Does the DSM need to be re-written?

I recently came across an interesting paper that looked at the likelihood that a person, once diagnosed with one mental disorder, would be diagnosed with another. (Exploring Comorbidity Within Mental Disorders Among a Danish National Population, by Oleguer Plana-Ripoll.)

This was a remarkable study in two ways. First, it had a sample size of 5,940,778, followed up for 83.9 million person-years–basically, the entire population of Denmark over 15 years. (Big Data indeed.)

Second, it found that for virtually every disorder, one diagnoses increased your chances of being diagnosed with a second disorder. (“Comorbid” is a fancy word for “two diseases or conditions occurring together,” not “dying at the same time.”) Some diseases were particularly likely to co-occur–in particular, people diagnosed with “mood disorders” had a 30% chance of also being diagnosed with “neurotic disorders” during the 15 years covered by the study.

Mood disorders includes bipolar, depression, and SAD;

Neurotic disorders include anxieties, phobias, and OCD.

Those chances were considerably higher for people diagnosed at younger ages, and decreased significantly for the elderly–those diagnosed with mood disorders before the age of 20 had a +40% chance of also being diagnosed with a neurotic disorder, while those diagnosed after 80 had only a 5% chance.

I don’t find this terribly surprising, since I know someone with at least five different psychological diagnoses, (nor is it surprising that many people with “intellectual disabilities” also have “developmental disorders”) but it’s interesting just how pervasive comorbidity is across conditions that are ostensibly separate diseases.

This suggests to me that either many people are being mis-diagnosed (perhaps diagnosis itself is very difficult,) or what look like separate disorders are often actually one, single disorder. While it is certainly possible, of course, for someone to have both a phobia of snakes and seasonal affective disorder, the person I know with five diagnoses most likely has only one “true” disorder that has just been diagnosed and treated differently by different clinicians. It seems likely that some people’s depression also manifests itself as deep-rooted anxiety or phobias, for example.

While this is a bit of a blow for many psychiatric diagnoses, (and I am quite certain that many diagnostic categories will need a fair amount of revision before all is said and done,) autism recently got a validity boost–How brain scans can diagnose Autism with 97% accuracy.

The title is overselling it, but it’s interesting anyway:

Lead study author Marcel Just, PhD, professor of psychology and director of the Center for Cognitive Brain Imaging at Carnegie Mellon University, and his team performed fMRI scans on 17 young adults with high-functioning autism and 17 people without autism while they thought about a range of different social interactions, like “hug,” “humiliate,” “kick” and “adore.” The researchers used machine-learning techniques to measure the activation in 135 tiny pieces of the brain, each the size of a peppercorn, and analyzed how the activation levels formed a pattern. …

So great was the difference between the two groups that the researchers could identify whether a brain was autistic or neurotypical in 33 out of 34 of the participants—that’s 97% accuracy—just by looking at a certain fMRI activation pattern. “There was an area associated with the representation of self that did not activate in people with autism,” Just says. “When they thought about hugging or adoring or persuading or hating, they thought about it like somebody watching a play or reading a dictionary definition. They didn’t think of it as it applied to them.” This suggests that in autism, the representation of the self is altered, which researchers have known for many years, Just says.

N=34 is not quite as impressive as N=Denmark, but it’s a good start.


Reminder: Hunter-Gatherers were not Peace Loving Pacifists

From Balancing Selection at the Prion Protein Gene Consistent with Prehistoric Kurulike Epidemics:

Kuru is an acquired prion disease largely restricted to the Fore linguistic group of the Papua New Guinea Highlands, which was transmitted during endocannibalistic feasts. Heterozygosity for a common polymorphism in the human prion protein gene (PRNP) confers relative resistance to prion diseases. Elderly survivors of the kuru epidemic, who had multiple exposures at mortuary feasts, are, in marked contrast to younger unexposed Fore, predominantly PRNP 129 heterozygotes. Kuru imposed strong balancing selection on the Fore, essentially eliminating PRNP 129 homozygotes. Worldwide PRNP haplotype diversity and coding allele frequencies suggest that strong balancing selection at this locus occurred during the evolution of modern humans.

Our ancestors–the ancestors of all humans–ate each other so often that they actually evolved resistance to prion diseases.

