A Colombian man’s lung tumors turned out to have an extremely unusual cause: The rapidly growing masses weren’t actually made of human cells, but were from a tapeworm living inside him, according to a report of the case.
This is the first known report of a person becoming sick from cancer cells that developed in a parasite, the researchers said.
“We were amazed when we found this new type of disease—tapeworms growing inside a person, essentially getting cancer, that spreads to the person, causing tumors,” said study researcher Dr. Atis Muehlenbachs, a staff pathologist at the Centers for Disease Control and Prevention’s Infectious Diseases Pathology Branch (IDPB).
The man had HIV, which weakens the immune system and likely played a role in allowing the development of the parasite cancer, the researchers said.
Fast forward to the spring of 2017. PreP had recently ushered in the second sexual revolution and everyone was now fucking each other like it was 1979. My wonderful boyfriend and I enjoyed a healthy sex life inside and outside our open relationship. Then he started experiencing stomach problems: diarrhea, bloating, stomach aches, nausea. All too familiar with those symptoms, I recommended he go to the doctor and ask for a stool test. …
His results came back positive for giardia. …
Well, just a few months later, summer of 2017, my boyfriend started experiencing another bout of diarrhea and stomach cramps. … This time the results came back positive for entamoeba histolytica. What the fuck is entamoeba histolytica?! I knew giardia. Giardia and I were on a first name basis. But entamoeba, what now?
Entamoeba histolytica, as it turns out, is another parasite common in developing countries spread through contaminated drinking water, poor hygiene when handling food, and…rimming. The PA treating him wasn’t familiar with entamoeba histolytica or how to treat it, so she had to research (Google?) how to handle the infection. The medical literature (Google search results?) led us back to metronidazole, the same antibiotic used to treat giardia.
When your urge to lick butts is so strong that this keeps happening, you’ve got to consider an underlying condition like toxoplasmosis or kamikaze horsehair worm.
While reading about the conditions in a Burmese prison around the turn of the previous century (The History and Romance of Crime: Oriental Prisons, by Arthur Griffiths)(not good) it occurred to me that there might have been some beneficial effect of the large amounts of tobacco smoke inside the prison. Sure, in the long run, tobacco is highly likely to give you cancer, but in the short run, is it noxious to fleas and other disease-bearing pests?
Meanwhile in Melanesia, (Pygmies and Papuans,) a group of ornithologists struggled up a river to reach an almost completely isolated tribe of Melanesians that barely practiced horticulture; even further up the mountain they met a band of pygmies (negritoes) whose existence had only been rumored of; the pygmies cultivated tobacco, which they traded with their otherwise not terribly interested in trading for worldy goods neighbors.
The homeless smoke at rates 3x higher than the rest of the population, though this might have something to do with the high correlation between schizophrenia and smoking–80% of schizophrenics smoke, compared to 20% of the general population. Obviously this correlation is best explained by tobacco’s well-noted psychological effects (including addiction,) but why is tobacco so ubiquitous in prisons that cigarettes are used as currency? Could they have, in unsanitary conditions, some healthful purpose?
On average, the more THC byproduct that Hagen’s team found in an Aka man’s urine, the fewer worm eggs were present in his gut.
“The heaviest smokers, with everything else being equal, had about half the number of parasitic eggs in their stool, compared to everyone else,” Hagen says. …
THC — and nicotine — are known to kill intestinal worms in a Petri dish. And many worms make their way to the gut via the lungs. “The worms’ larval stage is in the lung,” Hagan says. “When you smoke you just blast them with THC or nicotine directly.”
Smoking kills. But if you’re a bird and if you want to kill parasites, that can be a good thing. City birds have taken to stuffing their nests with cigarette butts to poison potential parasites. Nature reports:
“In a study published today in Biology Letters, the researchers examined the nests of two bird species common on the North American continent. They measured the amount of cellulose acetate (a component of cigarette butts) in the nests, and found that the more there was, the fewer parasitic mites the nest contained.”
Out in the State of Nature, parasites are extremely common and difficult to get rid of (eg, hookworm elimination campaigns in the early 1900s found that 40% of school-aged children were infected); farmers can apparently use tobacco as a natural de-wormer (but be careful, as tobacco can be poisonous.)
In the pre-modern environment, when many people had neither shoes, toilets, nor purified water, parasites were very hard to avoid.
Befoundalive recommends eating the tobacco from a cigarette if you have intestinal parasites and no access to modern medicine.
Overall, 8 intestinal parasite species have been recovered singly or in combinations from 146 (61.8 %) samples. The prevalence in prison population (88/121 = 72.7%) was significantly higher than that in tobacco farm (58/115 = 50.4%).
