We are fortunate to live in a state that is leading the way in the local farm and food movement. The number of young farmers is on the rise. Independent chefs and food entrepreneurs continue to put down roots and build sustainable businesses.
Quick, what do you know about Faecalibacterium, Lachnospira,Veillonella, and Rothia? Not much? Join the rest of us. But these four bacteria, FLVR for short, can really impact a child’s chances of developing asthma if given in the first three months of life.
Think of it as a bacterial gut vaccine or gut grass seed to avoid inflammation later in life. But why do we need them now? Asthma rates have been increasing dramatically in recent years. “Increased use of prenatal and perinatal antibiotics, increased urban living, and formula feeding in infancy may all play a role.”
The researchers were so impressed by their findings, they are hustling to patent their results. Currently, you can’t buy this mix anywhere, and your pediatrician is unlikely to know anything about it. Part of the problem is that we all have been taught to fear bacteria. “We need to revisit our relationship with bacteria,” Turvey says. “Our species have coevolved with them, and they’re really important for our health.”
My own contribution to increasing our knowledge has been a short book, Tending Your Internal Garden, in which I point out some current myths about our bacterial internal world and even some possible solutions.
Last year 118 children were paralyzed in the U.S. The only association (for most of the children) was a recent respiratory infection. At the time, enterovirus D68 was targeted, but less than 20% of the children had the virus present at the time of testing.
A recent report of the CDC cites Enterovirus C105 as another possible cause. The enterovirus C family includes 11 enteroviruses (previously Coxsackie A viruses) as well as the polioviruses. The most recent report is of a six-year-old girl who lost function in her right arm after a respiratory infection. Enterovirus C105 was found in her respiratory tract, and her MRI showed swelling in her spinal column.
Although the patient was started on immunoglobulin treatment, it had little effect. She has gradually regained the use of her arm over the eight months since her infection. (report here)
I love coconut oil. It takes great, and you feel vaguely virtuous for using a “healthy oil.” But I have misgivings about giving it a completely free pass and using it for everything. In Dr. Oz’s recent “99 Amazing Uses for Coconut Oil” he recommends it for everything from your morning coffee to treating cuts to everything you cook. It’s even good for a nursing mother’s nipples, introducing infants to coconut oil right along with mother’s milk.
Much of the hype surrounding coconut is because. “coconut oil comprises medium-chain fatty acids (MCFA). MCFA are unique in that they are easily absorbed and metabolised by the liver, and can be converted to ketones. Ketone bodies are an important alternative energy source in the brain.” (cite here) These health benefits are compared to the ill-effects of saturated fatty acids. But more recent analysis of the “data revealed that dietary saturated fatty acids (SFAs) are not associated with CAD and other adverse health effects or at worst are weakly associated” (cite here) So we’re using coconut to avoid something else that tastes as good and may not be any worse for us. In a trial of different fats versus transfats, all of them worked: “each 1% energy replacement of TFAs with SFAs, MUFAs or PUFAs, respectively, decreased the total cholesterol” (cite here)
Coconut isn’t just a replacement for saturated fats. “The parts of its fruit like coconut kernel and tender coconut water have numerous medicinal properties such as antibacterial, antifungal, antiviral, antiparasitic, antidermatophytic, antioxidant, hypoglycemic, hepatoprotective, (and) immunostimulant…The coconut palm is, therefore, eulogised as ‘Kalpavriksha’ (the all giving tree) in Indian classics” (cite here) I guess we should use it for everything.