(H/T Littlefoot,)

Of course, they weren’t necessarily hunting each other for the calories (humans are not a very good source of calories compared to other common food sources.) They might have just had a habit of eating the dead from their own communities–which is still pretty gruesome.

Of course, cannibalism didn’t stop when people adopted agriculture. The Aztecs were cannibals“Indigenous Culture Day” celebrates genocidal cannibals who were even worse than Columbus. The Anasazi were cannibals. The word “cannibal” itself comes from the language of the Carib Indians. And of course, there are still-living folks in many other parts of the world who have cannibalized others.

But the idea that ancient humans were some kind of angels is absurd.


I have some hopefully good, deep stuff I am working on, but in the meanwhile, here is a quick, VERY SPECULATIVE thread on my theory for why refined sugars are probably bad for you:

First, refined sugars are evolutionarily novel. Unless you’re a Hazda, your ancient ancestors never had this much sugar.

Pick up a piece of raw sugar cane and gnaw on it. Raw sugar cane has such a high fiber to sugar content that you can use it as a toothbrush after chewing it for a bit.

According to the internet, a stick of raw sugar cane has 10 grams of sugar in it. A can of Coke has 39. Even milk (whole, skim, or fat-free) contains 12 grams of natural milk sugars (lactose) per glass. Your body has no problem handling the normal amounts of unrefined sugars in regular foods, but to get the amount of sugar found in a single soda, you’d have to eat almost four whole stalks of sugarcane, which you certainly aren’t going to do in a few minutes.

It’s when we extract all of the sugar and throw away the rest of the fiber, fat, and protein in the food that we run into trouble.

(The same is probably also true of fat, though I am rather fond of butter.)

In my opinion, all forms of heavily refined sugar are suspect, including fruit juice, which is essentially refined fructose. People think that fruit juice is “healthy” because it comes from fruit, which is a plant and therefore “natural” and “good for you,” unlike, say, sugar, which comes from sugar cane, which is… also a plant. Or HFCS, which is totally unnatural because it comes from… corn. Which is a plant.

“They actually did studies on the sugar plantations back in the early 1900s. All of the workers were healthy and lived longer than the sugar executives who got the refined, processed product.”

I don’t know if I agree with everything he has to say, but refined fructose is no more natural than any other refined sugar. Again, the amount of sugar you get from eating an apple is very different from the amount you get from a cup of apple juice.

Now people are talking about reducing childhood obesity by eliminating the scourge of 100% fruit juice:

Excessive fruit juice consumption is associated with increased risk for obesity… sucrose consumption without the corresponding fiber, as is commonly present in fruit juice, is associated with the metabolic syndrome, liver injury, and obesity.

Regular fruit is probably good for you. Refined is not.

Here’s another study on the problems with fructose:

If calcium levels in the blood are low, our bodies produce more parathyroid hormone, stimulating the absorption of calcium by the kidneys, as well as the production of vitamin D (calcitriol), also in the kidneys. Calcitriol stimulates the absorption of calcium in the intestine, decreases the production of PTH and stimulates the release of calcium from the bone. …

… Ferraris fed rats diets with high levels of glucose, fructose or starch. He and his team studied three groups of lactating rats and three groups of non-pregnant rats (the control group).

“Since the amounts of calcium channels and of binding proteins depend on the levels of the hormone calcitriol, we confirmed that calcitriol levels were much greater in lactating rats,” said Ferraris.  … “However, when the rat mothers were consuming fructose, there were no increases in calcitriol levels,” Ferraris added. “The levels remained the same as those in non-pregnant rats, and as a consequence, there were no increases in intestinal and renal calcium transport.”

You then have two options: food cravings until you eat enough to balance the nutrients, or strip bones of calcium. This is what triggers tooth decay.

Sugar not only feeds the bacteria on your teeth (I think), it also weakens your teeth to pay the piper for sugar digestion. (Also, there may be something about sugar-fed bacteria lowering the pH in your mouth.)

The second thing that happens is your taste buds acclimate to excessive sugar. Soon “Sweet” tastes “normal.”

Now when you try to stop eating sugar, normal food tastes “boring” “sour” “bitter” etc.
This is where you just have to bite the bullet and cut sugar anyway. If you keep eating normal food, eventually it will start tasting good again.

