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.
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.
AND FOR GOODNESS SAKES DON’T PUT SUGAR IN FRUIT THINGS. JAM DOES NOT NEED SUGAR. NEITHER DOES PIE.
IF YOU ARE USING DECENT FRUIT THEN YOU DON’T NEED SUGAR. THE ONLY REASON YOU NEED SUGAR IS IF YOUR FRUIT IS CRAP. THEN JUST GO EAT SOMETHING ELSE.
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.
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.
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.
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.
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:
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.
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.
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.
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.
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.
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.
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.
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.
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.
A species may live in relative equilibrium with its environment, hardly changing from generation to generation, for millions of years. Turtles, for example, have barely changed since the Cretaceous, when dinosaurs still roamed the Earth.
But if the environment changes–critically, if selective pressures change–then the species will change, too. This was most famously demonstrated with English moths, which changed color from white-and-black speckled to pure black when pollution darkened the trunks of the trees they lived on. To survive, these moths need to avoid being eaten by birds, so any moth that stands out against the tree trunks tends to get turned into an avian snack. Against light-colored trees, dark-colored moths stood out and were eaten. Against dark-colored trees, light-colored moths stand out.
This change did not require millions of years. Dark-colored moths were virtually unknown in 1810, but by 1895, 98% of the moths were black.
The time it takes for evolution to occur depends simply on A. The frequency of a trait in the population and B. How strongly you are selecting for (or against) it.
Let’s break this down a little bit. Within a species, there exists a great deal of genetic variation. Some of this variation happens because two parents with different genes get together and produce offspring with a combination of their genes. Some of this variation happens because of random errors–mutations–that occur during copying of the genetic code. Much of the “natural variation” we see today started as some kind of error that proved to be useful, or at least not harmful. For example, all humans originally had dark skin similar to modern Africans’, but random mutations in some of the folks who no longer lived in Africa gave them lighter skin, eventually producing “white” and “Asian” skin tones.
(These random mutations also happen in Africa, but there they are harmful and so don’t stick around.)
Natural selection can only act on the traits that are actually present in the population. If we tried to select for “ability to shoot x-ray lasers from our eyes,” we wouldn’t get very far, because no one actually has that mutation. By contrast, albinism is rare, but it definitely exists, and if for some reason we wanted to select for it, we certainly could. (The incidence of albinism among the Hopi Indians is high enough–1 in 200 Hopis vs. 1 in 20,000 Europeans generally and 1 in 30,000 Southern Europeans–for scientists to discuss whether the Hopi have been actively selecting for albinism. This still isn’t a lot of albinism, but since the American Southwest is not a good environment for pale skin, it’s something.)
You will have a much easier time selecting for traits that crop up more frequently in your population than traits that crop up rarely (or never).
Second, we have intensity–and variety–of selective pressure. What % of your population is getting removed by natural selection each year? If 50% of your moths get eaten by birds because they’re too light, you’ll get a much faster change than if only 10% of moths get eaten.
Selection doesn’t have to involve getting eaten, though. Perhaps some of your moths are moth Lotharios, seducing all of the moth ladies with their fuzzy antennae. Over time, the moth population will develop fuzzier antennae as these handsome males out-reproduce their less hirsute cousins.
No matter what kind of selection you have, nor what part of your curve it’s working on, all that ultimately matters is how many offspring each individual has. If white moths have more children than black moths, then you end up with more white moths. If black moths have more babies, then you get more black moths.
So what happens when you completely remove selective pressures from a population?
Back in 1968, ethologist John B. Calhoun set up an experiment popularly called “Mouse Utopia.” Four pairs of mice were given a large, comfortable habitat with no predators and plenty of food and water.
Predictably, the mouse population increased rapidly–once the mice were established in their new homes, their population doubled every 55 days. But after 211 days of explosive growth, reproduction began–mysteriously–to slow. For the next 245 days, the mouse population doubled only once every 145 days.
The birth rate continued to decline. As births and death reached parity, the mouse population stopped growing. Finally the last breeding female died, and the whole colony went extinct.
As I’ve mentioned before Israel is (AFAIK) the only developed country in the world with a TFR above replacement.