Because of developing resistance to the existing anthelmintic drugs, there is a need for new anthelmintic agents. Tobacco plant has alkaloid materials that have antiparasitic effect. We investigated the in vitro anthelminthic effect of aqueous and alcoholic extract of Tobacco (Nicotiana tabacum) against M. marshalli. … Overall, extracts of Tobacco possess considerable anthelminthic activity and more potent effects were observed with the highest concentrations. Therefore, the in vivo study on Tobocco in animal models is recommended.
(Helminths are parasites; anthelmintic=anti-parasites.)
So it looks like, at least in the pre-sewers and toilets and clean water environment when people struggled to stay parasite free, tobacco (and certain other drugs) may have offered people an edge over the pests. (I’ve noticed many bitter or noxious plants seem to have been useful for occasionally flushing out parasites, but you certainly don’t want to be in a state of “flush” all the time.)
It looks like it was only when regular sanitation got good enough that we didn’t have to worry about parasites anymore that people started getting really concerned with tobacco’s long-term negative effects on humans.
Crohn‘s is an inflammatory disease of the digestive tract involving diarrhea, vomiting internal lesions, pain, and severe weight loss. Left untreated, Crohn’s can lead to death through direct starvation/malnutrition, infections caused by the intestinal walls breaking down and spilling feces into the rest of the body, or a whole host of other horrible symptoms, like pyoderma gangrenosum–basically your skin just rotting off.
Crohn’s disease has no known cause and no cure, though several treatments have proven effective at putting it into remission–at least temporarily.
The disease appears to be triggered by a combination of environmental, bacterial, and genetic factors–about 70 genes have been identified so far that appear to contribute to an individual’s chance of developing Crohn’s, but no gene has been found yet that definitely triggers it. (The siblings of people who have Crohn’s are more likely than non-siblings to also have it, and identical twins of Crohn’s patients have a 55% chance of developing it.) A variety of environmental factors, such as living in a first world country, (parasites may be somewhat protective against the disease), smoking, or eating lots of animal protein also correlate with Crohn’s, but since only 3.2/1000 people even in the West have it’s, these obviously don’t trigger the disease in most people.
Crohn’s appears to be a kind of over-reaction of the immune system, though not specifically an auto-immune disorder, which suggests that a pathogen of some sort is probably involved. Most people are probably able to fight off this pathogen, but people with a variety of genetic issues may have more trouble–according to Wikipedia, “There is considerable overlap between susceptibility loci for IBD and mycobacterial infections. ” Mycobacteria are a genus of of bacteria that includes species like tuberculosis and leprosy. A variety of bacteria–including specific strains of e coli, yersinia, listeria, and Mycobacterium avium subspecies paratuberculosis–are found in the intestines of Crohn’s suffers at higher rates than in the intestines of non-sufferers (intestines, of course, are full of all kinds of bacteria.)
Crohn’s treatment depends on the severity of the case and specific symptoms, but often includes a course of antibiotics, (especially if the patient has abscesses,) tube feeding (in acute cases where the sufferer is having trouble digesting food,) and long-term immune-system suppressants such as prednisone, methotrexate, or infliximab. In severe cases, damaged portions of the intestines may be cut out. Before the development of immunosuppressant treatments, sufferers often progressively lost more and more of their intestines, with predictably unpleasant results, like no longer having a functioning colon. (70% of Crohn’s sufferers eventually have surgery.)
A similar disease, Johne’s, infects cattle. Johne’s is caused by Mycobacterium avium subspecies paratuberculosis, (hereafter just MAP). MAP typically infects calves at birth, transmitted via infected feces from their mothers, incubates for two years, and then manifests as diarrhea, malnutrition, dehydration, wasting, starvation, and death. Luckily for cows, there’s a vaccine, though any infectious disease in a herd is a problem for farmers.
If you’re thinking that “paratuberculosis” sounds like “tuberculosis,” you’re correct. When scientists first isolated it, they thought the bacteria looked rather like tuberculosis, hence the name, “tuberculosis-like.” The scientists’ instincts were correct, and it turns out that MAP is in the same bacterial genus as tuberculosis and leprosy (though it may be more closely related to leprosy than TB.) (“Genus” is one step up from “species;” our species is “homo Sapiens;” our genus, homo, we share with homo Neanderthalis, homo Erectus, etc, but chimps and gorillas are not in the homo genus.)
The intestines of cattle who have died of MAP look remarkably like the intestines of people suffering from advanced Crohn’s disease.
MAP can actually infect all sorts of mammals, not just cows, it’s just more common and problematic in cattle herds. (Sorry, we’re not getting through this post without photos of infected intestines.)
So here’s how it could work:
The MAP bacteria–possibly transmitted via milk or meat products–is fairly common and infects a variety of mammals. Most people who encounter it fight it off with no difficulty (or perhaps have a short bout of diarrhea and then recover.)
A few people, though, have genetic issues that make it harder for them to fight off the infection. For example, Crohn’s sufferers produce less intestinal mucus, which normally acts as a barrier between the intestines and all of the stuff in them.
