It is popular to believe that aesthetic judgements of physical attractiveness – beauty – are arbitrary. Many people believe popular ideas about attractiveness are mostly social constructs. However science shows that this idea is incorrect.
Attractiveness is agreed upon by most people, across cultures and history, because it is defined by evolution by natural selection. What we experience as physical attraction is our brain’s innate ability to ascertain a potential mate’s health, mental fitness, and ability to reproduce (create healthy offspring.)
Attractiveness, from this scientific point of view, turns out be a person’s desire to seek an average mate: Note we are using a mathematical, scientific definition of the word “average.”
“Averageness” describes the physical beauty that results from averaging the facial features of people of the same gender and approximately the same age.
Scientific studies use photographic overlays of human faces, in which images are morphed together.
The term “average” here is a mathematical definition = arithmetic mean, = the sum of a collection of numbers divided by the count of numbers in the collection.
It turns out that an averaged face is not unremarkable, but is, in fact, quite good looking.
Nor is averageness typical in the sense of common or frequently occurring in the population, though it appears familiar, and is typical in the sense that it is a good example of a face that is representative of the category of faces.
The evolutionary explanation for averageness is koinophilia: animals seek mates with average features, because extreme or uncommon features indicate disadvantageous mutations.
Discerning mutations by just looking
Most humans have a good innate ability to discern whether a person has chromosomal damage just by looking at facial features. The shape of a person’s face is defined by instructions from our genes.
Thus if one has certain chromosomal mutations then other people pick up on that subconsciously.
There are characteristic changes in facial features created by Williams syndrome, Smith-Magenis syndrome, Fragile X syndrome, Jacobsen syndrome, trisomy 21 (classic mental retardation,) etc.
If one takes measurements, one can mathematically discern the existence of these chromosomal changes with a smartphone app (available only to doctors.)
The human face is sexually dimorphic, with the average male face differing from the average female face in the size and shape of, and distance between, the jaws, lips, eyes, nose and cheekbones.
Even within sex, there are considerable variations in these dimensions, leading to individuals appearing more or less feminine or masculine than the prototypical gendered face. While the origin of this variability remains unclear, there has been significant interest in the influence of the most abundant androgen, testosterone, in the development of face structure.
Genetic sex is determined at conception, but gonadal hormones play a vital role in the differentiation of male and female phenotypes throughout human development.
Andrew J. O. Whitehouse et al. Proceedings of the Royal Society B Biological Sciences 10/7/2015
Prenatal testosterone may have a powerful masculinizing effect on postnatal physical characteristics. However, no study has directly tested this hypothesis. Here, we report a 20-year follow-up study that measured testosterone concentrations from the umbilical cord blood of 97 male and 86 female newborns, and procured three-dimensional facial images on these participants in adulthood (range: 21–24 years).
Twenty-three Euclidean and geodesic distances were measured from the facial images and an algorithm identified a set of six distances that most effectively distinguished adult males from females.
From these distances, a ‘gender score’ was calculated for each face, indicating the degree of masculinity or femininity. Higher cord testosterone levels were associated with masculinized facial features when males and females were analysed together (n = 183; r = −0.59), as well as when males (n = 86; r = −0.55) and females (n = 97; r = −0.48) were examined separately (p-values < 0.001).
The relationships remained significant and substantial after adjusting for potentially confounding variables. Adult circulating testosterone concentrations were available for males but showed no statistically significant relationship with gendered facial morphology (n = 85, r = 0.01, p = 0.93).
This study provides the first direct evidence of a link between prenatal testosterone exposure and human facial structure.
Note (1) Grammer, K.; Thornhill, R. (October 1994). “Human (Homo sapiens) facial attractiveness and sexual selection: the role of symmetry and averageness”. Journal of Comparative Psychology. 108 (3): 233–42. doi:10.1037/0735-7036.108.3.233. PMID 7924253. Retrieved 4 May 2019.
Rhodes, Gillian; Zebrowitz, Leslie A. (2002). Facial Attractiveness: Evolutionary, Cognitive, and Social Perspectives. Ablex. ISBN 978-1-56750-636-5.
Jones, B. C., Little, A. C., Tiddeman, B. P., Burt, D. M., & Perrett, D. I. (2001). Facial symmetry and judgements of apparent health Support for a “‘ good genes ’” explanation of the attractiveness – symmetry relationship, 22, 417–429.
Alison Pearce Stevens writes “Research shows that people with more symmetrical faces don’t just look nice. They also tend to be healthier than asymmetrical people. Genes provide the instructions for how a cell is to perform. All people have the same number of genes. But people with more average faces tend to have a greater diversity in the genes they are born with. And that, research has shown, can lead to a stronger immune system and better health.” What makes a pretty face? Science News for Students
Iglesias-Julios M, Munoz-Reyes JA, Pita M et al. Facial Features: What Women Perceive as Attractive and What Men Consider Attractive. PLoS ONE. 2015.
Farmer H, McKay R, Tsakiris M. Trust in Me: Trustworthy Others Are Seen as More Physically Similar to the Self. Psychological Science. 2013.
Coetzee V, Keckp S, Kivleniece I et al. Facial attractiveness is related to women’s cortisol and body fat, but not with immune responsiveness. Biology Letters. 2013.
Students need to be aware of pseudoscience diets. Some of these claim that by eating more acidic or basic foods you can change your body’s pH level, and thus treat disease.
Not only is this entire idea incorrect, if a person does change their pH beyond even a tiny bit then they will almost immediately die. Changing one’s body pH is almost impossible, but when it happens it is fatal,
What are acids and bases? Acids are bases are complimentary types of chemicals. Acids perform one kind of chemical reaction; bases perform the opposite action. Learn more here about acids and bases.
Here’s the critical point: When it comes to living, what matters is whether acids and bases are working in a safe balance. Cells only work correctly in a very narrow range of conditions.
Too much or too little of any molecule, and they begin to malfunction or die. Homeostasis is the body’s way of keeping chemicals in a safe, dynamic balance.
In what they call the largest study ever done, researchers found using marijuana while pregnant may increase the risk that a child will develop autism.
“Women who used cannabis during pregnancy were 1.5 times more likely to have a child with autism,” said study author Dr. Darine El-Chaâr, a maternal fetal medicine specialist and clinical investigator at Ottawa Hospital Research Institute in Canada.
These are not reassuring findings. We highly discourage use of cannabis during pregnancy and breastfeeding,” she said.
Past studies have shown the use of marijuana during pregnancy is linked to low birth weight, impulsivity, hyperactivity, attention issues and other cognitive and behavioral issue in children, according to the US Centers for Disease Control and Prevention. Pregnant women who use marijuana, one study found, have a 2.3 times greater risk of stillbirth.
“Based on that, I’m not too surprised by these findings,” El-Chaâr said. “Fetal brain development occurs throughout all gestational ages.”
…. Use of marijuana by pregnant women has been growing in the United States in recent decades. An analysis last year of over 450,000 pregnant American women ages 12 to 44 by the National Institute on Drug Abuse found cannabis use more than doubled between 2002 and 2017. The vast majority of marijuana use was during the first three months of pregnancy, the study found, and was predominantly recreational rather than medical.
Yet the first trimester may be one of most sensitive times for the developing brain of a fetus, when it’s most susceptible to damage, El-Chaâr said.
Is Marijuana as Safe as We Think? Permitting pot is one thing; promoting its use is another.
Malcolm Gladwell, The New Yorker, January 14, 2019 Issue
A few years ago, the National Academy of Medicine convened a panel of sixteen leading medical experts to analyze the scientific literature on cannabis. The report they prepared, which came out in January of 2017, runs to four hundred and sixty-eight pages. It contains no bombshells or surprises, which perhaps explains why it went largely unnoticed. It simply stated, over and over again, that a drug North Americans have become enthusiastic about remains a mystery.
For example, smoking pot is widely supposed to diminish the nausea associated with chemotherapy. But, the panel pointed out, “there are no good-quality randomized trials investigating this option.” We have evidence for marijuana as a treatment for pain, but “very little is known about the efficacy, dose, routes of administration, or side effects of commonly used and commercially available cannabis products in the United States.” The caveats continue. Is it good for epilepsy? “Insufficient evidence.” Tourette’s syndrome? Limited evidence. A.L.S., Huntington’s, and Parkinson’s? Insufficient evidence. Irritable-bowel syndrome? Insufficient evidence. Dementia and glaucoma? Probably not. Anxiety? Maybe. Depression? Probably not.
Then come Chapters 5 through 13, the heart of the report, which concern marijuana’s potential risks. The haze of uncertainty continues. Does the use of cannabis increase the likelihood of fatal car accidents? Yes. By how much? Unclear. Does it affect motivation and cognition? Hard to say, but probably. Does it affect employment prospects? Probably. Will it impair academic achievement? Limited evidence. This goes on for pages.
We need proper studies, the panel concluded, on the health effects of cannabis on children and teen-agers and pregnant women and breast-feeding mothers and “older populations” and “heavy cannabis users”; in other words, on everyone except the college student who smokes a joint once a month. The panel also called for investigation into “the pharmacokinetic and pharmacodynamic properties of cannabis, modes of delivery, different concentrations, in various populations, including the dose-response relationships of cannabis and THC or other cannabinoids.”
Figuring out the “dose-response relationship” of a new compound is something a pharmaceutical company does from the start of trials in human subjects, as it prepares a new drug application for the F.D.A. Too little of a powerful drug means that it won’t work. Too much means that it might do more harm than good. The amount of active ingredient in a pill and the metabolic path that the ingredient takes after it enters your body—these are things that drugmakers will have painstakingly mapped out before the product comes on the market, with a tractor-trailer full of supporting documentation.