It just takes time for your brain to change its assumptions about what food tastes like.
But if you keep sweetening your food with “artificial” sweeteners, then you never give yourself a chance to recalibrate what food should taste like. You will keep craving sugar.
And it is really hard to stop eating sugar and let your body return to normal when you crave sugar.

If artificial sweeteners help you reduce sugar consumption and eventually stop using it altogether, then they’re probably a good idea, but don’t fall into the trap of thinking you’re going to get just as much cake and ice cream as always, just it won’t have any consequences anymore. No. Nature doesn’t work like that. Nature has consequences.

So I feel like I’ve been picking on fructose a lot in this post. I didn’t mean to. I am suspicious of all refined sugars; these are just the sources I happened across while researching today.

I am not sure about honey. I don’t eat a lot of honey, but maybe it’s okay. The Hadza of Tanzania eat a great deal of honey and they seem fine, but maybe they’re adapted to their diet in ways that we aren’t.

So what happens when you eat too much sugar? Aside from, obviously, food cravings, weight gain, mineral depletion, and tooth decay…

So here’s a theory:

Our bodies naturally cycle between winter and summer states. At least they do if you hail from a place that historically had winter; I can’t speak for people in radically different climates.

In the summer, plant matter (carbohydrates, fiber,) are widely available and any animal that can takes as much advantage of this as possible. As omnivores, we gorge on berries, leaves, fruits, tubers, really whatever we can. When we are satiated–when we have enough fat stores to last for the winter–our bodies start shutting down insulin production. That’s enough. We don’t need it anymore.

In the winter, there’s very little plant food naturally available, unless you’re a farmer (farming is relatively recent in areas with long winters.)

In the winter, you hunt animals for meat and fat.This is what the Inuit and Eskimo did almost all year round.

The digestion of meat and fat does not require insulin, but works on the ketogenic pathways which, long story short, also turn food into energy and keep people alive.

The real beauty of ketosis is that, apparently, it ramps up your energy production–that is, you feel physically warmer when running entirely off of meat and fat than when running off carbs. Given that ketosis is the winter digestive cycle, this is amazingly appropriate.

By spring, chances are you’ve lost a lot of the weight from last summer. Winters are harsh. With the fat gone, the body starts producing insulin again.

At this point, you go from hyperglycemia (too much sugar in your bloodstream if you eat anything sweet, due to no insulin,) to hypoglycemia–your body produces a lot of insulin to transform any plants you eat into energy FAST. (Remember the discussion above about how your body transforms fructose into fat? Back in our ancestral environment, that was a feature, not a bug!)

This lets you put on pounds quickly in the spring and summer, using now-available plants as your primary food source.

The difficulty with our society is we’ve figured out how to take the energy part out of the plants, refine it, and store up huge quantities of it so we can eat it any time we want, which is all the time.

Evolution makes us want to eat, obviously. Ancestors who didn’t have a good “eat now” drive didn’t eat whatever good food was available and didn’t become ancestors.

But now we’ve hacked that, and as a result we never go into the sugar-free periods we were built to occasionally endure.

I don’t think you need to go full keto or anti-bread or something to make up for this. Just cutting down on refined sugars (and most refined oils, btw) is probably enough for most people.

Note: Humans have been eating grains for longer than the domestication of plants–there’s a reason we thought it was a good idea to domesticate grains in the first place, and it wasn’t because they were a random, un-eaten weed. If your ancestors ate bread, then there’s a good chance that you can digest bread just fine.

But if bread causes you issues, then by all means, avoid it. Different people thrive on different foods.

Please remember that this thread is speculative.




Tapeworm-cancer-AIDS is a real thing

Tapeworm Spreads Deadly Cancer to Human:

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.

There’s not a lot I can add to this.

But there are probably more cases like this, if only because gay men seem to contract a lot of parasites:

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.

Greatest Hits: Can Ice Packs Help Stop a Seizure in Humans?


Source: WHO

Over the years, a few posts have proven surprising hits– Can Ice packs help stop a seizure (in humans)?, Turkey: Not very Turkic, Why do Native Americans Have so much Neanderthal DNA?, and Do Black Babies have Blue Eyes?

It’s been a while since these posts aired, so I thought it was time to revisit the material and see if anything new has turned up.

First, Ice packs and Epilepsy

Ice packs (cold packs) applied to the lower back at the first sign of a seizure may be able to halt or significantly decrease the severity of a seizure in humans.