Interestingly, parasite infections can increase intestinal mucus (some parasites feed on mucus), which in turn is protective against other forms of infection; decreasing parasite load can increase the chance of other intestinal infections.
Once MAP enters the intestinal walls, the immune system attempts to fight it off, but a genetic defect in microphagy results in the immune cells themselves getting infected. The body responds to the signs of infection by sending more immune cells to fight it, which subsequently also get infected with MAP, triggering the body to send even more immune cells. These lumps of infected cells become the characteristic ulcerations and lesions that mark Crohn’s disease and eventually leave the intestines riddled with inflamed tissue and holes.
The most effective treatments for Crohn’s, like Infliximab, don’t target infection but the immune system. They work by interrupting the immune system’s feedback cycle so that it stops sending more cells to the infected area, giving the already infected cells a chance to die. It doesn’t cure the disease, but it does give the intestines time to recover.
There were 70 reported cases of tuberculosis after treatment with infliximab for a median of 12 weeks. In 48 patients, tuberculosis developed after three or fewer infusions. … Of the 70 reports, 64 were from countries with a low incidence of tuberculosis. The reported frequency of tuberculosis in association with infliximab therapy was much higher than the reported frequency of other opportunistic infections associated with this drug. In addition, the rate of reported cases of tuberculosis among patients treated with infliximab was higher than the available background rates.
because it is actively suppressing the immune system’s ability to fight diseases in the TB family.
Luckily, if you live in the first world and aren’t in prison, you’re unlikely to catch TB–only about 5-10% of the US population tests positive for TB, compared to 80% in many African and Asian countries. (In other words, increased immigration from these countries will absolutely put Crohn’s suffers at risk of dying.)
There are a fair number of similarities between Crohn’s, TB, and leprosy is that they are all very slow diseases that can take years to finally kill you. By contrast, other deadly diseases, like smallpox, cholera, and yersinia pestis (plague), spread and kill extremely quickly. Within about two weeks, you’ll definitely know if your plague infection is going to kill you or not, whereas you can have leprosy for 20 years before you even notice it.
Tuberculosis is classified as one of the granulomatous inflammatory diseases. Macrophages, T lymphocytes, B lymphocytes, and fibroblasts aggregate to form granulomas, with lymphocytes surrounding the infected macrophages. When other macrophages attack the infected macrophage, they fuse together to form a giant multinucleated cell in the alveolar lumen. The granuloma may prevent dissemination of the mycobacteria and provide a local environment for interaction of cells of the immune system. However, more recent evidence suggests that the bacteria use the granulomas to avoid destruction by the host’s immune system. … In many people, the infection waxes and wanes.
Crohn’s also waxes and wanes. Many sufferers experience flare ups of the disease, during which they may have to be hospitalized, tube fed, and put through another round of antibiotics or sectioning (surgical removal of the intestines) before they improve–until the disease flares up again.
Leprosy is also marked by lesions, though of course so are dozens of other diseases.
Note: Since Crohn’s is a complex, multi-factorial disease, there may be more than one bacteria or pathogen that could infect people and create similar results. Alternatively, Crohn’s sufferers may simply have intestines that are really bad at fighting off all sorts of diseases, as a side effect of Crohn’s, not a cause, resulting in a variety of unpleasant infections.
The MAP hypothesis suggests several possible treatment routes:
Improving the intestinal mucus, perhaps via parasites or medicines derived from parasites
Improving the intestinal microbe balance
Antibiotics that treat Map
Anti-MAP vaccine similar to the one for Johne’s disease in cattle
To determine how the worms could be our frenemies, Cadwell and colleagues tested mice with the same genetic defect found in many people with Crohn’s disease. Mucus-secreting cells in the intestines malfunction in the animals, reducing the amount of mucus that protects the gut lining from harmful bacteria. Researchers have also detected a change in the rodents’ microbiome, the natural microbial community in their guts. The abundance of one microbe, an inflammation-inducing bacterium in the Bacteroides group, soars in the mice with the genetic defect.
The researchers found that feeding the rodents one type of intestinal worm restored their mucus-producing cells to normal. At the same time, levels of two inflammation indicators declined in the animals’ intestines. In addition, the bacterial lineup in the rodents’ guts shifted, the team reports online today in Science. Bacteroides’s numbers plunged, whereas the prevalence of species in a different microbial group, the Clostridiales, increased. A second species of worm also triggers similar changes in the mice’s intestines, the team confirmed.
To check whether helminths cause the same effects in people, the scientists compared two populations in Malaysia: urbanites living in Kuala Lumpur, who harbor few intestinal parasites, and members of an indigenous group, the Orang Asli, who live in a rural area where the worms are rife. A type of Bacteroides, the proinflammatory microbes, predominated in the residents of Kuala Lumpur. It was rarer among the Orang Asli, where a member of the Clostridiales group was plentiful. Treating the Orang Asli with drugs to kill their intestinal worms reversed this pattern, favoring Bacteroides species over Clostridiales species, the team documented.