With marijuana, apparently, we’re still waiting for this information. It’s hard to study a substance that until very recently has been almost universally illegal. And the few studies we do have were done mostly in the nineteen-eighties and nineties, when cannabis was not nearly as potent as it is now. Because of recent developments in plant breeding and growing techniques, the typical concentration of THC, the psychoactive ingredient in marijuana, has gone from the low single digits to more than twenty per cent—from a swig of near-beer to a tequila shot.
Are users smoking less, to compensate for the drug’s new potency? Or simply getting more stoned, more quickly? Is high-potency cannabis more of a problem for younger users or for older ones? For some drugs, the dose-response curve is linear: twice the dose creates twice the effect. For other drugs, it’s nonlinear: twice the dose can increase the effect tenfold, or hardly at all. Which is true for cannabis? It also matters, of course, how cannabis is consumed. It can be smoked, vaped, eaten, or applied to the skin. How are absorption patterns affected?
Last May, not long before Canada legalized the recreational use of marijuana, Beau Kilmer, a drug-policy expert with the rand Corporation, testified before the Canadian Parliament. He warned that the fastest-growing segment of the legal market in Washington State was extracts for inhalation, and that the mean THC concentration for those products was more than sixty-five per cent. “We know little about the health consequences—risks and benefits—of many of the cannabis products likely to be sold in nonmedical markets,” he said. Nor did we know how higher-potency products would affect THC consumption.
When it comes to cannabis, the best-case scenario is that we will muddle through, learning more about its true effects as we go along and adapting as needed—the way, say, the once extraordinarily lethal innovation of the automobile has been gradually tamed in the course of its history. For those curious about the worst-case scenario, Alex Berenson has written a short manifesto, “Tell Your Children: The Truth About Marijuana, Mental Illness, and Violence.”
Berenson begins his book with an account of a conversation he had with his wife, a psychiatrist who specializes in treating mentally ill criminals. They were discussing one of the many grim cases that cross her desk—“the usual horror story, somebody who’d cut up his grandmother or set fire to his apartment.” Then his wife said something like “Of course, he was high, been smoking pot his whole life.”
Of course? I said.
Yeah, they all smoke.
Well . . . other things too, right?
Sometimes. But they all smoke.
Berenson used to be an investigative reporter for the Times, where he covered, among other things, health care and the pharmaceutical industry. Then he left the paper to write a popular series of thrillers. At the time of his conversation with his wife, he had the typical layman’s view of cannabis, which is that it is largely benign. His wife’s remark alarmed him, and he set out to educate himself. Berenson is constrained by the same problem the National Academy of Medicine faced—that, when it comes to marijuana, we really don’t know very much. But he has a reporter’s tenacity, a novelist’s imagination, and an outsider’s knack for asking intemperate questions. The result is disturbing.
The first of Berenson’s questions concerns what has long been the most worrisome point about cannabis: its association with mental illness. Many people with serious psychiatric illness smoke lots of pot. The marijuana lobby typically responds to this fact by saying that pot-smoking is a response to mental illness, not the cause of it—that people with psychiatric issues use marijuana to self-medicate. That is only partly true. In some cases, heavy cannabis use does seem to cause mental illness. As the National Academy panel declared, in one of its few unequivocal conclusions, “Cannabis use is likely to increase the risk of developing schizophrenia and other psychoses; the higher the use, the greater the risk.”
Berenson thinks that we are far too sanguine about this link. He wonders how large the risk is, and what might be behind it. In one of the most fascinating sections of “Tell Your Children,” he sits down with Erik Messamore, a psychiatrist who specializes in neuropharmacology and in the treatment of schizophrenia.
Messamore reports that, following the recent rise in marijuana use in the U.S. (it has almost doubled in the past two decades, not necessarily as the result of legal reforms), he has begun to see a new kind of patient: older, and not from the marginalized communities that his patients usually come from. These are otherwise stable middle-class professionals. Berenson writes, “A surprising number of them seemed to have used only cannabis and no other drugs before their breaks. The disease they’d developed looked like schizophrenia, but it had developed later—and their prognosis seemed to be worse. Their delusions and paranoia hardly responded to antipsychotics.”
Messamore theorizes that THC may interfere with the brain’s anti-inflammatory mechanisms, resulting in damage to nerve cells and blood vessels. Is this the reason, Berenson wonders, for the rising incidence of schizophrenia in the developed world, where cannabis use has also increased?
In the northern parts of Finland, incidence of the disease has nearly doubled since 1993. In Denmark, cases have risen twenty-five per cent since 2000. In the United States, hospital emergency rooms have seen a fifty-per-cent increase in schizophrenia admissions since 2006. If you include cases where schizophrenia was a secondary diagnosis, annual admissions in the past decade have increased from 1.26 million to 2.1 million.
Berenson’s second question derives from the first. The delusions and paranoia that often accompany psychoses can sometimes trigger violent behavior. If cannabis is implicated in a rise in psychoses, should we expect the increased use of marijuana to be accompanied by a rise in violent crime, as Berenson’s wife suggested?
Once again, there is no definitive answer, so Berenson has collected bits and pieces of evidence. For example, in a 2013 paper in the Journal of Interpersonal Violence, researchers looked at the results of a survey of more than twelve thousand American high-school students. The authors assumed that alcohol use among students would be a predictor of violent behavior, and that marijuana use would predict the opposite. In fact, those who used only marijuana were three times more likely to be physically aggressive than abstainers were; those who used only alcohol were 2.7 times more likely to be aggressive. Observational studies like these don’t establish causation. But they invite the sort of research that could.
Berenson looks, too, at the early results from the state of Washington, which, in 2014, became the first U.S. jurisdiction to legalize recreational marijuana. Between 2013 and 2017, the state’s murder and aggravated-assault rates rose forty per cent—twice the national homicide increase and four times the national aggravated-assault increase. We don’t know that an increase in cannabis use was responsible for that surge in violence. Berenson, though, finds it strange that, at a time when Washington may have exposed its population to higher levels of what is widely assumed to be a calming substance, its citizens began turning on one another with increased aggression.
His third question is whether cannabis serves as a gateway drug. There are two possibilities. The first is that marijuana activates certain behavioral and neurological pathways that ease the onset of more serious addictions. The second possibility is that marijuana offers a safer alternative to other drugs: that if you start smoking pot to deal with chronic pain you never graduate to opioids.
Which is it? This is a very hard question to answer. We’re only a decade or so into the widespread recreational use of high-potency marijuana. Maybe cannabis opens the door to other drugs, but only after prolonged use. Or maybe the low-potency marijuana of years past wasn’t a gateway, but today’s high-potency marijuana is. Methodologically, Berenson points out, the issue is complicated by the fact that the first wave of marijuana legalization took place on the West Coast, while the first serious wave of opioid addiction took place in the middle of the country. So, if all you do is eyeball the numbers, it looks as if opioid overdoses are lowest in cannabis states and highest in non-cannabis states.
Not surprisingly, the data we have are messy. Berenson, in his role as devil’s advocate, emphasizes the research that sees cannabis as opening the door to opioid use. For example, two studies of identical twins—in the Netherlands and in Australia—show that, in cases where one twin used cannabis before the age of seventeen and the other didn’t, the cannabis user was several times more likely to develop an addiction to opioids. Berenson also enlists a statistician at N.Y.U. to help him sort through state-level overdose data, and what he finds is not encouraging: “States where more people used cannabis tended to have more overdoses.”
The National Academy panel is more judicious. Its conclusion is that we simply don’t know enough, because there haven’t been any “systematic” studies. But the panel’s uncertainty is scarcely more reassuring than Berenson’s alarmism. Seventy-two thousand Americans died in 2017 of drug overdoses. Should you embark on a pro-cannabis crusade without knowing whether it will add to or subtract from that number?
Drug policy is always clearest at the fringes. Illegal opioids are at one end. They are dangerous. Manufacturers and distributors belong in prison, and users belong in drug-treatment programs. The cannabis industry would have us believe that its product, like coffee, belongs at the other end of the continuum.
“Flow Kana partners with independent multi-generational farmers who cultivate under full sun, sustainably, and in small batches,” the promotional literature for one California cannabis brand reads. “Using only organic methods, these stewards of the land have spent their lives balancing a unique and harmonious relationship between the farm, the genetics and the terroir.”
But cannabis is not coffee. It’s somewhere in the middle. The experience of most users is relatively benign and predictable; the experience of a few, at the margins, is not. Products or behaviors that have that kind of muddled risk profile are confusing, because it is very difficult for those in the benign middle to appreciate the experiences of those at the statistical tails.
Low-frequency risks also take longer and are far harder to quantify, and the lesson of “Tell Your Children” and the National Academy report is that we aren’t yet in a position to do so. For the moment, cannabis probably belongs in the category of substances that society permits but simultaneously discourages. Cigarettes are heavily taxed, and smoking is prohibited in most workplaces and public spaces. Alcohol can’t be sold without a license and is kept out of the hands of children. Prescription drugs have rules about dosages, labels that describe their risks, and policies that govern their availability. The advice that seasoned potheads sometimes give new users—“start low and go slow”—is probably good advice for society as a whole, at least until we better understand what we are dealing with.
Late last year, the commissioner of the Food and Drug Administration, Scott Gottlieb, announced a federal crackdown on e-cigarettes. He had seen the data on soaring use among teen-agers, and, he said, “it shocked my conscience.” He announced that the F.D.A. would ban many kinds of flavored e-cigarettes, which are especially popular with teens, and would restrict the retail outlets where e-cigarettes were available.
In the dozen years since e-cigarettes were introduced into the marketplace, they have attracted an enormous amount of attention. There are scores of studies and papers on the subject in the medical and legal literature, grappling with the questions raised by the new technology. Vaping is clearly popular among kids. Is it a gateway to traditional tobacco use? Some public-health experts worry that we’re grooming a younger generation for a lifetime of dangerous addiction. Yet other people see e-cigarettes as a much safer alternative for adult smokers looking to satisfy their nicotine addiction. That’s the British perspective.