It has long been known that overcrowding leads to population stress and reduced reproduction, but overcrowding can only explain why the mouse population began to shrink–not why it died out. Surely by the time there were only a few breeding pairs left, things had become comfortable enough for the remaining mice to resume reproducing. Why did the population not stabilize at some comfortable level?
Professor Bruce Charlton suggests an alternative explanation: the removal of selective pressures on the mouse population resulted in increasing mutational load, until the entire population became too mutated to reproduce.
Unfortunately, randomly changing part of your genetic code is more likely to give you no skin than skintanium armor.
But only the worst genetic problems that never see the light of day. Plenty of mutations merely reduce fitness without actually killing you. Down Syndrome, famously, is caused by an extra copy of chromosome 21.
While a few traits–such as sex or eye color–can be simply modeled as influenced by only one or two genes, many traits–such as height or IQ–appear to be influenced by hundreds or thousands of genes:
Differences in human height is 60–80% heritable, according to several twin studies and has been considered polygenic since the Mendelian-biometrician debate a hundred years ago. A genome-wide association (GWA) study of more than 180,000 individuals has identified hundreds of genetic variants in at least 180 loci associated with adult human height. The number of individuals has since been expanded to 253,288 individuals and the number of genetic variants identified is 697 in 423 genetic loci.
Obviously most of these genes each plays only a small role in determining overall height (and this is of course holding environmental factors constant.) There are a few extreme conditions–gigantism and dwarfism–that are caused by single mutations, but the vast majority of height variation is caused by which particular mix of those 700 or so variants you happen to have.
The general figure for the heritability of IQ, according to an authoritative American Psychological Association report, is 0.45 for children, and rises to around 0.75 for late teens and adults. In simpler terms, IQ goes from being weakly correlated with genetics, for children, to being strongly correlated with genetics for late teens and adults. … Recent studies suggest that family and parenting characteristics are not significant contributors to variation in IQ scores; however, poor prenatal environment, malnutrition and disease can have deleterious effects.…
Despite intelligence having substantial heritability2 (0.54) and a confirmed polygenic nature, initial genetic studies were mostly underpowered3, 4, 5. Here we report a meta-analysis for intelligence of 78,308 individuals. We identify 336 associated SNPs (METAL P < 5 × 10−8) in 18 genomic loci, of which 15 are new. Around half of the SNPs are located inside a gene, implicating 22 genes, of which 11 are new findings. Gene-based analyses identified an additional 30 genes (MAGMA P < 2.73 × 10−6), of which all but one had not been implicated previously. We show that the identified genes are predominantly expressed in brain tissue, and pathway analysis indicates the involvement of genes regulating cell development (MAGMA competitive P = 3.5 × 10−6). Despite the well-known difference in twin-based heritability2 for intelligence in childhood (0.45) and adulthood (0.80), we show substantial genetic correlation (rg = 0.89, LD score regression P = 5.4 × 10−29). These findings provide new insight into the genetic architecture of intelligence.
The greater number of genes influence a trait, the harder they are to identify without extremely large studies, because any small group of people might not even have the same set of relevant genes.
High IQ correlates positively with a number of life outcomes, like health and longevity, while low IQ correlates with negative outcomes like disease, mental illness, and early death. Obviously this is in part because dumb people are more likely to make dumb choices which lead to death or disease, but IQ also correlates with choice-free matters like height and your ability to quickly press a button. Our brains are not some mysterious entities floating in a void, but physical parts of our bodies, and anything that affects our overall health and physical functioning is likely to also have an effect on our brains.
The study focused, for the first time, on rare, functional SNPs – rare because previous research had only considered common SNPs and functional because these are SNPs that are likely to cause differences in the creation of proteins.
The researchers did not find any individual protein-altering SNPs that met strict criteria for differences between the high-intelligence group and the control group. However, for SNPs that showed some difference between the groups, the rare allele was less frequently observed in the high intelligence group. This observation is consistent with research indicating that rare functional alleles are more often detrimental than beneficial to intelligence.