This sounds unethical unless they were merely tagging along with another team of doctors who were de-worming the Orangs for normal health reasons and didn’t intend on potentially inflicting Crohn’s on people. Nevertheless, it’s an interesting study.
At any rate, so far they haven’t managed to produce an effective medicine from parasites, possibly in part because people think parasites are icky.
But if parasites aren’t disgusting enough for you, there’s always the option of directly changing the gut bacteria: fecal microbiota transplants (FMT). A fecal transplant is exactly what it sounds like: you take the regular feces out of the patient and put in new, fresh feces from an uninfected donor. (When your other option is pooping into a bag for the rest of your life because your colon was removed, swallowing a few poop pills doesn’t sound so bad.) EG, Fecal microbiota transplant for refractory Crohn’s:
Approximately one-third of patients with Crohn’s disease do not respond to conventional treatments, and some experience significant adverse effects, such as serious infections and lymphoma, and many patients require surgery due to complications. .. Herein, we present a patient with Crohn’s colitis in whom biologic therapy failed previously, but clinical remission and endoscopic improvement was achieved after a single fecal microbiota transplantation infusion.
Antibiotics are another potential route. The Redhill Biopharma is conducting a phase III clinical study of antibiotics designed to fight MAP in Crohn’s patients. Redhill is expected to release some of their results in April.
Mechanism of action: The vaccine is what is called a ‘T-cell’ vaccine. T-cells are a type of white blood cell -an important player in the immune system- in particular, for fighting against organisms that hide INSIDE the body’s cells –like MAP does. Many people are exposed to MAP but most don’t get Crohn’s –Why? Because their T-cells can ‘see’ and destroy MAP. In those who do get Crohn’s, the immune system has a ‘blind spot’ –their T-cells cannot see MAP. The vaccine works by UN-BLINDING the immune system to MAP, reversing the immune dysregulation and programming the body’s own T-cells to seek out and destroy cells containing MAP. For general information, there are two informative videos about T Cells and the immune system below.
Efficacy: In extensive tests in animals (in mice and in cattle), 2 shots of the vaccine spaced 8 weeks apart proved to be a powerful, long-lasting stimulant of immunity against MAP. To read the published data from the trial in mice, click here. To read the published data from the trial in cattle, click here.
Dr. Borody (who was influential in the discovery that ulcers are caused by the h. pylori bacteria and not stress,) has had amazing success treating Crohn’s patients with a combination of infliximab, anti-MAP antibiotics, and hyperbaric oxygen. Here are two of his before and after photos of the intestines of a 31 yr old Crohn’s sufferer:
Here are some more interesting articles on the subject:
Last week, Davis and colleagues in the U.S. and India published a case report in Frontiers of Medicine http://journal.frontiersin.org/article/10.3389/fmed.2016.00049/full . The report described a single patient, clearly infected with MAP, with the classic features of Johne’s disease in cattle, including the massive shedding of MAP in his feces. The patient was also ill with clinical features that were indistinguishable from the clinical features of Crohn’s. In this case though, a novel treatment approach cleared the patient’s infection.
The patient was treated with antibiotics known to be effective for tuberculosis, which then eliminated the clinical symptoms of Crohn’s disease, too.
Through luck, hard work, good fortune, perseverance, and wonderful doctors, I seem to be one of the few people in the world who can claim to be “cured” of Crohn’s Disease. … In brief, I was treated for 6 years with medications normally used for multidrug resistant TB and leprosy, under the theory that a particular germ causes Crohn’s Disease. I got well, and have been entirely well since 2004. I do not follow a particular diet, and my recent colonoscopies and blood work have shown that I have no inflammation. The rest of these 3 blogs will explain more of the story.
What about removing Johne’s disease from the food supply? Assuming Johne’s is the culprit, this may be hard to do, (it’s pretty contagious in cattle, can lie dormant for years, and survives cooking) but drinking ultrapasteurized milk may be protective, especially for people who are susceptible to the disease.
However… there are also studies that contradict the MAP theory. For example, a recent study of the rate of Crohn’s disease in people exposed to Johne’s disease found no correllation. (However, Crohn’s is a pretty rare condition, and the survey only found 7 total cases, which is small enough that random chance could be a factor, but we are talking about people who probably got very up close and personal with feces infected with MAP.)