Last year, a Parliamentary committee recommended cutting taxes on e-cigarettes and allowing vaping in areas where it had previously been banned. Since e-cigarettes are as much as ninety-five per cent less harmful than regular cigarettes, the committee argued, why not promote them? Gottlieb said that he was splitting the difference between the two positions—giving adults “opportunities to transition to non-combustible products,” while upholding the F.D.A.’s “solemn mandate to make nicotine products less accessible and less appealing to children.” He was immediately criticized.
“Somehow, we have completely lost all sense of public-health perspective,” Michael Siegel, a public-health researcher at Boston University, wrote after the F.D.A. announcement:
Every argument that the F.D.A. is making in justifying a ban on the sale of electronic cigarettes in convenience stores and gas stations applies even more strongly for real tobacco cigarettes: you know, the ones that kill hundreds of thousands of Americans each year. Something is terribly wrong with our sense of perspective when we take the e-cigarettes off the shelf but allow the old-fashioned ones to remain.
Among members of the public-health community, it is impossible to spend five minutes on the e-cigarette question without getting into an argument. And this is nicotine they are arguing about, a drug that has been exhaustively studied by generations of scientists. We don’t worry that e-cigarettes increase the number of fatal car accidents, diminish motivation and cognition, or impair academic achievement. The drugs through the gateway that we worry about with e-cigarettes are Marlboros, not opioids. There are no enormous scientific question marks over nicotine’s dosing and bio-availability. Yet we still proceed cautiously and carefully with nicotine, because it is a powerful drug, and when powerful drugs are consumed by lots of people in new and untested ways we have an obligation to try to figure out what will happen.
A week after Gottlieb announced his crackdown on e-cigarettes, on the ground that they are too enticing to children, Siegel visited the first recreational-marijuana facility in Massachusetts. Here is what he found on the menu, each offering laced with large amounts of a drug, THC, that no one knows much about:
Prenatal Exposure to Cannabis Affects the Developing Brain
Children born to moms who smoked or ingested marijuana during pregnancy suffer higher rates of depression, hyperactivity, and inattention.
By Andrew Scheyer, The Scientist, 1/1/2019
Excerpt
A Lifetime of Consequences?
Large-scale, longitudinal studies of humans whose mothers smoked marijuana once or more per week and experimental work on rodents exposed to cannabinoids in utero have yielded remarkably consistent intellectual and behavioral correlates of fetal exposure to this drug. Some exposed individuals exhibit deficits in memory, cognition, and measures of sociability.
These aberrations appear during infancy and persist through adulthood and are tied to changes in the expression of multiple gene families, as well as more global measures of brain responsiveness and plasticity. Researchers currently consider these perturbations to be mediated by changes to the endocannabinoid system caused by the active compounds in cannabis.
How Cannabis Affects the Function of Neurons
The human body contains two primary cannabinoid receptors: CB1R and CB2R. CB1R is present in the human fetal cerebrum by the first weeks of the second trimester, and is the brain’s most abundant G-protein coupled receptor. Located at the presynaptic terminal of neurons, CB1R is activated by endocannabinoids, which are synthesized from fatty acids in the postsynaptic neuron.
The receptors’ activation modulates the presynaptic release of neurotransmitters, thereby affecting synaptic function and a range of downstream signaling agents, from glutamate, dopamine, and serotonin to neuropeptides and hormones. The function of CB2Rs in the brain is still poorly understood, but there is some evidence that they exist both pre- and post-synaptically, as well as on glia and astrocytes. One recent paper suggests that, like CB1Rs, CB2Rs regulate neurotransmitter release (Synapse, 72:e22061, 2018).
When people smoke or ingest marijuana, exogenous cannabinoids enter the nervous system and activate these receptors. Stimulation by these high-affinity agonists results in stronger binding and greater activation of CB1R, triggering the process of receptor downregulation. Specifically, the greater binding causes the receptors to be internalized and degraded, such that they are no longer as available for cannabinoid signaling, and can thereby alter neuronal firing and other downstream events.
As the drug becomes more popular, concerns have been raised that its use can lead to psychotic disorders. Here’s what scientists know for sure, and what they don’t.
By Benedict Carey, The New York Times, 1/17/2019
Nearly a century after the film “Reefer Madness” alarmed the nation, some policymakers and doctors are again becoming concerned about the dangers of marijuana, although the reefers are long gone.
Experts now distinguish between the “new cannabis” — legal, highly potent, available in tabs, edibles and vapes — and the old version, a far milder weed passed around in joints. Levels of T.H.C., the chemical that produces marijuana’s high, have been rising for at least three decades, and it’s now possible in some states to buy vape cartridges containing little but the active ingredient.
The concern is focused largely on the link between heavy usage and psychosis in young people. Doctors first suspected a link some 70 years ago, and the evidence has only accumulated since then. In a forthcoming book, “Tell Your Children,” Alex Berenson, a former Times reporter, argues that legalization is putting a generation at higher risk of schizophrenia and other psychotic syndromes. Critics, including leading researchers, have called the argument overblown, and unfaithful to the science.
Can heavy use cause schizophrenia or other syndromes?
That is the big question, and so far the evidence is not strong enough to answer one way or the other. Even top scientists who specialize in marijuana research are divided, drawing opposite conclusions from the same data.
“I’ve been doing this research for 25 years, and it’s polarizing even among academics,” said Margaret Haney, a professor of neurobiology at Columbia University Medical Center. “This is what the marijuana field is like.”
The debate centers on the distinction between correlation and causation. People with psychotic problems often use cannabis regularly; this is a solid correlation, backed by numerous studies. But it is unclear which came first, the cannabis habit or the psychoses. Children who later develop schizophrenia often seem to retreat into their own world, stalked periodically by bizarre fears and fantasies well outside the range of usual childhood imagination, and well before they are exposed to cannabis. Those who go on to become regular marijuana users often use other substances as well, including alcohol and cigarettes, making it more difficult for researchers to untangle causation.
Consider cigarettes, the least mind-altering of these substances. In a 2015 study, a team led by Dr. Kenneth S. Kendler of Virginia Commonwealth University analyzed medical data on nearly two million people in Sweden. The data followed the individuals over time, from young adulthood, when most schizophrenia diagnoses occur, to middle age. Smoking was a predictor for later development of the disorder, and in what doctors call a dose-response relationship: the more a person smoked, the higher the risk.
Yet nicotine attracts nowhere near the concern that cannabis does, in part because the two drugs are so different in their everyday effects: mildly stimulated versus stoned. Indeed, some scientists have studied nicotine as a partial treatment for schizophrenia, to blunt the disorders effects on thinking and memory.
Is it biologically plausible that cannabis could cause a psychotic disorder?
Yes. Brain scientists know very little about the underlying biology of psychotic conditions, other than that hundreds of common gene variants are likely involved. Schizophrenia, for instance, is not a uniform disorder but an umbrella term for an array of unexplained problems involving recurrent psychosis, and other common symptoms.
Even so, there is circumstantial evidence for a biological mechanism. Psychotic disorders tend to emerge in late adolescence or early adulthood, during or after a period of rapid brain development. In the teenage years, the brain strips away unneeded or redundant connections between brain cells, in a process called synaptic pruning. This editing is concentrated in the prefrontal cortex, the region behind the forehead where thinking and planning occur — and the region that is perturbed in psychotic conditions.
The region is rich with so-called CB1 receptors, which are involved in the pruning, and are engaged by cannabis use. And alterations to the pruning process may well increase schizophrenia risk, according to recent research at the Broad Institute of M.I.T. and Harvard. In a 2016 analysis, scientists there found that people with the disorder often have a gene variant that appears to accelerate the pruning process.
What does this mean for me?
Experts may debate whether cannabis use can lead to psychotic disorders, but they mostly agree on how to minimize one’s risk.
Psychotic conditions tend to run in families, which suggests there is an inherited genetic vulnerability. Indeed, according to some studies, people prone to or at heightened risk of psychosis seem to experience the effects of cannabis differently than peers without such a history. The users experience a more vivid high, but they also are more likely to experience psychosis-like effects such as paranoia.
The evidence so far indicates that one’s familial risk for psychotic disorders outweighs any added effect of cannabis use. In a 2014 study, a team led by Ashley C. Proal and Dr. Lynn E. DeLisi of Harvard Medical School recruited cannabis users with and without a family history of schizophrenia, as well as non-users with and without such a history. The researchers made sure the cannabis users did not use other drugs in addition, a factor that muddied earlier studies. The result: there was a heightened schizophrenia risk among people with a family history, regardless of cannabis use.
“My study clearly shows that cannabis does not cause schizophrenia by itself,” said Dr. DeLisi. “Rather, a genetic predisposition is necessary. It is highly likely, based on the results of this study and others, that cannabis use during adolescence through to age 25, when the brain is maturing and at its peak of growth in a genetically vulnerable individual, can initiate the onset of schizophrenia.”
Because marijuana has been illegal for so long, research that could settle the question has been sorely lacking, although that has begun to change. The National Institutes of Health have launched a $300 million project that will track thousands of children from the age of 9 or 10 through adolescence, and might help clarify causation.
For the near future, expert opinions likely will be mixed. “Usually it is the research types who are doing ‘the sky is falling’ bit, but here it is switched,” said Dr. Jay Geidd, a professor of psychiatry at the University of California, San Diego. “The researchers are wary of overselling the dangers, as was clearly done in the past. However, clinicians overwhelmingly endorse seeing many more adolescents with ‘paranoia’” of some kind.
In short: Regularly using the new, high-potency cannabis may indeed be a risk for young people who are related to someone with a psychotic condition. On that warning, at least, most experts seem to agree.