Greg Cochran has some interesting Thoughts on Genetic Load. (Currently, the most interesting candidate genes for potentially increasing IQ also have terrible side effects, like autism, Tay Sachs and Torsion Dystonia. The idea is that–perhaps–if you have only a few genes related to the condition, you get an IQ boost, but if you have too many, you get screwed.) Of course, even conventional high-IQ has a cost: increased maternal mortality (larger heads).
the difference between the fitness of an average genotype in a population and the fitness of some reference genotype, which may be either the best present in a population, or may be the theoretically optimal genotype. … Deleterious mutation load is the main contributing factor to genetic load overall. Most mutations are deleterious, and occur at a high rate.
There’s math, if you want it.
Normally, genetic mutations are removed from the population at a rate determined by how bad they are. Really bad mutations kill you instantly, and so are never born. Slightly less bad mutations might survive, but never reproduce. Mutations that are only a little bit deleterious might have no obvious effect, but result in having slightly fewer children than your neighbors. Over many generations, this mutation will eventually disappear.
(Some mutations are more complicated–sickle cell, for example, is protective against malaria if you have only one copy of the mutation, but gives you sickle cell anemia if you have two.)
Throughout history, infant mortality was our single biggest killer. For example, here is some data from Jakubany, a town in the Carpathian Mountains:
We can see that, prior to the 1900s, the town’s infant mortality rate stayed consistently above 20%, and often peaked near 80%.
When I first ran a calculation of the infant mortality rate, I could not believe certain of the intermediate results. I recompiled all of the data and recalculated … with the same astounding result – 50.4% of the children born in Jakubany between the years 1772 and 1890 would diebefore reaching ten years of age! …one out of every two! Further, over the same 118 year period, of the 13306 children who were born, 2958 died (~22 %) before reaching the age of one.
Historical infant mortality rates can be difficult to calculate in part because they were so high, people didn’t always bother to record infant deaths. And since infants are small and their bones delicate, their burials are not as easy to find as adults’. Nevertheless, Wikipedia estimates that Paleolithic man had an average life expectancy of 33 years:
Based on the data from recent hunter-gatherer populations, it is estimated that at 15, life expectancy was an additional 39 years (total 54), with a 0.60 probability of reaching 15.
In other words, a 40% chance of dying in childhood. (Not exactly the same as infant mortality, but close.)
Wikipedia gives similarly dismal stats for life expectancy in the Neolithic (20-33), Bronze and Iron ages (26), Classical Greece(28 or 25), Classical Rome (20-30), Pre-Columbian Southwest US (25-30), Medieval Islamic Caliphate (35), Late Medieval English Peerage (30), early modern England (33-40), and the whole world in 1900 (31).
Over at ThoughtCo: Surviving Infancy in the Middle Ages, the author reports estimates for between 30 and 50% infant mortality rates. I recall a study on Anasazi nutrition which I sadly can’t locate right now, which found 100% malnutrition rates among adults (based on enamel hypoplasias,) and 50% infant mortality.
As Priceonomics notes, the main driver of increasing global life expectancy–48 years in 1950 and 71.5 years in 2014 (according to Wikipedia)–has been a massive decrease in infant mortality. The average life expectancy of an American newborn back in 1900 was only 47 and a half years, whereas a 60 year old could expect to live to be 75. In 1998, the average infant could expect to live to about 75, and the average 60 year old could expect to live to about 80.
Michael A Woodley suggests that what was going on [in the Mouse experiment] was much more likely to be mutation accumulation; with deleterious (but non-fatal) genes incrementally accumulating with each generation and generating a wide range of increasingly maladaptive behavioural pathologies; this process rapidly overwhelming and destroying the population before any beneficial mutations could emerge to ‘save; the colony from extinction. …
The reason why mouse utopia might produce so rapid and extreme a mutation accumulation is that wild mice naturally suffer very high mortality rates from predation. …
Thus mutation selection balance is in operation among wild mice, with very high mortality rates continually weeding-out the high rate of spontaneously-occurring new mutations (especially among males) – with typically only a small and relatively mutation-free proportion of the (large numbers of) offspring surviving to reproduce; and a minority of the most active and healthy (mutation free) males siring the bulk of each generation.
However, in Mouse Utopia, there is no predation and all the other causes of mortality (eg. Starvation, violence from other mice) are reduced to a minimum – so the frequent mutations just accumulate, generation upon generation – randomly producing all sorts of pathological (maladaptive) behaviours.