But this magical tree doesn’t necessarily result in the expected benefits. Natives who consumed lots of coconuts did not have more heart disease, but also did not have less of it. (cite here) When calves are fed either coconut oil (CO) or tallow: “Feeding on the CO diet induced an 18-fold increase in the hepatic concentration of triacylglycerols” (cite here)
Sometimes coconut and palm oil are discussed as equally healthy. Palm oil clearly is not. “for every additional kilogram of palm oil consumed per-capita annually, IHD mortality rates increased by 68 deaths per 100,000 (95% CI [21-115]), whereas, in similar settings, stroke mortality rates increased by 19 deaths per 100,000” (cite here) In rats, coconut oil benefits rats “suffering” from heated palm oil.(cite here)
Rather than an all-or-nothing approach to any foodstuff, it’s better to consider the advantages and disadvantages of each. In a rat trial of the heart: “The cardiac mitochondria from rats fed with coconut oil showed the lowest concentration of oxidized proteins and peroxidized lipids.” We could conclude “Yes! Coconut oil is great!” The researchers went on: “The fish oil diet leads to the highest oxidative stress in cardiac mitochondria, an effect that could be partly prevented by the antioxidant probucol.” We could conclude that fish oil is a terrible choice, so why are all of our doctors recommending it? But the next sentence tells a different story: “Total and LDL cholesterols decreased in plasma of rats fed fish oil, compared to olive and coconut oils fed rats.” So now we have a better picture of what the oils do in rats. We don’t have that clear a picture about what happens in humans, regardless of the current fad. (cite here)
Human prion diseases are rare. So when, for the first time in fifty years, a new one is discovered, you’d think there would have been more media coverage.
The last time we had a new prion disease, Creutzfeldt–Jaekob disease, (CJD), it was associated with cannibalism and more recently mad cows. This one is connected to an orphan disease, Multiple system atrophy (MSA). It looks sometimes like Parkinsons and sometimes like something else.
Having Parkinsons is a poor enough diagnosis, but having MSA Parkinsons is worse. Rather than simply having your nerve cells fill with alpha-synuclein, MSA Parkinsons patients have the alpha-synuclein fill up their oligodendroglia, the cells that help sheath your nerves in protective myelin. So not only do you have Parkinsons symptoms, you have all the symptoms of an immune system that is shorting out, much like multiple sclerosis.
Currently, there are no treatments or cure, so this disease is managed by cobbling together treatments from other areas as supportive measures.
But researchers noticed a strange behavior in the plaques of MSA patients: ““toxic α-Syn aggregates exhibit prion-like behavior spreading from cell to cell.” This month they announced that, indeed, MSA was a prion based illness. Mice who were injected with Parkinsons plaques did not develop the disease, but mice who were injected with MSA plaques all got the illness. The researchers concluded: ” α-synuclein is the first new human prion to be identified, to our knowledge, since the discovery a half century ago that CJD was transmissible.”
Now we need to think about how many current patients with Parkinsons might have MSA. Differentiating the diagnosis takes a lot of testing, and many patients with symptoms may not have had that testing but simply been diagnosed with Parkinsons. One of the basic realities of prion diseases is that common sterilizing practices (autoclaving) are not effective at removing all infectious material.
At the same time, there may be a treatment for people who currently have MSA Parkinsons. Just last month a team of researchers found that polythiophenes (chemicals that make samples glow during experiments) bind preferentially to prions. Infected mice exhibited an 80% increase in survival. They were building on previous research by another group.
So, in the span of two months, we have a new terrible specter of a surgerical and blood passed infectious prion and a possible treatment for many currently affected individuals.
In Phil Zuckerman’s book, Atheism and Secularity, (p.95) he describes atheists and agnostics as a tiny minority. But my experience of atheists is that they describe themselves as far more prevalent and under-represented because too few of them will speak out. They also think of themselves as more intelligent, creating the need to evangelize their truth to the rest of us.
To compile his information about atheists, Zuckerman used members of the Bright movement, founded in 2003 by Futrell and Geisert. The Bright movement is currently maintained by Daniel Dennett (Tufts) and Richard Dawkins. A Bright maintains a naturalistic worldview free of mystical and supernatural elements. There are 40,000 Brights in over 140 countries.
Zuckerman’s information places atheists at 2% of the U.S. population, while agnostics hold 4%. Agnostics were more educated than atheists or believers. Over half of atheist and agnostics continued to identify themselves as belonging to a religion despite their lack of belief. They also continue to attend church services, giving credence to the idea of “being in the closet” about their atheism.
But this contradiction is also maintained in their personal spiritual life. Only a third of atheists and agnostics claim they never pray. Many continue to attend weekly religious services despite minimal external pressure.
While more liberal than believers, atheists are almost twice as likely as agnostics to be against homosexuality. Atheists who continue to continue to attend church services are more than twice as likely to acknowledge homophobia as those who do not.
Despite this, atheists or agnostics are almost three times as likely as believers to be homosexual. (p.98) Zuckerman explores the subject of homosexuality within the Bright community, noting that over 7% of online conversations revolved around homosexuality both as a moral issue and as a model for Brights themselves to come out of the closet and go main stream.