I consider this one of the most important posts I’ve written, because it is the only one that offers useful, real-life advice: if someone is having a seizure, grab an ice pack or two and press them against the person’s back/neck. There is very little you can do for someone who is already having a seizure besides making sure they don’t accidentally hurt themselves, but using ice packs may help decrease the duration and severity of the seizure.

I have received some very positive responses to the post, including this one, by Tom Coventry:

We have been using an ice pack on our 13 yr old Son’s neck to stop seizures for nearly a year now and it works without fail to bring the seizures to an end within seconds of applying the ice. This is an old technique used before medications were invented, you can read about it at The Meridian Foundation papers on Edgar Case and Abdominal epilepsy.

Here is a relevant quote from Cayce’s paper on abdominal epilepsy:

… Also note that the reflex from the abdomen was mediated through the medulla oblongata, a important nerve center at the upper portion of the spinal cord where it enters the skull.  This is significant because Cayce sometimes recommended that a piece of ice be placed at this area during the aura or at the beginning of the seizure.  This simple technique has proven effective in several contemporary cases where Cayce’s therapeutic model has been utilized. Incidentally, this technique for preventing seizures was also used by osteopathic physicians during the early decades of this century and is included in the therapeutic model developed by the Meridian Institute. …

If the subject is currently experiencing seizures and can sense the beginning of the episode, they are encouraged to use a piece of ice at the base of the brain for one to two minutes.

I encountered the ice packs trick on forums where people were talking about treating seizures in dogs. (Yes, there are dogs with epilepsy.) There are many accounts of people successfully stopping or preventing their dogs from going into a seizure by grabbing a cold pack at the first warning signs and putting it directly onto the dog’s lower back:

We have been using ice packs to help manage our girl’s seizures for over a year now. From what I have heard first hand from others is that it either doesn’t work at all or it works fabulously. With our girl it “works fabulously”. It is not the miracle cure and it does not prevent future seizures but it definitely stops her grand mal right in its tracks. It is the most amazing thing I have ever seen. … If we get the ice pack on her within the first 15 seconds or so, the grand mal just suddenly stops. Like a light switch. All motor movement comes to a halt. She continues to be incoherent for a bit but all movements stop.

Oddly, though, I haven’t found much discussion of the use of ice packs on humans. But if it works on dogs, why wouldn’t it work on people? On the grand evolutionary scale, our nervous systems are pretty similar–we’re both mammals with neocortexes, after all.

From The Hidden Genetics of Epilepsy

My epileptic friend has also reported continued good success with the technique; her husband says he can feel an immediate change in the pattern of the seizure

My original post outlines some of the scientific evidence in favor of the technique; I’ll just quote one bit:

The Journal of American Holistic Veterinary Medical Association published an article on the use of ice packs to stop seizures in dogs, A Simple, Effective Technique for Arresting Canine Epileptic Seizures, back in 2004. You can read it for a mere $95, or check out the highlights on Dawg Business’s blog:

Fifty-one epileptic canine patients were successfully treated during an epileptic seizure with a technique involving the application of ice on the back (T10 to L4). This technique was found to be effective in aborting or shortening the duration of the seizure.

I suspect the “ice trick” was once fairly well-known before there were medications for preventing seizures, but modern doctors are just taught about the medications. And ice packs, to be clear, can’t cure epilepsy. But they can help people who are in the midst of a seizure.

Any doctors out there, please do some research on this. I think a lot of people could benefit.

A mercifully short note on Lice and the Invention of Clothes

Lice apparently come in three varieties: head, body, and pubic. The body louse’s genome was published in 2010 and is the shortest known insect genome. (Does parasitism reduce genome length?) According to Wikipedia:

Pediculus humanus humanus (the body louse) is indistinguishable in appearance from Pediculus humanus capitis (the head louse) but will interbreed only under laboratory conditions. In their natural state, they occupy different habitats and do not usually meet. In particular, body lice have evolved to attach their eggs to clothes, whereas head lice attach their eggs to the base of hairs.

So when did the clothes-infesting body louse decide to stop associating with its hair-clinging cousins?

The body louse diverged from the head louse at around 100,000 years ago, hinting at the time of the origin of clothing.[7][8][9]

So, did Neanderthals have clothes? Or did they survive winters in ice age Europe by being really hairy?