Today, almost everyone in the developed world has plenty of food, a comfortable home, and doesn’t have to worry about dying of bubonic plague. We live in humantopia, where the biggest factor influencing how many kids you have is how many you want to have.
Back in 1930, infant mortality rates were highest among the children of unskilled manual laborers, and lowest among the children of professionals (IIRC, this is Brittish data.) Today, infant mortality is almost non-existent, but voluntary childlessness has now inverted this phenomena:
Yes, the percent of childless women appears to have declined since 1994, but the overall pattern of who is having children still holds. Further, while only 8% of women with post graduate degrees have 4 or more children, 26% of those who never graduated from highschool have 4+ kids. Meanwhile, the age of first-time moms has continued to climb.
Take a moment to consider the high-infant mortality situation: an average couple has a dozen children. Four of them, by random good luck, inherit a good combination of the couple’s genes and turn out healthy and smart. Four, by random bad luck, get a less lucky combination of genes and turn out not particularly healthy or smart. And four, by very bad luck, get some unpleasant mutations that render them quite unhealthy and rather dull.
Infant mortality claims half their children, taking the least healthy. They are left with 4 bright children and 2 moderately intelligent children. The three brightest children succeed at life, marry well, and end up with several healthy, surviving children of their own, while the moderately intelligent do okay and end up with a couple of children.
On average, society’s overall health and IQ should hold steady or even increase over time, depending on how strong the selective pressures actually are.
Or consider a consanguineous couple with a high risk of genetic birth defects: perhaps a full 80% of their children die, but 20% turn out healthy and survive.
Today, by contrast, your average couple has two children. One of them is lucky, healthy, and smart. The other is unlucky, unhealthy, and dumb. Both survive. The lucky kid goes to college, majors in underwater intersectionist basket-weaving, and has one kid at age 40. That kid has Down Syndrome and never reproduces. The unlucky kid can’t keep a job, has chronic health problems, and 3 children by three different partners.
Your consanguineous couple migrates from war-torn Somalia to Minnesota. They still have 12 kids, but three of them are autistic with IQs below the official retardation threshold. “We never had this back in Somalia,” they cry. “We don’t even have a word for it.”
People normally think of dysgenics as merely “the dumb outbreed the smart,” but genetic load applies to everyone–men and women, smart and dull, black and white, young and especially old–because we all make random transcription errors when copying our DNA.
I could offer a list of signs of increasing genetic load, but there’s no way to avoid cherry-picking trends I already know are happening, like falling sperm counts or rising (diagnosed) autism rates, so I’ll skip that. You may substitute your own list of “obvious signs society is falling apart at the genes” if you so desire.
Nevertheless, the transition from 30% (or greater) infant mortality to almost 0% is amazing, both on a technical level and because it heralds an unprecedented era in human evolution. The selective pressures on today’s people are massively different from those our ancestors faced, simply because our ancestors’ biggest filter was infant mortality. Unless infant mortality acted completely at random–taking the genetically loaded and unloaded alike–or on factors completely irrelevant to load, the elimination of infant mortality must continuously increase the genetic load in the human population. Over time, if that load is not selected out–say, through more people being too unhealthy to reproduce–then we will end up with an increasing population of physically sick, maladjusted, mentally ill, and low-IQ people.
If all of the above is correct, then I see only 4 ways out:
Do nothing: Genetic load increases until the population is non-functional and collapses, resulting in a return of Malthusian conditions, invasion by stronger neighbors, or extinction.
Sterilization or other weeding out of high-load people, coupled with higher fertility by low-load people
Abortion of high load fetuses
#1 sounds unpleasant, and #2 would result in masses of unhappy people. We don’t have the technology for #4, yet. I don’t think the technology is quite there for #2, either, but it’s much closer–we can certainly test for many of the deleterious mutations that we do know of.
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.
(If I’m correct, then this is the most important post on this blog, so please share.)
After researching ways to stop seizures, I suggested this to a friend with epilepsy. Her previous seizure lasted for 5 minutes (absolutely terrifying); this time her husband ran to the fridge, got two ice packs on her back, and the seizure immediately began slowing.
