or other respiratory irritants, immune suppression, and crowded housing or crowded environment. Avoid exposing your child to these triggers as much as possible by smoking cessation, avoiding crowded living spaces if possible, boosting the immune system, etc., and engaging in a generally healthy lifestyle. If your child has a known exposure to HiB, prompt evaluation by a physician for prophylactic antibiotics may be prudent.

Breastfeeding offers significant protection against HiB, lasting several years after weaning. If breastfeeding is not possible due to adoption or other issues, look into relactation, pumping, or donor milk.

 

How effective are the vaccines at preventing asymptomatic carriage?

HiB carriage is reduced but not eliminated by vaccination. Extremely high vaccination rates reduce but do not eliminate HiB disease. As mentioned above, the bacteria can jump from asymptomatic carrier to asymptomatic carrier regardless of the carrier’s vaccine status before causing disease in a susceptible individual. Therefore, because the vaccine does not prevent asymptomatic carriage, it cannot be relied upon for herd immunity.

 

How effective is the HiB vaccine?

Prior to the introduction of the vaccine, HiB caused over 80% of all invasive H. influenzae disease among children. The incidence of HiB began to drop before the introduction of the vaccine and continued to drop after the introduction of the vaccine.

The HiB vaccine’s efficacy ranges from -69% (increased risk) to 88% (decreased risk), with the efficacy seeming to depend not only on the type of HiB vaccine used, but also on the populations in which it was used. It varies drastically even from state to state or province to province in the same country.

HiB vaccination is associated with *decreased* type B H. influenzae (HiB) disease and death but *increased* non-B H. influenzae disease and death. The overall net effect of HiB vaccination has been **a net increase in H. influenzae disease and death**. This is likely due to the crippling effect of “original antigenic sin,” where the body is trained to produce antibodies against one strain and becomes unable to produce antibodies against different strains. This makes the vaccinated person at **increased risk of contracting other strains**. Furthermore, the greatest increase in H. influenzae disease and death was in the (unvaccinated) elderly. If herd immunity existed with this vaccine, we would expect a decreased risk in the unvaccinated. However, HiB vaccination of infants was followed by an increased risk in all age groups (vaccinated or unvaccinated) but especially in the (unvaccinated) elderly, suggesting a negative herd effect.

 

Are there other infectious diseases related to HiB vaccination?

It appears that pertussis vaccination caused an increase in (more dangerous, less treatable) HiB, hence the HiB vaccine; HiB vaccination caused an increase in pneumococcal (even more dangerous, less treatable) infections, hence the PCV vaccine; and the PCV caused an increased in (still more dangerous, less treatable) meningococcal infections, hence the MCV vaccine. There is concern that the MCV will also be followed by the sudden increase of another more dangerous and less treatable bacterial disease.

 

What are the risks of the vaccine?

Type 1 Diabetes. The HiB vaccine increases the risk of type 1 diabetes with just one dose, and the risk increases with more doses. In fact, the long-term complications from HiB-vaccine-induced type 1 diabetes alone outweigh the long-term complications from HiB disease if no children were vaccinated against HiB.

H. influenzae non-B Invasive Disease. As discussed above, the vaccine is associated with an overall increased incidence in H. influenzae infections and deaths. This is because the increase in non-B infections is more than the decrease in type B infections. The increase in non-B H. influenzae disease and death alone outweighs the drop in type B disease and death.

HiB Invasive Disease. HiB vaccination increases the risk of HiB invasive disease and death in the first week after vaccinating. This has happened as shortly as 3 hours after vaccinating and after a second vaccine when there was no reaction to the first.

Others. Other known or suspected reactions include transverse myelitis, Guillain-Barre Syndrome, thrombocytopenia, SIDS, asthma and allergies, epiglottitis, autism, encephalitis, convulsions (seizures), and allergic reactions to the vaccine (including anaphylaxis).

 

So what’s the bottom line?

The bottom line is that HiB is so common that 100% of the population carries it at some point and virtually 100% of the population is immune to it by age 5. The vaccine does not prevent asymptomatic carriage and so cannot be relied upon for herd immunity. The vaccine simultaneously decreases the risk of H. influenzae type B, which makes up a minority of strains today, and increases the risk of all other H. influenzae strains. Vaccination of children is associated with an overall increased risk of H. influenzae invasive disease and death in both children and adults, especially the elderly. HiB vaccination is also associated with increased incidence of other more dangerous and less treatable bacterial infections. The vaccine is associated with type 1 diabetes, and the complications of vaccine-induced type 1 diabetes alone outweighs the risk of HiB disease when not vaccinated. The vaccine is also associated with other adverse events such as asthma, allergies, epiglottitis, an increased incidence of HiB disease in the first week after vaccination, and more. The bottom line is the risk of death is higher with the vaccine than without.