Daily Marijuana Use And Highly Potent Weed Linked To Psychosis
NPR, 3/19/2019, by Rhitu Chatterjee
Several past studies have found that more frequent use of pot is associated with a higher risk of psychosis — that is, when someone loses touch with reality. Now a new study published Tuesday in the The Lancet Psychiatry shows that consuming pot on a daily basis and especially using high-potency cannabis increases the odds of having a psychotic episode later.
“This is more evidence that the link between cannabis and psychosis matters,” says Krista M. Lisdahl, a clinical neuropsychologist at the University of Wisconsin, Milwaukee, who wasn’t involved in the study.
The study authors consider high-potency cannabis to be products with more than 10 percent tetrahydrocannabinol or THC, the compound responsible for the drug’s psychoactive effects. The fact that consuming high-THC cannabis products has a greater risk is concerning, Lisdahl says, because these products are more common in the market now.
The study also shows that three European cities — London, Paris and Amsterdam — where high-potency weed is most commonly available actually have higher rates of new cases of psychosis than the other cities in the study.
The researchers identified 901 people aged 18 to 64 who were diagnosed with their first episode of psychosis between May 2010 and April 2015, at a mental health facility anywhere in 11 cities, including London, Paris, Amsterdam, Barcelona, other cities across Europe and one site in Brazil.
The researchers then asked these individuals and a control group of 1,200-plus other healthy people about their habits, including their use of weed. “We asked people if they used cannabis, when did they start using it and what kind of cannabis,” explains study author Marta Di Forti, a psychiatrist and clinician scientist at King’s College London.
People reported the names of weed strains they used, such as skunk in the U.K. or the Dutch Nederwiet, which allowed the researchers to identify the THC content in each product through data gathered by the European Monitoring Center for Drugs and Drug Addiction and national data from the different countries.
The study found that those who used pot daily were three times more likely to have a psychotic episode compared with someone who never used the drug.
Those who started using cannabis at 15 or younger had a slightly more elevated risk than those who started using in later years.
Use of high-potency weed almost doubled the odds of having psychosis compared with someone who had never smoked weed, explains Di Forti.
And for those who used high-potency pot on a daily basis, the risk of psychosis was even greater — four times greater than those who had never used.
The easy availability of high-THC weed is a recent phenomenon, she notes. “Almost 20 years ago, there wasn’t much high-potency cannabis available [in the market].”
One recent study showed that high-potency cannabis is increasingly dominating markets. It found that the average potency of weed in Europe and the U.S. in 2017 was 17.1 percent, up from 8.9 percent in 2008.
And some products can be even more potent. For example, in the Netherlands, the THC content of one product that’s gained popularity, locally produced Dutch resin Nederhasj, can be as high as 67 percent.
“What this paper has done that’s really nice is they look at rates of psychosis and cannabis use in lots of different places where underlying rates of psychosis are different,” says Suzanne Gage, a psychologist and epidemiologist at the University of Liverpool, who wrote a commentary linked to the study in The Lancet Psychiatry.
This allowed the researchers to compare incidence of psychosis with the availability and use of high-THC cannabis in the different cities, she says.
The study found that the three European cities — London, Paris and Amsterdam — had the highest rates of new diagnoses of psychosis — 45.7 per 100,000 person-years in London, 46.1 in Paris and 37.9 in Amsterdam.
These are also cities where high-potency weed is most easily available and commonly used.
Other European cities in Spain, Italy and France on the other hand have less than 10 percent THC content in most popular cannabis products on the market. These cities also have lower rates of new psychosis diagnosis, according to the study.
“One of the things that’s really novel is that they could show that variation of use and potency of cannabis was related to rates of first-episode psychosis,” Lisdahl says.
One critique of the theory that weed contributes to psychosis risk has been that while more people are using weed worldwide, there hasn’t been a corresponding rise in rates of psychosis, Gage explains. But the new study shows that cities with more easily available high-THC weed do have a higher rate of new diagnoses of psychosis.
“That’s a really interesting finding, and that’s not something anyone has done before,” she adds.
However, the study doesn’t prove causality, cautions Dr. Diana Martinez, a psychiatrist and addiction researcher at Columbia University. “You can’t say that cannabis causes psychosis,” she says. “It’s simply not supported by the data,” she says.
Lisdahl agrees. In order to show causality, one would have to follow people over time — before they started using weed to years later when they have their psychotic episodes, she says. “You need twins in the studies, you need genetic information,” among all other kinds of data, she says.
Psychotic disorders such as schizophrenia and bipolar are complicated, “multifaceted disorders,” Gage notes.
“In all psychotic disorders, there is this multiple hit hypothesis,” Martinez says. Many factors influence whether and how these disorders manifest.
Genetics is known to play a major role, as are a host of environmental factors. “Children who have risk of schizophrenia but grow up in stable homes … they may not go on to develop schizophrenia,” she adds.
The Adolescent Brain Cognitive Development study, which is funded by the U.S. National Institutes of Health, is attempting to tease out the various influences, Lisdahl says. “The NIH has now invested in that question.”
In the meantime, the new findings should be of interest to anyone using cannabis, says study author Di Forti. “There are people across the world who use cannabis for a variety of reasons,” she says. “Some of them recreationally, some of them for medicinal purposes.” They should be aware that using high-potency cannabis comes with a risk, she says.
“They need to know what to look for and ask for help, if they come across characteristics of a psychotic disorder,” she adds.
— – – — – – – – –
In response to The contribution of cannabis use to variation in the incidence of psychotic disorder across Europe (EU-GEI): a multicentre case-control study , Suzanne H. Gage, in Cannabis and psychosis: triangulating the evidence, writes
…It is perfectly possible that the association between cannabis and psychosis is bidirectional, as suggested by other work using genetic variables as proxies for the exposures of interest in a Mendelian randomisation design. Di Forti and colleagues’ study adds a new and novel study design to the evidence available, which consistently indicates that for some individuals there is an increased risk of psychosis resulting from daily use of high potency cannabis. Given the changing legal status of cannabis across the world, and the associated potential for an increase in use, the next priority is to identify which individuals are at risk from daily potent cannabis use, and to develop educational strategies and interventions to mitigate this.
Samuel T. Wilkinson, Rajiv Radhakrishnan, and Deepak Cyril D’Souza write:
The link between cannabis use and psychosis comprises three distinct relationships: acute psychosis associated with cannabis intoxication; acute psychosis that lasts beyond the period of acute intoxication; and persistent psychosis not time-locked to exposure. Experimental studies reveal that cannabis, delta-9-tetrahydrocannabinol (THC) and synthetic cannabinoids reliably produce transient positive, negative, and cognitive symptoms in healthy volunteers. Case studies indicate that cannabinoids can induce acute psychosis that lasts beyond the period of acute intoxication but resolves within a month. Exposure to cannabis in adolescence is associated with a risk for later psychotic disorder in adulthood; this association is consistent, temporally related, shows a dose response, and is biologically plausible. However, cannabis is neither necessary nor sufficient to cause a persistent psychotic disorder. More likely, it is a component cause that interacts with other factors to result in psychosis. The link between cannabis and psychosis is moderated by age at onset of cannabis use, childhood abuse, and genetic vulnerability. While more research is needed to better characterize the relationship between cannabinoid use and the onset and persistence of psychosis, clinicians should be mindful of the potential risk of psychosis, especially in vulnerable populations, including adolescents and those with a psychosis diathesis.
PreK–12 Standard 10: Tobacco, Alcohol, & Substance Use/Abuse Prevention
Students will acquire the knowledge and skills to be competent in making health-enhancing decisions regarding the use of medications and avoidance of substances, and in communicating about substance use/abuse prevention for healthier homes, schools, and communities.
Through the study of Effects on the Body students will
10.5 Describe addictions to alcohol, tobacco, and other drugs, and methods for intervention, treatment, and cessation
10.6 List the potential outcomes of prevalent early and late adolescent risk behaviors related to tobacco, alcohol, and other drugs, including the general pattern and continuum of risk behaviors involving substances that young people might follow
Students generate ideas of what the term “gateway” means in relation to substance abuse and map out a series of behaviors that begin with such “gateway” behaviors
Through the study of Healthy Decisions students will
10.7 Identify internal factors (such as character) and external factors (such as family, peers, community, faith-based affiliation, and media) that influence the decision of young people to use or not to use drugs
10.8 Demonstrate ways of refusing and of sharing preventive health information about tobacco, alcohol, and other drugs with peers. Students research and give an oral report on the effects of second-hand smoke.
By the end of grade 12
Through the study of Effects on the Body students will
10.9 Describe the relationship between multi-drug use and the increased negative effects on the body, including the stages of addiction, and overdose. Students research the increased chances of death from alcohol poisoning when alcohol is combined with marijuana.
10.10 Describe the harmful effects of tobacco, alcohol, and other substances on pregnant women and their unborn children.
+++++++++++++++++++++++++++++++++++++++++++++++++
This website is educational. Materials within it are being used in accord with the Fair Use doctrine, as defined by United States law.
§107. Limitations on Exclusive Rights: Fair Use. Notwithstanding the provisions of section 106, the fair use of a copyrighted work, including such use by reproduction in copies or phone records or by any other means specified by that section, for purposes such as criticism, comment, news reporting, teaching (including multiple copies for classroom use), scholarship, or research, is not an infringement of copyright. In determining whether the use made of a work in any particular case is a fair use, the factors to be considered shall include: the purpose and character of the use, including whether such use is of a commercial nature or is for nonprofit educational purposes; the nature of the copyrighted work; the amount and substantiality of the portion used in relation to the copyrighted work as a whole; and the effect of the use upon the potential market for or value of the copyrighted work. (added pub. l 94-553, Title I, 101, Oct 19, 1976, 90 Stat 2546)
We currently don’t know the cause of all forms of Alzheimer’s disease. There may be more than one cause. But today we have increasingly strong evidence that many cases are caused by a combination of a genetic mutation and Herpes virus.
Prions
Two proteins central to the pathology of Alzheimer’s disease act as prions—misshapen proteins that spread through tissue like an infection by forcing normal proteins to adopt the same misfolded shape—according to new UC San Francisco research.