Logistic regression showed no significant association with measures of potential contamination of water sources with MAP, water intake, or water treatment. Multivariate analysis showed that consumption of pasteurized milk (per kg/month: odds ratio (OR) = 0.82, 95% confidence interval (CI): 0.69, 0.97) was associated with a reduced risk of Crohn’s disease. Meat intake (per kg/month: OR = 1.40, 95% CI: 1.17, 1.67) was associated with a significantly increased risk of Crohn’s disease, whereas fruit consumption (per kg/month: OR = 0.78, 95% CI: 0.67, 0.92) was associated with reduced risk.
So even if Crohn’s is caused by MAP or something similar, it appears that people aren’t catching it from milk.
There are other theories about what causes Crohn’s–these folks, for example, think it’s related to consumption of GMO corn. Perhaps MAP has only been found in the intestines of Crohn’s patients because people with Crohn’s are really bad at fighting off infections. Perhaps the whole thing is caused by weird gut bacteria, or not enough parasites, insufficient Vitamin D, or industrial pollution.
Let’s consider the similarities between the fairy fountains found in Nintendo’s new Legend of Zelda installment, Breath of the Wild, and the enormous blooms of our terrestrial Rafflesia genus.
Rafflesia Arnoldii hold the record for world’s largest flowers, growing regularly to a width of 3 feet and weighing up to 24 pounds. Their central chamber is large enough to put a baby in, if you aren’t too perturbed by their odd spiky structures and horrific smell.
The Fairy Fountain is obviously the largest flower in Breath of the Wild and has a central chamber similar to Rafflesia’s; an enormous fairy woman lives inside.
Rafflesia is a parasitic plant which actually has no stems, leaves, roots, or even chlorophyll! (This has made tracing its genetic relationships to other plants difficult for scientists, because most of what we know about plant relationships is based off comparing differences in their chlorophyll’s DNA.) The only visible parts of the plant are its buds and, subsequently, the flowers they open into.
Likewise, the Fairy Fountain has no leaves, stems, or other visible plant parts–it is just a bud that opens into a flower. (However, the fairy fountain bud is green. Perhaps it would have looked too much like a giant nut if it were brown like the true Rafflesia.)
The rest of Rafflesia’s structure is hidden within the vines it parasitizes. When not in bloom, it’s just a network within the vine, just as a mushroom’s principle structures lie hidden within the ground or rotting logs.
The Fairy Fountain is surrounded by mushrooms, which suggest their similarity to the fountain’s hidden structure.
Rafflesia’s enormous size is due to the fact that it is pollinated by carrion flies, who are attracted to the largest carcasses they can find. Unfortunately, this also means that Rafflesia smells like rotting meat, earning it various unsavory names like “corpse flower.” It also possesses the remarkable ability to generate heat, creating a warm, comfortable environment for flies to congregate in.
In Breath of the Wild, the Fairy Fountain is also home to flies, though these are thankfully the much less smelly, tiny winged fairy kind.
“The pollen is incredible,” Davis continues. In most plants, the pollen is powdery, but in Rafflesia, it is “produced as a massive quantity of viscous fluid, sort of like snot, that dries on the backs of these flies—and presumably remains viable for quite a long time,” perhaps weeks. In their pollinating efforts, the flies may travel as much as 12 to 14 miles.
I don’t have a very good sense of scale in Breath of the Wild, but 12 or 14 miles between Fairy Fountains sounds about right. By picking up fairies at one fountain and carrying them to the next, Link is helping this likely endangered Hylian species reproduce.
Likewise, the center of the enormous Fairy Fountains is filled not with powder, but some kind of… liquid.
Or it might just be water:
Vines move massive quantities of water, which may be one of the physiological reasons that Rafflesia colonize them, he explains. The flowers, which to the touch are like “a Nerf football that is wet,” are mostly water themselves, and the exponential growth of the blooms in the final stages of development is made possible “primarily by pumping massive quantities of water into the flower.”
That’s a lot like what I imagine the Fairy Fountain would feel like, too.
But the really interesting thing about Rafflesia is their genes:
Given his mandate to establish a phylogeny for the order Malpighiales, Davis set out, dutifully, to duplicate the published result for Rafflesia. What he found was not just unexpected. It absolutely astounded him. Some of the genes he sequenced confirmed that Rafflesia were indeed part of Malpighiales—but other sequenced genes placed them in an entirely different order (Vitales)—with their host plants. Davis had stumbled upon a case of massive horizontal gene transfer, the exchange of genetic information between two organisms without sex. …
The work is also facilitating the identification of Rafflesia’s past hosts, since many of the transgenes Davis found came from lineages of plants other than Tetrastigma, the current host. These ancient parasite/host associations, a kind of molecular fossil record, could be used to elucidate the timing and origin of plant parasitism itself.