 

Meningococcal Vaccine (Meningitis) (SHORT)

This is the short version of the meningococcal vaccine post. For the long version and references, check here.

400px-NMeningitidis

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 will be discussed here and the others in future Weekly Topics.

What is meningococcus?

Neisseria meningitidis, the meningococcal bacteria, is passed by coughing or contact with saliva and is normally present in the respiratory tracts of healthy people without causing disease. Probably 100% of people become infected at some point and about 5-35% of the population is infected with the bacteria at any time. Asymptomatic carriers carry the bacteria for months or even years.

N. meningitidis is divided into serogroups (not strains). Serogroup B is responsible for 60% of U.S. cases of meningococcal disease and is targeted by one vaccine. Serogroups A, C, Y, and W-135 are less common and are targeted by another vaccine (some countries have a C-only vaccine). Natural infection with one serogroup or with a different species called N. lactamica confers immunity to all serogroups and it’s rare for an unvaccinated individual to become infected with one serogroup and later become infected with a different serogroup.

According to the CDC, “For unknown reasons, incidence has declined since the peak of disease in the late 1990s…. This decline began before implementation of routine use of meningococcal vaccines in adolescents and have occurred in all serogroups.” Last year (2014), there were a total of 386 meningococcal disease cases and an estimated 39-58 deaths.

Meningococcal disease occurs most frequently in those with suppressed immune systems. Risk factors and prevention techniques are in the longer version of this post.

How effective are the vaccines at preventing asymptomatic carriage?

One study suggested that A/C/Y/W-135 vaccination may reduce the length of (but not eliminate) asymptomatic carriage. However, the vaccine against serogroup B does not prevent asymptomatic carriage. Thus, the vaccines should not be relied upon for herd immunity.

How effective are the vaccines at preventing disease?

As discussed above, natural infection with one serogroup or a related species confers immunity against all serogroups. However, the vaccine potentially protects against only the serogroup in the vaccine. It’s said to be 85% effective, but has never been proven to prevent disease, only to induce an antibody response.

As also discussed above, it’s rare for an unvaccinated individual to become infected with one serogroup and later become infected with another serogroup. However, when N. meningitidis infects a vaccinated individual, the bacteria can change its serogroup in a matter of days to one against which the vaccine offered no protection, whereby it causes disease in and kills the vaccinated individual.

How great is the antibody response produced by the vaccine?

As discussed above, the vaccine has never been proven to prevent disease, only to induce an antibody response. However, following three doses, about half of recipients do not develop an appropriate antibody response, and following four doses, 87% do not respond. Furthermore, the antibodies wane in less than 7 months.

In fact, New Zealand saw an increased incidence of meningococcal disease following three doses of the vaccine. After the four-year vaccination campaign, the New Zealand Herald reported on 109 cases of the vaccine-targeted strain in vaccinated people. For 2006-2008, there were 12 meningococcal deaths, all in vaccinated children. There were no meningococcal deaths in unvaccinated children. Furthermore, the meningococcal disease rate was dropping prior to the introduction of the vaccine but increased during the vaccination campaign.

Is the vaccine safe?

The short version is a resounding no. We will assume the previously discussed false statistic of 85% efficacy is true and combine that with the package inserts’ serious adverse event rate of 1% (A/C/Y/W-135) and 2% (B), the CDC’s estimated 0.3% rate of death following adverse events, and Fall 2015’s U.S. college enrollment of 20.2 million students. If all U.S. college students receive only one injection of each meningococcal vaccine in one year, there will be an estimated 606,000 serious adverse events and 1,818 deaths from meningococcal vaccination of all U.S. college students. Compare that to last year’s 386 meningococcal disease cases and estimated 39-58 deaths in all age groups in the U.S.

Are the meningococcal vaccines linked to autoimmune diseases?

Meningococcal serogroup C or A/C/Y/W-135 vaccines have been definitively or tentatively linked to three autoimmune diseases: Henoch-Schönlein purpura, bullous phemigoid, and Guillain-Barré Syndrome. The serogroup B vaccine took so long to develop primarily because its antigens look very similar to structures on human brain cells, which may increase the risk of neurological autoimmune diseases. However, the serogroup B vaccine is too new to know yet whether it increases the risk of autoimmune diseases.

So what’s the bottom line?

The bottom line is that meningococcal bacteria infect probably 100% of the population and exceptionally rarely cause disease. Natural infection with one serogroup confers immunity against all serogroups whereas vaccination provides immunity only against the serogroups targeted by the vaccine and increase one’s risk to serogroups not included in the vaccine. After infecting a vaccinated person, the bacteria can change their serogroup to one against which the vaccinated individual has no protection. Furthermore, in some populations, vaccination was demonstrated to increase the incidence of meningococcal disease and death. The risk of death from the vaccine far outweighs the risk of death from the disease. The vaccine does not prevent asymptomatic carriage, so the vaccine offers no herd immunity effect.