Using novel laboratory tests, the researchers were able to detect and measure specific, self-propagating prion forms of the proteins amyloid beta (A-β) and tau in postmortem brain tissue of 75 Alzheimer’s patients. In a striking finding, higher levels of these prions in human brain samples were strongly associated with early-onset forms of the disease and younger age at death.
Alzheimer’s: The heretical and hopeful role of infection
David Robson writes
…. The “amyloid beta hypothesis” has inspired countless trials of drugs that aimed to break up these toxic plaques. Yet this research has ended in many disappointments, without producing the desired improvements in patients’ prognosis. This has led some to wonder whether the amyloid beta hypothesis may be missing an important part of the story. “The plaques that Alzheimer observed are the manifestation of the disease, not the cause,” says geriatrics scientist Tamas Fulop at the University of Sherbrooke in Canada.
Scientists studying Alzheimer’s have also struggled to explain why some people develop the disease while others don’t. Genetic studies show that the presence of a gene variant – APOE4 – can vastly increase someone’s chances of building the amyloid plaques and developing the disease.
But the gene variant does not seal someone’s fate as many people carry APOE4 but don’t suffer from serious neurodegeneration. Some environmental factors must be necessary to set off the genetic time bomb, prompting the build-up of the toxic plaques and protein tangles.
Early evidence
Could certain microbes act as a trigger? That’s the central premise of the infection hypothesis.
Itzhaki has led the way with her examinations into the role of the herpes simplex virus (HSV1), which is most famous for causing cold sores on the skin around the mouth. Importantly, the virus is known to lie dormant for years, until times of stress or ill health, when it can become reactivated – leading to a new outbreak of the characteristic blisters.
While it had long been known that the virus could infect the brain – leading to a dangerous swelling called encephalitis that required immediate treatment – this was thought to be a very rare event. In the early 1990s, however, Itzhaki’s examinations of post-mortem tissue revealed that a surprising number of people showed signs of HSV1 in their neural tissue, without having suffered from encephalitis.
Importantly, the virus didn’t seem to be a risk for the people without the APOE4 gene variant, most of whom did not develop dementia. Nor did the presence of APOE4 make much difference to the risk of people without the infection.
Instead, it was the combination of the two that proved to be important. Overall, Itzhaki estimates that the two risk factors make it 12 times more likely that someone will develop Alzheimer’s, compared to people without the gene variant or the latent infection in their brain.
Itzhaki hypothesised that this was due to repeated reactivation of the latent virus – which, during each bout, invades the brain and somehow triggers the production of amyloid beta, until eventually, people start to show the cognitive decline that marks the onset of dementia.
Itzhaki says that her findings were met with a high degree of scepticism by other scientists. “We had the most awful trouble getting it published.” Many assumed that the experiments were somehow contaminated, she says, leading to an illusory result. Yet she had been careful to avoid this possibility, and the apparent link between HSV1 infection and Alzheimer’s disease has now been replicated in many different populations.
One paper, published earlier this year, examined cohorts from Bordeaux, Dijon, Montpellier and rural France. By tracking certain antibodies, they were able to detect who had been infected with the herpes simplex virus. The researchers found that the infection roughly tripled the risk of developing Alzheimer’s in APOE4 carriers over a seven-year follow-up period – but had no effect in people who were not carrying the gene.
“The herpes virus was only able to have a deleterious effect if there was APOE4,” says Catherine Helmer at the University of Bordeaux in France, who conducted the research.
“It’s a result that is so striking, it’s hard to believe,” says Anthony Komaroff, a professor at Harvard Medical School and a senior physician at Brigham and Women’s Hospital in Boston, who recently reviewed the current state of the research into the infection hypothesis for the Journal of the American Medical Association. Although he remains cautious about lending too much confidence to any single study, he is now convinced that the idea demands more attention. “It’s such a dramatic result that it must be taken seriously,” he says.
Komaroff knows of no theoretical objections to the theory. “I haven’t heard anyone, even world-class Alzheimer’s experts who are dubious about the infection hypothesis, give a good reason why it has to be bunkum,” he adds. We simply need more studies providing direct evidence for the link, he says, to be able to convince the sceptics.
As interest in the infection hypothesis has grown, scientists have started to investigate whether any other pathogens may trigger a similar response – with some intriguing conclusions. A 2017 study suggested that the virus behind shingles and chickenpox can moderately increase the risk of Alzheimer’s disease.
In the short term, this could be highly advantageous, preventing the infection from spiralling out of control so that it poses an immediate danger to someone’s life. But if the pathogen is repeatedly reactivated during times of stress, the amyloid beta could accumulate in the toxic plaques, harming the cells it is meant to be protecting.
Connection to coronavirus, covid-19
During the current pandemic, some scientists have started to worry that the coronavirus could increase the risk of dementia. As scientists from Mount Sinai School of Medicine, New York warned in the Journal of Alzheimer’s Disease last year: “It is possible that there may be an existing population who have become unknowingly predisposed to neurodegeneration through silent viral entry into the brain.”
This could just be another consequence of the overall assault on the body, including the increased inflammation that comes with the disease. But some animal studies and analyses of human autopsies suggest that the coronavirus can invade the brain. And laboratory experiments suggest that this infection may, in turn, trigger neural damage.
Such findings ring alarm bells for Fulop. “Sars-Cov-2 may act exactly as HSV-1,” he proposes. Others – including Gopalakrishnan – are more cautious, however. “We have demonstrated that the virus can infect human neurons, and it can cause some sort of neuronal stress,” he says. “And this may have some unexpected effects.” Much more research will be necessary to assess any long-term risks for neurological disease
Ruth Itzhaki, Professor Emeritus of Molecular Neurobiology, University of Manchester
More than 30m people worldwide suffer from Alzheimer’s disease – the most common form of dementia. Unfortunately, there is no cure, only drugs to ease the symptoms. However, my latest review, suggests a way to treat the disease. I found the strongest evidence yet that the herpes virus is a cause of Alzheimer’s, suggesting that effective and safe antiviral drugs might be able to treat the disease. We might even be able to vaccinate our children against it.
The virus implicated in Alzheimer’s disease, herpes simplex virus type 1 (HSV1), is better known for causing cold sores. It infects most people in infancy and then remains dormant in the peripheral nervous system (the part of the nervous system that isn’t the brain and the spinal cord). Occasionally, if a person is stressed, the virus becomes activated and, in some people, it causes cold sores.
We discovered in 1991 that in many elderly people HSV1 is also present in the brain. And in 1997 we showed that it confers a strong risk of Alzheimer’s disease when present in the brain of people who have a specific gene known as APOE4.
The virus can become active in the brain, perhaps repeatedly, and this probably causes cumulative damage. The likelihood of developing Alzheimer’s disease is 12 times greater for APOE4 carriers who have HSV1 in the brain than for those with neither factor.
Later, we and others found that HSV1 infection of cell cultures causes beta-amyloid and abnormal tau proteins to accumulate. An accumulation of these proteins in the brain is characteristic of Alzheimer’s disease.
We believe that HSV1 is a major contributory factor for Alzheimer’s disease and that it enters the brains of elderly people as their immune system declines with age. It then establishes a latent (dormant) infection, from which it is reactivated by events such as stress, a reduced immune system and brain inflammation induced by infection by other microbes.
Reactivation leads to direct viral damage in infected cells and to viral-induced inflammation. We suggest that repeated activation causes cumulative damage, leading eventually to Alzheimer’s disease in people with the APOE4 gene.
Presumably, in APOE4 carriers, Alzheimer’s disease develops in the brain because of greater HSV1-induced formation of toxic products, or less repair of damage.
New treatments? The data suggest that antiviral agents might be used for treating Alzheimer’s disease. The main antiviral agents, which are safe, prevent new viruses from forming, thereby limiting viral damage.
In an earlier study, we found that the anti-herpes antiviral drug, acyclovir, blocks HSV1 DNA replication, and reduces levels of beta-amyloid and tau caused by HSV1 infection of cell cultures.
It’s important to note that all studies, including our own, only show an association between the herpes virus and Alzheimer’s – they don’t prove that the virus is an actual cause. Probably the only way to prove that a microbe is a cause of a disease is to show that an occurrence of the disease is greatly reduced either by targeting the microbe with a specific anti-microbial agent or by specific vaccination against the microbe.
Excitingly, successful prevention of Alzheimer’s disease by use of specific anti-herpes agents has now been demonstrated in a large-scale population study in Taiwan. Hopefully, information in other countries, if available, will yield similar results.
=================================
Corroboration of a Major Role for Herpes Simplex Virus Type 1 in Alzheimer’s Disease
Ruth F. Itzhaki, Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, United Kingdom
Strong evidence has emerged recently for the concept that herpes simplex virus type 1 (HSV1) is a major risk for Alzheimer’s disease (AD). This concept proposes that latent HSV1 in brain of carriers of the type 4 allele of the apolipoprotein E gene (APOE-ε4) is reactivated intermittently by events such as immunosuppression, peripheral infection, and inflammation, the consequent damage accumulating, and culminating eventually in the development of AD….
===================
How an outsider in Alzheimer’s research bucked the prevailing theory — and clawed for validation
Sharon Begley, Stat News, 10/29/2018
Robert Moir was damned if he did and damned if he didn’t. The Massachusetts General Hospital neurobiologist had applied for government funding for his Alzheimer’s disease research and received wildly disparate comments from the scientists tapped to assess his proposal’s merits.
It was an “unorthodox hypothesis” that might “fill flagrant knowledge gaps,” wrote one reviewer, but another said the planned work might add little “to what is currently known.” A third complained that although Moir wanted to study whether microbes might be involved in causing Alzheimer’s, no one had proved that was the case.
As if scientists are supposed to study only what’s already known, an exasperated Moir thought when he read the reviews two years ago.