Davis found that the host plant contributed about 2 percent to 3 percent of Rafflesia’s expressed nuclear genome (genes in the cell nucleus), and as much as 50 percent of its mitochondrial genome (genes that govern energy production). The sheer scale of the transfer was so far-fetched, his collaborator at the time at first didn’t believe that the findings could be accurate. The paper, published in 2012, demonstrated that intimate host/parasite connections are potentially an important means by which horizontal gene transfers can occur. And it showed that the physiological invisibility of Rafflesia within the host is echoed in its genes: the host and parasite share so much biology that the boundaries between them have become blurred.
Intriguingly, some of the transferred genes swap in at precisely the same genetic location as in the parasite’s own genome. “One of the ideas that we are exploring,” says Davis, “is whether maintaining these transferred genes might provide a fitness advantage for the parasite. Might these transfers be providing a kind of genetic camouflage so that the host can’t mount an immune response to the parasite that lives within it?”
And finally, Rafflesia flowers and the Fairy Fountain are basically the same color: both are both reddish with white mottling.
Okay, yes, obviously when you take the gut parasites out of people, they tend to gain weight immediately after. That’s not exactly what I’m talking about.
First, let’s assume you come from a place where humans and hookworms have co-existed for a long, long time. The hookworms that just about everybody in the American South used to have appear to have come from Africa, so I think it safe to assume that hookworms have probably been infecting a lot of people in Africa for a long time. I don’t know how long–could be anywhere from a few hundred years, if they’d come from somewhere else or recently mutated or something, or could be tens of thousands or hundreds of thousands of years, if they’ve just always been hanging around. Let’s just go with tens of thousands, because if it wasn’t them, it was probably something else.
Over a few thousand years of constant infection, you’d expect to develop some sort of biological response to minimize the chances of death–that is, your ancestors would have evolved over time to be less susceptible to the parasite. Obviously not getting the parasite is one great way to avoid getting killed by it, but let’s assume that’s not an option.
Another solution would be to just absorb food differently–faster, say, or in a manner that circumvents the parts of the gut that are normally infected. Over time, humans and parasites might tend toward an equilibrium–humans stepping up their digestion to make up for what’s lost to the parasite.
Remove the parasite, and equilibrium is lost: suddenly the human starts gaining a lot of weight, especially compared to people from populations that did not adapt to the parasite.
That functional a gut isn’t needed anymore, but it might persist for a while if there are no counter-evolutionary pressures.
Like our lack of fur, acne remains an evolutionary mystery to me.
Do other furless mammals get acne? Like elephants or whales? Or even chimps; their faces don’t have fur. If so, everyone’s keeping it a secret–I’ve never even seen an add for bonobo anti-acne cream, and with bonobos’ social lives, you know they’d want it. :)
So far, Google has returned no reports of elephants or whales with acne.
Now, a few skin blemishes here and there are not terribly interesting or mysterious. The weird thing about acne (IMO) is that it pops up at puberty*, and appears to have a genetic component.
Considering that kids with acne tend to feel rather self-conscious about it, I think it reasonable to assume that people with more severe acne have more difficulty with dating than people without. (Remember, some people have acne well into their 30s or beyond.)
Wouldn’t the non-acne people quickly out-compete the acne-people, resulting in less acne among humans? (Okay, now I really want to know if someone has done a study on whether people with more acne have fewer children.) Since acne is extremely common and shows up right as humans reach puberty, this seems like a pretty easy thing to study/find an effect if there is any.
Anyway, I totally remember a reference to acne in Dr. Price’s Nutrition and Physical Degeneration, (one of my favorite books ever,) but can’t find it now. Perhaps I am confusing it with Nutrition and Western Disease or a book with a similar title. At any rate, I recall a picture of a young woman’s back with a caption to the effect that none of the people in this tropical local had acne, which the author could tell rather well since this was one of those tropical locals where people typically walk around with rather little clothing.
“Rates appear to be lower in rural societies. While some find it affects people of all ethnic groups, it may not occur in the non-Westernized people of Papua New Guinea and Paraguay.
Acne affects 40 to 50 million people in the United States (16%) and approximately 3 to 5 million in Australia (23%). In the United States, acne tends to be more severe in Caucasians than people of African descent.”
I consider these more “hints” than “conclusive proof of anything.”
Back when I was researching hookworms, I ran across these bits:
“The [Hygiene Hypothesis] was first proposed by David P. Strachan who noted that hay fever and eczema were less common in children who belonged to large families. Since then, studies have noted the effect of gastrointestinal worms on the development of allergies in the developing world. For example, a study in Gambia found that eradication of worms in some villages led to increased skin reactions to allergies among children. … [bold mine.]
Moderate hookworm infections have been demonstrated to have beneficial effects on hosts suffering from diseases linked to overactive immune systems. … Research at the University of Nottingham conducted in Ethiopia observed a small subset of people with hookworm infections were half as likely to experience asthma or hay fever. Potential benefits have also been hypothesized in cases of multiple sclerosis, Crohn’s Disease and diabetes.”