Coming out of the closet for atheists may be a daunting task according to Robert Altemeyer’s The Atheists. They face a much larger group in the U.S., Evangelical Fundamentalists, who roughly outnumber them as 36% of the population to their 3%. The U.S. is the worst place to be an atheist, 3% vs. 9% in Canada and as high as 19% in France. In the U.S. being an outspoken atheist can cost you friends and job prospects, as well as alienate your family and relatives.
So the next time you meet an atheist, spend a moment in their shoes. They see around them a world defined by religion. Even the books written by atheists for atheists are largely defined by arguments against God and religion, not positive discussions of a positive, humanistic atheist world view. For the most part an atheist expects derision and argument as well as prejudice and discrimination. It makes sense that an atheist might be a little disagreeable, a little argumentative, so let them vent a little without taking it personally. Be polite and change the subject if you find the religious discussion objectionable.
You’d think a super bug with a 50% death rate would get more press. But maybe because KPC is complicated, it doesn’t get the same kind of media frenzy as its far less deadly media rival Ebola. There was one article (in the Australian press) trying to explain KPC.
The problem isn’t helped by a name change. Just call KPC “the superbug formerly known as KPC but now known as CRE.” The first name at least defined a specific bug: Klebsiella pneumoniae carbapenemase, which used to be the major host of antibiotic resistance. But now it’s given its antibiotic resistance to a whole bunch of its friends like e. coli, so together the gang is called: carbapenem-resistant Enterobacteriaceae (CRE). (Here’s a table of the gang members.)
Since it was KPC before it became CRE, let’s follow little KPC. The first sighting was in Japan in 1994, followed by a sighting in North Carolina in 2001. It made some serious inroads in the New York area in 2003-2004 and spread worldwide. By 2009, the CDC recommended CRE as the new name, but nobody has really made the switch, even in the medical literature.
We’re talking about a growing resistance that really puts other antibiotic resistance to shame. And it originated in the U.S., spreading elsewhere from us. “In New York City, the percentage of carbapenem-resistant K pneumoniae rose from 9% in 2002 to 18% in 2004, then further to 38% in 2008. In 2005, the first report of a clinical isolate producing a KPC outside of the US occurred in France from a patient who had recently been hospitalized in New York City.10 The first outbreak outside the US was in Israel,11 and KPCs are now endemic in both Israel and Greece. Enterobacteriaceae-producing KPCs have also been reported in Brazil, China, Colombia, Norway, United Kingdom, India, Sweden,5 and more recently, Italy and Finland.” (study here)
But we haven’t just sent it overseas. “To date, KPC-producing bacteria have been isolated in at least 33 states.” When we say resistant, we don’t mean just to carbapenem antibiotics (hospital use only). “these bacteria had reduced susceptibility or resistance to all beta-lactams including penicillins, cephalosporins, monobactams, and carbapenems. Moreover, in vitro studies of 95 KPC isolates from Brooklyn hospitals during 2003-2004 revealed approximately half to be susceptible to aminoglycosides and very few to be susceptible to fluoroquinolones.” In other words, we’re talking almost global resistance, not just one or two antibiotics. So when you get sick, it’s very possible that they may not have anything to help you. That explains the high death rate.
What makes this worse is that you may not know you’re in trouble even after you know you have an infection: “automated systems will identify seven to eighty-seven percent of KPC-producing K pneumoniae as susceptible to imipenem or meropenem” The computer may not catch that your bacterial infection is resistant until it’s too late to change antibiotics. “A small series of patients with bloodstream infections caused by KPC-producing bacteria from New York City hospitals in 2005 revealed mortality rates of 47% to 66%.” Even when they try to culture out the bacteria, the system may not catch the resistance: “A study of 36 patients in an intensive care unit (ICU) in New York City during a KPC outbreak revealed 39% of all patients had gastrointestinal colonization while only 14% were identified by previous clinical culture.”
So, should we all be terrified? Maybe? We don’t know how far and how fast the problem is spreading because CRE can live happily in your system as long as you don’t get sick. Health care workers exposed to CRE in the hospital can disseminate them out to their entire communities without any ill effects until a community member gets another illness. Given that we have no way to moniter KPC, and that it has transferred incredibly rapidly in less than ten years from New York to worldwide, I would have to agree with the study headline: ”
In a busy world, it’s nice to know that some researchers have time to brew a cuppa for themselves. Of course, they have to ruin it by making it an experiment. With math!