He’d just had a paper published in a leading journal, providing strong data for his idea that beta-amyloid, a hallmark of Alzheimer’s disease, might be a response to microbes in the brain. If true, the finding would open up vastly different possibilities for therapy than the types of compounds virtually everyone else was pursuing.
But the inconsistent evaluations doomed Moir’s chances of winning the $250,000 a year for five years that he was requesting from the National Institutes of Health. While two reviewers rated his application highly, the third gave him scores in the cellar. Funding rejected.
Complaints about being denied NIH funding are as common among biomedical researchers as spilled test tubes after a Saturday night lab kegger. The budgets of NIH institutes that fund Alzheimer’s research at universities and medical centers cover only the top 18 percent or so of applications. There are more worthy studies than money.
Moir’s experience is notable, however, because it shows that, even as one potential Alzheimer’s drug after another has failed for the last 15 years (the last such drug, Namenda, was approved in 2003), researchers with fresh approaches — and sound data to back them up — have struggled to get funded and to get studies published in top journals. Many scientists in the NIH “study sections” that evaluate grant applications, and those who vet submitted papers for journals, have so bought into the prevailing view of what causes Alzheimer’s that they resist alternative explanations, critics say.
“They were the most prominent people in the field, and really good at selling their ideas,” said George Perry of the University of Texas at San Antonio and editor-in-chief of the Journal of Alzheimer’s Disease. “Salesmanship carried the day.”
Dating to the 1980s, the amyloid hypothesis holds that the disease is caused by sticky agglomerations, or plaques, of the peptide beta-amyloid, which destroy synapses and trigger the formation of neuron-killing “tau tangles.” Eliminating plaques was supposed to reverse the disease, or at least keep it from getting inexorably worse. It hasn’t. The reason, more and more scientists suspect, is that “a lot of the old paradigms, from the most cited papers in the field going back decades, are wrong,” said MGH’s Rudolph Tanzi, a leading expert on the genetics of Alzheimer’s.
Even with the failure of amyloid orthodoxy to produce effective drugs, scientists who had other ideas saw their funding requests repeatedly denied and their papers frequently rejected. Moir is one of them.
For years in the 1990s, Moir, too, researched beta-amyloid, especially its penchant for gunking up into plaques and “a whole bunch of things all viewed as abnormal and causing disease,” he said. “The traditional view is that amyloid-beta is a freak, that it has a propensity to form fibrils that are toxic to the brain — that it’s irredeemably bad. In the 1980s, that was a reasonable assumption.”
But something had long bothered him about the “evil amyloid” dogma. The peptide is made by all vertebrates, including frogs and lizards and snakes and fish. In most species, it’s identical to humans’, suggesting that beta-amyloid evolved at least 400 million years ago. “Anything so extensively conserved over that immense span of time must play an important physiological role,” Moir said.
What, he wondered, could that be?
In 1994, Moir changed hemispheres to work as a postdoctoral fellow with Tanzi. They’d hit it off over beers at a science meeting in Amsterdam. Moir liked that Tanzi’s lab was filled with energetic young scientists — and that in cosmopolitan Boston, he could play the hyper-kinetic (and bone-crunching) sport of Australian rules football. Tanzi liked that Moir was the only person in the world who could purify large quantities of the molecule from which the brain makes amyloid.
Moir initially focused on genes that affect the risk of Alzheimer’s — Tanzi’s specialty. But Moir’s intellectual proclivities were clear even then. His mind is constantly noodling scientific puzzles, colleagues say, even during down time. Moir took a vacation in the White Mountains a decade ago with his then-6-year-old son and a family friend, an antimicrobial expert; in between hikes, Moir explained a scientific roadblock he’d hit, and the friend explained a workaround.
Moir’s inclination toward unconventional thinking took flight in 2007. He was (and still is) in the habit of spending a couple of hours Friday afternoons on what he calls “PubMed walkabouts,” casually perusing that database of biomedical papers. One summer day, a Corona in hand, he came across a paper on something called LL37. It was described as an “antimicrobial peptide” that kills viruses, fungi, and bacteria, including — maybe especially — in the brain.
What caught his eye was that LL37’s size and structure and other characteristics were so similar to beta-amyloid, the two might be twins.
Moir hightailed it to Tanzi’s office next door. Serendipitously, Tanzi (also Corona-fueled) had just received new data from his study of genes that increase the risk of Alzheimer’s disease. Many of the genes, he saw, are involved in innate immunity, the body’s first line of defense against germs. If immune genetics affect Alzheimer’s, and if the chief suspect in Alzheimer’s (beta-amyloid) is a virtual twin of an antimicrobial peptide, maybe beta-amyloid is also an antimicrobial, Moir told Tanzi.
If so, then the plaques it forms might be the brain’s last-ditch effort to protect itself from microbes, a sort of Spider-Man silk that binds up pathogens to keep them from damaging the brain. Maybe they save the brain from pathogens in the short term only to themselves prove toxic over the long term.
Tanzi encouraged Moir to pursue that idea. “Rob was trained [by Marshall] to think out of the box,” Tanzi said. “He thinks so far out of the box he hasn’t found the box yet.”
Moir spent the next three years testing whether beta-amyloid can kill pathogens. He started simple, in test tubes and glass dishes. Those are relatively cheap, and Tanzi had enough funding to cover what Moir was doing: growing little microbial gardens in lab dishes and then trying to kill them.
Day after day, Moir and his junior colleagues played horticulturalists. They added staph and strep, the yeast candida, and the bacteria pseudomonas, enterococcus, and listeria to lab dishes filled with the nutrient medium agar. Once the microbes formed a thin layer on top, they squirted beta-amyloid onto it and hoped for an Alexander Fleming discovery-of-penicillin moment.
This website is educational. Materials within it are being used in accord with the Fair Use doctrine, as defined by United States law.
§107. Limitations on Exclusive Rights: Fair Use. Notwithstanding the provisions of section 106, the fair use of a copyrighted work, including such use by reproduction in copies or phone records or by any other means specified by that section, for purposes such as criticism, comment, news reporting, teaching (including multiple copies for classroom use), scholarship, or research, is not an infringement of copyright. In determining whether the use made of a work in any particular case is a fair use, the factors to be considered shall include: the purpose and character of the use, including whether such use is of a commercial nature or is for nonprofit educational purposes; the nature of the copyrighted work; the amount and substantiality of the portion used in relation to the copyrighted work as a whole; and the effect of the use upon the potential market for or value of the copyrighted work. (added pub. l 94-553, Title I, 101, Oct 19, 1976, 90 Stat 2546)
The ingredients can be combined in hundreds of ways to make a delicious dinner.
It often takes just 15 minutes of prep and 15 minutes of cooking.
photo by Anna Ivanova
Start – pick one protein
Chicken breast or thigh meat, cut into pieces
Vegan chik’n (e.g. Trader Joe’s or Gardein Chik’n)
Beef strips/tips
Vegan beef (e.g. Trader Joe’s or Gardein Beef-less tips)
Tofu (firm)
Tempeh
Any other favorite protein source
Pick a carbohydrate
Cook these in a separate pot. Lay this down as the base for your meal. The vegetables, proteins and sauce go aside or over this.
Brown rice
Farro
Quinoa
Spaghetti or angel hair pasta
Mung bean vermicelli
Rice pasta
Pick a few veggies
Have a different combination each time!
Broccoli
Red bell peppers, green bell peppers, yellow or orange bell peppers
Yellow onions, vidalia onions
Summer squash
Carrots
Snow pea pods
Bamboo shoots
Miniature corn
Water chestnuts
If you like, add nuts
peanuts, cashews, etc.
Stir fry sauce
Kung Pao sauce
Red curry sauce and coconut milk
Teriyaki sauce
Sesame ginger sauce
Thai Peanut Satay
Orange Sauce
Szechuan sauce
Island Mango
Instructions
Dice your meat/protein source into small pieces, like the size of pieces you see at those food court restaurants at the shopping mall.
Add a small amount of oil to the wok. Usually peanut oil, but can be olive oil or any other favorite cooking oil.
In a separate pot, boil water. When boiling add your carb/pasta/grains.
Drop the meat (or faux meat) into the wok. Rotate and move all the pieces so that each is covered in oil.
Cook on a medium flame for a few minutes.
If you use real meat you must stir-fry this first; it takes more time to fully and safely cook.
Once the meat is cooked you then add in all of the other ingredients into the wok.
At this point continue cooking until all of the ingredients are done to your liking.
A neuroscientist argues that it’s time to change our minds on the roots of substance abuse, Laura Miller, for Salon. 6/27/15
A psychologist and former addict insists that the illness model for addiction is wrong, and dangerously so.
The mystery of addiction — what it is, what causes it and how to end it — threads through most of our lives. Experts estimate that one in 10 Americans is dependent on alcohol and other drugs, and if we concede that behaviors like gambling, overeating and playing video games can be addictive in similar ways, it’s likely that everyone has a relative or friend who’s hooked on some form of fun to a destructive degree. But what exactly is wrong with them? For several decades now, it’s been a commonplace to say that addicts have a disease. However, the very same scientists who once seemed to back up that claim have begun tearing it down.
Once, addictions were viewed as failures of character and morals, and society responded to drunks and junkies with shaming, scolding and calls for more “will power.” This proved spectacularly ineffective, although, truth be told, most addicts do quit without any form of treatment. Nevertheless, many do not, and in the mid-20th century, the recovery movement, centered around the 12-Step method developed by the founders of Alcoholics Anonymous, became a godsend for those unable to quit drinking or drugging on their own. The approach spread to so-called “behavioral addictions,” like gambling or sex, activities that don’t even involve the ingestion of any kind of mind-altering substance.
Much of the potency of AA comes from its acknowledgement that willpower isn’t enough to beat this devil and that blame, rather than whipping the blamed person into shape, is counterproductive. The first Step requires admitting one’s helplessness in the face of addiction….