Behavioral modernity–such as intentional burials and cave painting–is thought to have emerged around 50,000 years ago. Some people push this date back to 80,000 years ago, possibly just before the Out of Africa event (something that made people smarter and better at making tools may have been necessary for OOA to succeed.)

But perhaps we should consider the invention of clothing alongside other technological breakthroughs that made us modern–after all, I don’t think we hairless apes could have had much success at conquering the planet without clothes.

(On the other hand, other Wikipedia pages give other estimates for the origin of clothing, some even also citing louse studies, so I’m not sure of the 100k YA date, but surely clothes were invented before we went anywhere cold.)

Oddly, though, there appears to have been at least one human group that managed to survive in a cold climate without much in the way of clothes, the Yaghan people of Tierra del Fuego. In fact, the whole reason the region got named Tierra del Fuego (translation: Land of the fire) is because the nearly-naked locals carried fire with them wherever they went to stay warm.

Only 100-1,600 Yaghans remain; their language is an isolate with only one native speaker, and she’s 89 years old.

Unfortunately, searching for “people with no clothes” does not return any useful information about other groups that might have led similar lifestyles.

PS: Pubic lice evolved from gorilla lice 3 million yeas ago. I bet you didn’t want to know that. Someone should look for that introgression event.

Native Americans appear to also carry a strain of head lice that had previously occupied Homo erectus’s hair, suggesting that H.e. and the ancestors of today’s N.A.s once met. Since these lice aren’t found elsewhere, it’s evidence that H. e. might have survived somewhere out there until fairly recently.

Did tobacco become popular because it kills parasites?

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?

From NPR: Pot For Parasites? Pygmy Men Smoke out Worms:

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.”

Smithsonian reports that Birds Harness the Deadly Power of Nicotine to Poison Parasites:

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.

Here’s a study comparing parasite rates in tobacco workers vs. prisoners in Ethiopia:

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%).

In vitro anthelmintic effect of Tobacco (Nicotiana tabacum) extract on parasitic nematode, Marshallagia marshalli reports:

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.

RIP Professor Hawking

Stephen Hawking

Stephen Hawking was one of the 20th century’s greatest scientists, not only because of his prodigious intellect, but also because he succeeded in the face of one of the most debilitating diseases possible. ALS normally kills people in 3 to 4 years; Hawking survived for decades.

So far there is no word on what finally killed him, only the description that he “died peacefully in his home.”

Given the horrible hand fate dealt him, it would have been understandable for Hawking to turn bitter and resentful. Instead he remained positive, never accepting defeat.

Hawking wanted his most famous formula, the equation for describing the entropy of a black hole, engraved on his tombstone. In this he joins other greats, like Boltzmann and Archimedes.

Rest in peace, Professor Hawking. I hope your spirit is finally free. You will be missed down here on Earth.


Is Crohn’s Disease Tuberculosis of the Intestines?

Source: Rise in Crohn’s Disease admission rates, Glasgow

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.[62] ” 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.)

Source: The Gutsy Group

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.)

A: Crohn’s Disease in Humans. Figure B: Johne’s Disease in Animals. Greenstein Lancet Infectious Disease, 2004, H/T Human Para Foundation

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.

Unfortunately, this means infliximab raises your chance of developing TB:

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.

TB, like Crohn’s, creates granulomas:

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.[63] 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:

  1. Improving the intestinal mucus, perhaps via parasites or medicines derived from parasites
  2. Improving the intestinal microbe balance
  3. Antibiotics that treat Map
  4. Anti-MAP vaccine similar to the one for Johne’s disease in cattle
  5. Eliminate map from the food supply

Here’s an article about the parasites and Crohn’s:

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.

Here’s a Chinese doctor who appears to have good success with FMTs to treat Crohn’s–improvement in 87% of patients one month after treatment and remission in 77%, though the effects may wear off over time. Note: even infliximab, considered a “wonder drug” for its amazing abilities, only works for about 50-75% of patients, must be administered via regular IV infusions for life (or until it stops working,) costs about $20,000 a year per patient, and has some serious side effects, like cancer. If fecal transplants can get the same results, that’s pretty good.

Little known fact: “In the United States, the Food and Drug Administration (FDA) has regulated human feces as an experimental drug since 2013.”

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.

A Crohn’s MAP vaccine trial is underway in healthy volunteers:

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.