Obviously this is only an anecdote, but if you or a loved one has seizures, I can’t imagine it would hurt to try.
Let’s run through the evidence in favor of ice packs:
Seizures can definitely be triggered by being too hot–febrile seizures are somewhat common in children with fevers. Hyperthermia (heat stroke) can also cause seizures. And, yes, you can induce seizures in rats by heating them up. In the rat experiment, note that the seizure-prone rats’s temperatures went up more than the seizure-resistant rats–seizures may be more common in people whose bodies have difficulty regulating their temperatures.
That said, seizure-prone people don’t need to be cold all the time–summer weather doesn’t cause an overall uptick in seizures (and some people’s seizures are actually triggered by being cold. If you are one of these people, ice packs may not be for you.)
We have a precious little Jack Russell Terrier named Scamp. … he is one of many dogs who have epilepsy. This has broken our hearts over the last three-and-a-half years. …
Recently my husband and I did research on the Internet regarding dogs with epilepsy. What we found was amazing. Something the eight or so vets we have seen over the past years had never even mentioned to us. It’s as simple as keeping a bag of ice in your freezer.
We had never tried this until this morning at 5:00 a.m. when Scamp began seizuring. I’ve never seen anything work so fast in my life. As I write this this morning I’m still amazed and can’t believe that what ended a seziure was as simple as a bag of ice and 2 teaspoons of vanilla ice cream to elevate his blood sugar level.
Here’s how it works: all you do is fill a food storage bag (at least one quart size) with crushed ice and leave it in the freezer. When your dog starts to seizure remove the bag of ice from the freezer and place it firmly on his lower back. Scamp came out of his seizure in about 30 to 60 seconds. …
He came out of the seizure smoothly and with no post-ictal symptoms whatsoever. He began to walk and followed my husband and I right into the kitchen. I went to the freezer and took out vanilla ice cream and took two teaspoons out of the carton. … he lapped it up. He was fine. He wanted to go outside so my husband followed him out to make sure he would be OK. He went to the bathroom, roamed around the yard for a bit and came in and went back to sleep on our bed. I’m still in shock.
The ice cream is to help get the dog’s blood sugar levels back up to normal. Humans might also find this useful.
Here’s another testimonial, from one of the links above:
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. I would love to get it on video but as you all know a seizure is such a highly emotionally time that grabbing the camera is the last thing on my mind. 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.
“Lani” is a 65 lb. Lab with a pretty thick coat. Our first attempts did not go so well because those little blue ice packs or baggies did nothing. So I custom made her packs using large seal a meal bags with water and rubbing alcohol that I keep in the freezer. It is perfect because its super cold but pliable so you can form it over their back. Every seizure she has is treated with the ice packs. She is also on high doses of meds, supplements, etc. but my personal belief is that the ice pack treatment helps to significantly reduce the length of the seizure.
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.
The technique doesn’t work for all dogs, but it works for enough that it really seems like there must be something there.
But I haven’t read any cases of people using ice packs to treat seizures in humans–the (small quantity of) veterinary literature doesn’t appear to have made it over to human trials. But if it works for dogs, why not try it on people? It would be simplest, cheapest, least side-effect-inducing option for millions of people whose seizures can’t be fully controlled by medication.
Why does it work?
I don’t know. The ice packs probably aren’t in contact with the dogs for long enough to significantly lower the dog’s brain temperature, although they might lower the temperature of spinal nerves.
Perhaps the sudden cold just has an overwhelming effect on the brain that interrupts whatever feedback loop is causing the seizure.
Why not just medicate the seizures away?
Seizures are serious, potentially life-threatening conditions (actually, a friend of the family who had epilepsy died of a seizure that occurred while taking a bath.) Seizure medications, by necessity, are also serious and can have major side effects. According to the WHO, 70% of epileptics respond well to medication and live normal lives–leaving 30% of people who don’t. For many people, especially children, treatment is about trying to find a balance between minimizing harm from seizures and minimizing harm from anti-seizure medications.
So for anyone out there with epilepsy or another seizure condition, please consider ice packs as one more tool in your arsenal. And for any doctors out there, please do some research on this; there’s got to be some medical award for anyone who can prove it.