…. Another factor promoting the disease model is that it has ushered addiction under the aegis of the healthcare industry, whether in the form of an illness whose treatment can be charged to an insurance company or as the focus of profit-making rehab centers.
….The recovery movement and rehab industry (two separate things, although the latter often employs the techniques of the former) have always had their critics, but lately some of the most vocal have been the neuroscientists whose findings once lent them credibility.
One of those neuroscientists is Marc Lewis, a psychologist and former addict himself, also the author of a new book “The Biology of Desire: Why Addiction is Not a Disease.”
Lewis’s argument is actually fairly simple: The disease theory, and the science sometimes used to support it, fail to take into account the plasticity of the human brain. Of course, “the brain changes with addiction,” he writes. “But the way it changes has to do with learning and development — not disease.” All significant and repeated experiences change the brain; adaptability and habit are the brain’s secret weapons. The changes wrought by addiction are not, however, permanent, and while they are dangerous, they’re not abnormal.
Through a combination of a difficult emotional history, bad luck and the ordinary operations of the brain itself, an addict is someone whose brain has been transformed, but also someone who can be pushed further along the road toward healthy development. (Lewis doesn’t like the term “recovery” because it implies a return to the addict’s state before the addiction took hold.)
“The Biology of Desire” is grouped around several case studies, each one illustrating a unique path to dependency. A striving Australian entrepreneur becomes caught up in the “clarity, power and potential” he feels after smoking meth, along with his ability to work long hours while on the drug. A social worker who behaves selflessly in her job and marriage constructs a defiant, selfish, secret life around stealing and swallowing prescription opiates. A shy Irishman who started drinking as a way to relax in social situations slowly comes to see social situations as an occasion to drink and then drinking as a reason to hole up in his apartment for days on end.
Each of these people, Lewis argues, had a particular “emotional wound” the substance helped them handle, but once they started using it, the habit itself eventually became self-perpetuating and in most cases ultimately served to deepen the wound.
Each case study focuses on a different part of the brain involved in addiction and illustrates how the function of each part — desire, emotion, impulse, automatic behavior — becomes shackled to a single goal: consuming the addictive substance. The brain is built to learn and change, Lewis points out, but it’s also built to form pathways for repetitive behavior, everything from brushing your teeth to stomping on the brake pedal, so that you don’t have to think about everything you do consciously. The brain is self-organizing. Those are all good properties, but addiction shanghais them for a bad cause.
As Lewis sees it, addiction really is habit; we just don’t appreciate how deeply habit can be engraved on the brain itself. “Repeated (motivating) experience” — i.e., the sensation of having one’s worries wafted away by the bliss of heroin — “produce brain changes that define future experiences… So getting drunk a lot will sculpt the synapses that determine future drinking patterns.”
More and more experiences and activities get looped into the addiction experience and trigger cravings and expectations like the bells that made Pavlov’s dogs salivate, from the walk home past a favorite bar to the rituals of shooting up. The world becomes a host of signs all pointing you in the same direction and activating powerful unconscious urges to follow them. At a certain point, the addictive behavior becomes compulsive, seemingly as irresistibly automatic as a reflex. You may not even want the drug anymore, but you’ve forgotten how to do anything else besides seek it out and take it.
Yet all of the addicts Lewis interviewed for “The Biology of Desire” are sober now, some through tried-and-true 12-Step programs, others through self-designed regimens, like the heroin addict who taught herself how to meditate in prison. Perhaps it’s no surprise that a psychologist would argue for some form of talk therapy addressing the underlying emotional motivations for turning to drugs. But Lewis is far from the only expert to voice this opinion, or to recommend cognitive behavioral therapy as a way to reshape the brain and redirect its systems into less self-destructive patterns.
Without a doubt, AA and similar programs have helped a lot of people. But they’ve also failed others. One size does not fit all, and there’s a growing body of evidence that empowering addicts, rather than insisting that they embrace their powerlessness and the impossibility of ever fully shedding their addiction, can be a road to health as well.
If addiction is a form of learning gone tragically wrong, it is also possible that it can be unlearned, that the brain’s native changeability can be set back on track. “Addicts aren’t diseased,” Lewis writes, “and they don’t need medical intervention in order to change their lives. What they need is sensitive, intelligent social scaffolding to hold the pieces of their imagined future in place — while they reach toward it.”
Its faith-based 12-step program dominates treatment in the United States. But researchers have debunked central tenets of AA doctrine and found dozens of other treatments more effective. By Gabrielle Glaser, The Atlantic 4/2015 The Irrationality of Alcoholics Anonymous, The Atlantic
The Surprising Failures of 12 Steps
How a pseudoscientific, religious organization birthed the most trusted method of addiction treatment. By Jake Flanagan 3/25/2014
Why the Disease Definition of Addiction Does Far More Harm Than Good.
Among other problems, it has obstructed other channels of investigation, including the social, psychological and societal roots of addiction. By Marc Lewis on February 9, 2018
…Viewing addiction as pathology has other, more direct detriments. If you feel that your addiction results from an underlying pathology, as implied by the brain disease model, and if that pathology is chronic, as highlighted by both NIDA and the 12-step movement, then you are less likely to believe that you will ever be free of it or that recovery can result from your own efforts. This characterization of addiction flies in the face of research indicating that a great majority of those addicted to any substance or behavior do in fact recover, and most of those who recover do so without professional care.
By Mark Lewis, Neuroethics, April 2017, Volume 10, Issue 1, pp 7–18
I review the brain disease model of addiction promoted by medical, scientific, and clinical authorities in the US and elsewhere. I then show that the disease model is flawed because brain changes in addiction are similar to those generally observed when recurrent, highly motivated goal seeking results in the development of deep habits, Pavlovian learning, and prefrontal disengagement. This analysis relies on concepts of self-organization, neuroplasticity, personality development, and delay discounting. It also highlights neural and behavioral parallels between substance addictions, behavioral addictions, normative compulsive behaviors, and falling in love. I note that the short duration of addictive rewards leads to negative emotions that accelerate the learning cycle, but cortical reconfiguration in recovery should also inform our understanding of addiction. I end by showing that the ethos of the disease model makes it difficult to reconcile with a developmental-learning orientation.
The chronic disease concept of addiction: Helpful or harmful?
Thomas K. Wiens & Lawrence J. Walker. Addiction Research & Theory, Volume 23, 2015 – Issue 4
This study provides empirical support to the notion that framing addiction within a biological conceptualisation, as opposed to a psychological and social framework, weakens perceptions of agency in relation to drinking. Likewise, no evidence was found to support the common assertion that the disease model reduces feelings of stigma and shame.
Most People With Addiction Simply Grow Out of It: Why Is This Widely Denied?
By Maia Szalavitz, Addictionblog.org 6/22/2015
The idea that addiction is typically a chronic, progressive disease that requires treatment is false, the evidence shows. Yet the “aging out” experience of the majority is ignored by treatment providers and journalists.
Most of Us Still Don’t Get It: Addiction Is a Learning Disorder
By Maia Szalavitz
Addiction is not about our brains being “hijacked” by drugs or experiences—it’s about learned patterns of behavior. Our inability to understand this leads to no end of absurdities.
5 Addiction Myths. A book review of Unbroken Brain: A Revolutionary New Way of Understanding Addiction. Laurel Sindewald, Handshake Media, 6/20/2016
Learned behavior model also explains wide array human behaviors, including political anger
Author David Brin writes
“For years I’ve followed advances that investigate reinforcement processes in the human brain, especially those involving dopamine and other messenger chemicals that are active in mediating pleasure response. One might call this topic chemically-mediated states of arousal that self-reinforce patterns of behavior.
Of course, what this boils down to — at one level — is addiction. But not only in the sense of illegal drug abuse. In very general terms, “addiction” may include desirable things, like bonding with our children and “getting high on life.” These good patterns share with drug addiction the property of being reinforced by repeated chemical stimulus, inside the brain…
Consider studies of gambling. Researchers led by Dr. Hans Breiter of Massachusetts General Hospital examined with functional magnetic resonance imaging (fMRI) which brain regions activate when volunteers won games of chance — regions that overlapped with those responding to cocaine!…
Moving along the spectrum toward activity that we consider more “normal” — neuroscientists at Harvard have found a striking similarity between the brain-states of people trying to predict financial rewards (e.g., via the stock market) and the brains of cocaine and morphine users.
… researchers at Emory University monitored brain activity while asking staunch party members, from both left and right, to evaluate information that threatened their preferred candidate prior to the 2004 Presidential election. “We did not see any increased activation of the parts of the brain normally engaged during reasoning,” said Drew Westen, Emory’s director of clinical psychology. “Instead, a network of emotion circuits lit up… reaching biased conclusions by ignoring information that could not rationally be discounted. Significantly, activity spiked in circuits involved in reward, similar to what addicts experience when they get a fix,” Westen explained.
Addicted to Self-Righteousness? An Open Letter to Researchers In the Fields of Addiction, Brain Chemistry, and Social Psychology
This website is educational. Materials within it are being used in accord with the Fair Use doctrine, as defined by United States law.
§107. Limitations on Exclusive Rights: Fair Use
Notwithstanding the provisions of section 106, the fair use of a copyrighted work, including such use by reproduction in copies or phone records or by any other means specified by that section, for purposes such as criticism, comment, news reporting, teaching (including multiple copies for classroom use), scholarship, or research, is not an infringement of copyright. In determining whether the use made of a work in any particular case is a fair use, the factors to be considered shall include: the purpose and character of the use, including whether such use is of a commercial nature or is for nonprofit educational purposes; the nature of the copyrighted work; the amount and substantiality of the portion used in relation to the copyrighted work as a whole; and the effect of the use upon the potential market for or value of the copyrighted work. (added pub. l 94-553, Title I, 101, Oct 19, 1976, 90 Stat 2546)
“People got in their head, well, if it’s man-made somehow it’s potentially dangerous, but if it’s natural, it isn’t. That doesn’t really fit with anything we know about toxicology. When we understand how animals are resistant to chemicals, the mechanisms are all independent of whether it’s natural or synthetic. And in fact, when you look at natural chemicals, half of those tested came out positive [for toxicity in humans].” –Bruce Ames
Organic food is food produced by organic farming, a set of techniques that mixes scientific knowledge of soil depletion and enrichment with anti-scientific beliefs and myths about nature and the natural.