Have a look at this tea equation: dcdt=k1(c−c∞)2(1). That’s not a nice look for any poor cup of tea.
But we can all benefit from the hard work of researchers. Here are the results.
Say you’re in a hurry, so you grab a cup and dip your teabag in. You want the caffeine, but you don’t want to mess with the teabag later. So as soon as the color starts spreading in the cup, you dump the bag and race off to your meeting. Hold on Speedy!
Along with that teabag you just dumped your caffeine fix. According to the researchers, who had very consistent results, you need a minimum of two minutes of steeping time before you get your caffeine. Otherwise, all you get is colored water. The caffeine keeps coming in for a few more minutes, giving you a steep time of up to eight minutes. Isn’t eight minutes an entire “lunch hour” these days? But at least give your teabag two minutes to bask in that warm water before jettisoning it in the wastebasket.
There are a lot more reasons for drinking tea than the caffeine, and you can see that to get the maximum bang out of your bag eight minutes is really peak steeping time. All the benefits of tea will then be yours. Care to look at your benefit package in that slim little tea bag?
“polyphenols present in tea have shown a wide range of biological and pharmaceutical benefits, including prevention of cancer , obesity , type 2 diabetes , depressive symptoms  cardiovascular diseases and cerebral ischemic damage . Further tea possesses insulin-enhancing , antioxidative , hypolipidemic , antimicrobial , immune-stimulatory, anti-inflammatory , neuroprotective  and bone mineralization enhancement activities.” (All cites from the original article here)
I’ve thought a lot about antibiotic resistance, but I haven’t thought it through like Maryn McKenna in her TED talk.
What Ms. McKenna makes brutally clear is that we’re not talking about the end of dealing with infections. We’re talking about the end of safe surgery, the end of a fear free life where we can scratch ourselves and have antibiotics to fall back on if we need them.
So walk with me through a hospital in 2050, when antibiotics no longer work. Do you want to be there, where all the infections are rampant? Would you get a knee replacement, a hip surgery? A colonoscopy, a laparoscopic surgery, an in-vitro fertilization? What about having a routine exam of any kind at the doctor’s office, where other infectious patients still congregate even though antibiotics aren’t available for them? What about the nursing homes, which have now become the pneumonia wards?
We have been living in the golden age of modern medicine, if less than a century can be considered a golden age. The coming centuries do not look as rosy.
But will technology turn it around? Don’t hold your breath. The bacteria trade antibiotic resistant genes every twenty minutes. It takes a drug company ten years to get a new antibiotic on the market. The math is not in our favor.
Unlike Ms. McKenna, I don’t feel completely disheartened. It’s not because I believe we won’t continue to feed 80% of our antibiotics to animals to fatten them up (speeding up antibiotic resistance at the same time). It’s because drug companies aren’t the only source of antibiotic compounds. I realized this in medical school, and I’ve placed myself firmly in the area that we need when the antibiotics fail. Our drug pipeline won’t save us, but our herb garden is an untapped source of antibiotics, and the complex compounds found in herbs can be synthesized without patent technology. So far they haven’t been because a drug company can’t really patent oregano. But when the antibiotics fail, your modern doctor will be reaching into a spice rack to save lives.
One of the most pejorative things someone can say to you is: “you’re too old.” Yet doctors fall into this trap all the time. “You’re just getting old,” is second only to the favorite “it’s just in your mind” as a medical cop out. Too often treatment that would benefit someone for decades goes by the wayside because the doctor doesn’t pursue it further.
So what happens if you decide to ignore the naysayers and start training at 77? You might just end up like Olga Kotelko, who bypassed other athletes and kept right on going until her death at 95. Ms. Kotelko also lent us her brain to examine and they found that her brain did not seem as old as her age. Researchers looking at older patients found that: “the most physically active elderly volunteers, according to their activity tracker data, had better oxygenation and healthier patterns of brain activity than the more sedentary volunteers — especially in parts of the brain, including the hippocampus, that are known to be involved in improved memory and cognition.” (NYT article here)