So I got to thinking, if allergies and eczema are auto-immune reactions (I know someone in real life, at least, whose skin cracks to the point of bleeding if they eat certain foods, but is otherwise fine if they don’t eat those foods,) why not acne?
Acne is generally considered a minor problem, so people haven’t necessarily spent a ton of time researching it. Googling “acne autoimmune” gets me some Paleo-Dieter folks talking about curing severe cases with a paleo-variant (they’re trying to sell books, so they didn’t let on the details, but I suspect the details have to do with avoiding refined sugar, milk, and wheat.)
While I tend to caution against over-enthusiastic embrace of a diet one’s ancestors most likely haven’t eaten in thousands or ten thousand years, if some folks are reporting a result, then I’d love to see scientists actually test it and try to confirm or disprove it.
The problem with dietary science is that it is incredibly complicated, full of confounds, and most of the experiments you might think up in your head are completely illegal and impractical.
For example, scientists figured out that Pellagra is caused by nutritional deficiency–rather than an infectious agent–by feeding prisoners an all-corn diet until they started showing signs of gross malnutrition. (For the record, the prisoners joined the program voluntarily. “All the corn you can eat” sounded pretty good for the first few months.) Likewise, there was a program during WWII to study the effects of starvation–on voluntary subjects–and try to figure out the best way to save starving people, started because the Allies knew they would have a lot of very real starvation victims on their hands very soon.
These sorts of human experiments are no longer allowed. What a scientist can do to a human being is pretty tightly controlled, because no one wants to accidentally kill their test subjects and universities and the like don’t like getting sued. Even things like the Milgram Experiments would have trouble getting authorized today.
So most of the time with scientific studies, you’re left with using human analogs, which means rats. And rats don’t digest food the exact same way we do–Europeans and Chinese don’t digest food the exact same way, so don’t expect rats to do it the same way, either. An obvious oversight as a result of relying on animal models is that most animals can synthesize Vitamin C, but humans can’t. This made figuring out this whole Vitamin C thing a lot trickier.
Primates are probably a little closer, digestively, to humans, but people get really squeamish about monkey research, and besides, they eat a pretty different diet than we do, too. Gorillas are basically vegan (I bet they eat small bugs by accident all the time, of course,) and chimps have almost no body fat–this is quite remarkable, actually. Gorillas and orangutans have quite a bit of body fat, “normal” levels by human standards. Hunter-gatherers, agriculturalists, and sedentary butt-sitters like us have different amounts, but they still all have some. But chimps and bonobos have vanishingly little; male chimps and bonobos have almost zero body fat, even after being raised in zoos and fed as much food as they want.
Which means that if you’re trying to study diet, chimps and bonobos are probably pretty crappy human analogs.
(And I bet they’re really expensive to keep, relative to mice or having humans fill out surveys and promise to eat more carbs.)
So you’re left with trying to figure out what people are eating and tinker with it in a non-harmful, non-invasive way. You can’t just get a bunch of orphans and raise them from birth on two different diets and see what happens. You get people to fill out questionnaires about what they eat and then see if they happen to drop dead in the next 40 or 50 years.
And that doesn’t even take into account the fact that “corn” can mean a dozen different things to different people. Someone whose ancestors were indigenous to North and South America may digest corn differently than someone from Europe, Africa, or Asia. Different people cook corn differently–we don’t typically use the traditional method of mixing it with lime (the mineral), which frees up certain nutrients and traditionally protected people from Pellagra. We don’t all eat corn in the same combinations with other foods (look at the interaction between the calcium in milk and Vitamin D for one of the ways which combining foods can complicate matters.) And we aren’t necessarily even cooking the same “corn”. Modern hybrid corns may not digest in exactly the same way as corn people were growing a hundred or two hundred years ago. Small differences are sometimes quite important, as we discovered when we realized the artificially-created trans-fats we’d stuck in our foods to replace saturated fats were causing cancer–our bodies were trying to use these fats like normal fats, but when we stuck them into our cell walls, their wonky shapes (on a chemical level, the differences between different kinds of fats can be mostly understood that they are shaped differently, and trans fats have been artificially modified to have a different shape than they would have otherwise,) fucked up the structure of the cells they were in.
In short, this research is really hard, but I still encourage people to go do it and do it well.
Anyway, back on topic, here’s another quote from the Wikipedia, on the subject of using parasites to treat autoimmunie disorders:
“While it is recognized that there is probably a genetic disposition in certain individuals for the development of autoimmune diseases, the rate of increase in incidence of autoimmune diseases is not a result of genetic changes in humans; the increased rate of autoimmune-related diseases in the industrialized world is occurring in too short a time to be explained in this way. There is evidence that one of the primary reasons for the increase in autoimmune diseases in industrialized nations is the significant change in environmental factors over the last century. …
Genetic research on the interleukin genes (IL genes) shows that helminths [certain kinds of parasites] have been a major selective force on a subset of these human genes. In other words, helminths have shaped the evolution of at least parts of the human immune system, especially the genes responsible for Crohn’s disease, ulcerative colitis, and celiac disease — and provides further evidence that it is the absence of parasites, and in particular helminths, that has likely caused a substantial portion of the increase in incidence of diseases of immune dysregulation and inflammation in industrialized countries in the last century. …
Studies conducted on mice and rat models of colitis, muscular sclerosis, type 1 diabetes, and asthma have shown helminth-infected subjects to display protection from the disease.”