Before: Fistula in the intestines, 31 year old Crohn’s patient–Dr Borody, Combining infliximab, anti-MAP and hyperbaric oxygen therapy for resistant fistulizing Crohn’s disease

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:

Sources: Is Crohn’s Disease caused by a Mycobacterium? Comparisons with Tuberculosis, Leprosy, and Johne’s Disease.

What is MAP?

Researcher Finds Possible link Between Cattle and Human Diseases:

Last week, Davis and colleagues in the U.S. and India published a case report in Frontiers of Medicine . 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.

After: The same intestines, now healed

Psychology Today: Treating Crohn’s Disease:

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.)

Another study found a negative correlation between Crohn’s and milk consumption:

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.

The condition remains very much a mystery.

2 Interesting studies: Early Humans in SE Asia and Genetics, Relationships, and Mental Illness

Ancient Teeth Push Back Early Arrival of Humans in Southeast Asia :

New tests on two ancient teeth found in a cave in Indonesia more than 120 years ago have established that early modern humans arrived in Southeast Asia at least 20,000 years earlier than scientists previously thought, according to a new study. …

The findings push back the date of the earliest known modern human presence in tropical Southeast Asia to between 63,000 and 73,000 years ago. The new study also suggests that early modern humans could have made the crossing to Australia much earlier than the commonly accepted time frame of 60,000 to 65,000 years ago.

I would like to emphasize that nothing based on a couple of teeth is conclusive, “settled,” or “proven” science. Samples can get contaminated, machines make errors, people play tricks–in the end, we’re looking for the weight of the evidence.

I am personally of the opinion that there were (at least) two ancient human migrations into south east Asia, but only time will tell if I am correct.

Genome-wide association study of social relationship satisfaction: significant loci and correlations with psychiatric conditions, by Varun Warrier, Thomas Bourgeron, Simon Baron-Cohen:

We investigated the genetic architecture of family relationship satisfaction and friendship satisfaction in the UK Biobank. …

In the DSM-55, difficulties in social functioning is one of the criteria for diagnosing conditions such as autism, anorexia nervosa, schizophrenia, and bipolar disorder. However, little is known about the genetic architecture of social relationship satisfaction, and if social relationship dissatisfaction genetically contributes to risk for psychiatric conditions. …

We present the results of a large-scale genome-wide association study of social
relationship satisfaction in the UK Biobank measured using family relationship satisfaction and friendship satisfaction. Despite the modest phenotypic correlations, there was a significant and high genetic correlation between the two phenotypes, suggesting a similar genetic architecture between the two phenotypes.

Note: the two “phenotypes” here are “family relationship satisfaction” and “friendship satisfaction.”

We first investigated if the two phenotypes were genetically correlated with
psychiatric conditions. As predicted, most if not all psychiatric conditions had a significant negative correlation for the two phenotypes. … We observed significant negative genetic correlation between the two phenotypes and a large cross-condition psychiatric GWAS38. This underscores the importance of social relationship dissatisfaction in psychiatric conditions. …

In other words, people with mental illnesses generally don’t have a lot of friends nor get along with their families.

One notable exception is the negative genetic correlation between measures of cognition and the two phenotypes. Whilst subjective wellbeing is positively genetically correlated with measures of cognition, we identify a small but statistically significant negative correlation between measures of correlation and the two phenotypes.

Are they saying that smart people have fewer friends? Or that dumber people are happier with their friends and families? I think they are clouding this finding in intentionally obtuse language.

A recent study highlighted that people with very high IQ scores tend to report lower satisfaction with life with more frequent socialization.

Oh, I think I read that one. It’s not the socialization per se that’s the problem, but spending time away from the smart person’s intellectual activities. For example, I enjoy discussing the latest genetics findings with friends, but I don’t enjoy going on family vacations because they are a lot of work that does not involve genetics. (This is actually something my relatives complain about.)

…alleles that increase the risk for schizophrenia are in the same haplotype as
alleles that decrease friendship satisfaction. The functional consequences of this locus must be formally tested. …

Loss of function mutations in these genes lead to severe biochemical consequences, and are implicated in several neuropsychiatric conditions. For
example, de novo loss of function mutations in pLI intolerant genes confers significant risk for autism. Our results suggest that pLI > 0.9 genes contribute to psychiatric risk through both common and rare genetic variation.