Right, so I’m curious if acne falls into this category, too.
The humble-but disgusting hookworm’s scientific name is “Necator americanus”–American Killer. (Actually, there are several hookworm species, but if you live in the US, this is the one to worry aboutt.)
This parasite, like many others, originated in sub-Saharan Africa, where it still infects about 200 million people. East Asia has another 150 million infected.
Each worm lays lays 9,000 to 10,000 eggs per day in your bowels. You helpfully “deposit” these eggs–prior to indoor plumbing, somewhere on the ground. The eggs hatch, and a week later, the baby worms are ready to burrow their way into the foot of any poor sod unlucky enough to step on them.
The babies go into your bloodstream, burrow into your lungs and throat, and then get coughed and swallowed down into your guts, where they make themselves comfortable, drinking your blood and laying more eggs.
Each individual worm only sucks a drop of blood per day, but no one has just one worm; your intestines soon fill with thousands of the bastards.
One of the interesting side effects of horrible infections and diseases is that, given enough exposure, a population will eventually evolve some sort of immunity. Sickle Cell Anemia, while imperfect, is one such adaptation, rendering some folks in malaria-prone regions less susceptible to the disease. People who do not have these adaptations are easy prey for the disease; so Smallpox, vicious murderer of Europeans, tore through native communities like an atomic bomb, killing some 90% of everyone it got near.
So when some idiot had the bright idea to import slaves from Sub-Saharan Africa, not only did millions of humans suffer and die, but Necator americanus jumped the Atlantic and found a new, less resistant host to infect. Poor southern whites, barefoot and often malnourished (un-nixtamalized corn is a culprit here), became unwitting hosts for an organism against which they had no defenses.
No one knew what was going on. The germ theory of disease hadn’t been developed, and no one was autopsying “white trash” kids when they died.
Historian Thomas D. Clark claims, “By modern American Standards of physical, mental, and moral fitness… more than half of the Johnny Rebs who shelled the woods at Shiloh, Chancellorsville, and Gettysburg, or stood with Pemberton at Vicksburg, might have been kept at home. No one can say how much Pellagra and hookworm helped to sustain the union.” (Quoted in “Parasites: Tales of Humanity’s Most Unwelcome Guests,” by Rosemary Drisdelle.)
The hookworm turned against the Union, though. As Driselle describes, it passed from infected Southerners to Northerners in the horrifying conditions of the POW camps.
At Andersonville, 13,000 people died of starvation, malnutrition, and disease. Driselle estimates that a third were felled by hookworms, but it is hard to imagine that anyone forced to drink Andersonville’s feces-laden stagnant water would have escaped infection.
It was only in the 1880s and 90s that people started putting together the hookworm infection pieces; in the early 1900s, hookworm eradication campaigns started in the American south. (Tips: Wear shoes; Poop in a toilet.) The parasite that had taken down so many Americans was thus formally dubbed the American Killer, Necator americanus, a great anti-disease naming move if I ever saw one, though not quite as great as the bee parasite, Varroa destructor. I mean, do you want something called V. destructor infecting your bees? Obviously not!
(Seriously, who names a disease AIDS? That makes it sound helpful. Should have named it MURDER disease or something like that.)
Hookworm eradication had notable effects on things like health, school performance, and not dying, which is almost always a good thing. (About that time we also figured out that you can’t live on a 100% corn diet for very long.)
From time to time, people ungracefully express their dislike of others in terms fear of disease, describing foreigners as “dirty” or otherwise infectious. While such sentiments are crude and insulting, the fact remains that even the most wonderful of strangers may in fact be carrying diseases to which you have no immunity. And with diseases, like devils, better the disease your ancestors might have survived than one they didn’t.
This morning I found a strange, worm-like creature wiggling around in the garden. It was about 5 inches long and thinner than a pin–completely wrong proportions for an earthworm, and further, it was waving its upper end in the air in a manner that earthworms can’t.
I am not worm expert, but my assumption is that there’s only one good reason to be that thin and that long: to make burrowing into someone else’s body easier.
Being a stupid hippie, I wear sandals everywhere (except in snow; I have found it more comfortable to be barefoot in snow than in sandals, and I do not find it comfortable to be barefoot in the snow.)
Forget that shit. I now have nice, sturdy boots for the garden.