This belief is contradicted by the vast majority of scientific studies that have been done on these subjects (Morris and Bate 1999; Taverne 2006; NCPA study). The United States Department of Agriculture (USDA) has put in place a set of national standards that food labeled “organic” must meet, whether it is grown in the United States or imported from other countries.
“USDA makes no claims that organically produced food is safer or more nutritious than conventionally produced food. Organic food differs from conventionally produced food in the way it is grown, handled, and processed.”*
Harm from bacterial contamination is a much greater possibility from natural fertilizers (Stossel 2005: 194). (For those of you who hate John Stossel, read the newspaper. The most dangerous bacteria in America’s food supply is E. coli, which is found in abundance in cattle manure, a favorite “natural” fertilizer of organic farming.)
The residues from pesticides on food, natural or synthetic, are not likely to cause harm to consumers because they occur in minute quantities.* (This fact does not make either kind of pesticide safe for those who work with them and are exposed to large quantities on a regular basis. I refer to residues on foods you and I are likely to find on fruits and vegetable we buy at the store or market.)
Using natural biological controls rather than synthetic pesticides is more dangerous to the environment (Morris and Bate 1999). The amounts of pesticide residue produced by plants themselves or introduced by organic farmers are significantly greater than the amounts of synthetic pesticide residues.
Almost all of the pesticides we ingest in food are naturally produced by plants to defend themselves against insects, fungi, and animal predators (Ames and Gold 1997). The bottom line is that fresh fruits and vegetables are good for you and it doesn’t matter whether they’re organic.
Over 30 separate investigations of about 500,000 people have shown that farmers, millers, pesticide-users, and foresters, occupationally exposed to much higher levels of pesticide than the general public, have much lower rates of cancer overall (Taverne 2006: 73.)
Groups like IFOAM refer to synthetic pesticides as “toxic,” even though the amount of pesticides people are likely to ingest through food are always in non-toxic amounts.
Although IFOAM has no official position on the quality of organic food, it’s easy to conclude that the overall nutritional and health-promoting value of food is compromised by farming methods that utilize synthetic fertilizers and toxic pesticides.
It’s easy to conclude—as long as you ignore the bulk of the scientific evidence that is available.
the myth of organic superiority
The evidence for the superiority of organic food is mostly anecdotal and based more on irrational assumptions and wishful thinking than on hard scientific evidence. There is no significant difference between a natural molecule and one created in the laboratory. Being natural or organic does not make a substance safe* nor does being synthetic make a substance unsafe.
Organic food does not offer special protection against cancer or any other disease. Organic food is not “healthier” than food produced by conventional farming, using synthetic pesticides and herbicides. Organic farming is not necessarily better for the environment than conventional farming. There is scant scientific evidence that most people can tell the difference in taste between organic and conventional foods. The bottom line is: fresher is better. Organic produce that travels thousands of miles to market is generally inferior to the same produce from local farmers, organic or not.
Is there any difference between organic and conventional fruits and vegetables? According to one scientific paper, there are several differences:
Based on the results of our literature review and experiment we conclude that there are substantial differences between organic and conventional fruits and vegetables. They differ with respect to production method, labeling, marketing, price and potentially other parameters.
You don’t need to do a scientific study to know that organic foods are produced differently from conventionally farmed foods. Anyone who has been to the market knows that you will pay substantially more for food labeled “organic.”
… The aforementioned scientific study did find that the literature provides evidence for one nutritional difference between organic and conventional foods: vitamin C was found to be higher for organic food.
coddling by the media
The way the media treat “green” issues accounts for one reason that the organic-is-better myth is pervasive. Here’s an example from BBC News:
Growing apples organically is not only better for the environment than other methods but makes them taste better than normal apples, US scientists say.
The study is among the first to give scientific credence to the claim that organic farming really is the better option.
The researchers found organic cultivation was more sustainable than either conventional or integrated farming, which cuts the use of chemicals.
The scientists, from Washington State University in Pullman, found the organic apples were rated highest for sweetness by amateur tasting panels.
They reported: “Escalating production costs, heavy reliance on non-renewable resources, reduced biodiversity, water contamination, chemical residues in food, soil degradation and health risks to farm workers handling pesticides all bring into question the sustainability of conventional farming systems.”
The headline for the story reads: Organic apples tickle tastebuds.
Most people might stop reading the story after five paragraphs of nothing but positive statements about organic farming and the mention of a number of problems ahead for conventional farming. For those who persevere, however, the following bits of information are also provided:
…organic farming systems were “less efficient, pose greater health risks and produce half the yields of conventional farming”.
…the tests “found no differences among organic, conventional and integrated apples in texture or overall acceptance”.
…Growers of more sustainable systems may be unable to maintain profitable enterprises without economic incentives, such as price premiums or subsidies for organic and integrated products.
Apparently, the measure used to determine that organic farming was “better for the environment” was based on physical, chemical, and biological soil properties. The scientists created their own index and found that organic was better mainly because of the addition of compost and mulch.
Certainly, there are going to be some organic farms that use methods of composting and mulching that improve growing conditions. But there are also methods conventional farmers can use to accomplish the same thing.
Finally, there are some organic farmers who used methods of composting and mulching that don’t improve anything except the chances of bacterial infection. Only a “green” journalist or scientist could turn being less efficient, posing greater health risks, no different in texture or appearance, and producing half the yields of conventional farming into “better than conventional farming.”
The article was published in the Journal of Agricultural and Food Chemistry, a peer-reviewed journal of the American Chemical Society. The article got some good press from “green” journalists, who proclaimed that the study showed that organic foods have significantly higher levels of antioxidants than conventional foods.
(Examples of glowing press reports can be found here and here.) There is a strong belief among promoters of organic foods that there is good scientific support for the claim that diets rich in antioxidants contribute to significantly lower cancer rates.
The data, however, do not support this belief. “Study after study has shown no benefit of antioxidants for heart disease, cancer, Parkinson’s disease, Alzheimer’s disease, or longevity” (Hall 2011).
The study compared total phenolic metabolites and ascorbic acid in only two crops, marionberries and corn. Both crops were grown organically and conventionally on different farms. The organic berries were grown on land that had been used for growing berries for four years; the conventional berries were grown on land that had been used to grow conventional berries for 21-22 years.
The crops were grown on different soil types: the organic soil was “sandy, clay, loam”; the conventional was “sandy, Ritzville loam.” The soil for the conventional corn had been used before for wheat; the soil for the organic corn had been used for green beans. The conventional farm used well water; the organic farm used a combination of well and creek water. (I don’t mention the strawberry listed in the title of the article because no organic strawberries were tested.)
As you can tell from the title of the article, the metabolites measured were not taken from fresh berries or corn but from samples that had been freeze-dried and air-dried. Though not mentioned in the title, the scientists also compared samples that were simply frozen.
The data provided by the authors in their published study shows clearly that there was not enough measurable ascorbic acid (AA) in either of the marionberry samples to compare the organic to the conventional. As already noted, no organic strawberries were studied. There was not enough measurable AA for the freeze-dried or air-dried corn to be compared.
So, the only data on AA is for the frozen corn: organic had a value of 3.2 and conventional had a value of 2.1. You can read the study yourself to find out what these numbers represent, but whatever they represent they do not merit the conclusion drawn by the authors of the study: “Levels of AA in organically grown … samples were consistently higher than the levels for the conventionally grown crops.”
The study also compared what it calls “sustainable agricultural practices” to organic and conventional practices. Sustainable practices in this study included the use of synthetic fertilizers.
“Our results indicate,” the authors write, “that TPs [total phenolics] were highest in the crops grown by sustainable agricultural methods as compared to organic methods.” Dr. Mitchell is quoted in the press as saying that their study “helps explain why the level of antioxidants is so much higher in organically grown food.” Yet, her study clearly states that the evidence for this claim is anecdotal. In fact, the authors write of the comparative studies that have been done:
These data demonstrate inconsistent differences in the nutritional quality of conventionally and organically produced vegetables with the exception of nitrate and ascorbic acid (AA) in vegetables.
distortion of evidence by scientists
One thing these “green” advocates are good at is distorting data to make lead appear to be gold. Another study led by Mitchell claims that organic tomatoes have “statistically higher levels (P < 0.05) of quercetin and kaempferol aglycones” than conventional tomatoes. The increase of these flavonoids corresponds “with reduced manure application rates once soils in the organic systems had reached equilibrium levels of organic matter.”
In fact, the study suggests that it is the nitrogen “in the organic and conventional systems that most strongly influence these differences.” The authors suggest that “overfertilization (conventional or organic) might reduce health benefits from tomatoes.” The argument is that the flavonoids are a protective response by the plants and one of the things they respond to is the amount of nitrogen in the soil.
In any case, the thrust of these and similar studies is that both organic and conventional crops can be manipulated to yield higher levels of antioxidants. At least one study has found “organic food products have a higher total antioxidant activity and bioactivity than the conventional foods.”* That study, however, involved only ten Italian men, aged 30-65 years.
I have to say that I am underwhelmed by the studies I have reviewed that claim to have found organic foods are more nourishing or healthy than conventional fruits and vegetables. At present, there is no strong body of scientific evidence that supports the contention that organic fruits and vegetables are superior to conventional produce.
A best case scenario for the organic folks would be that to achieve the recommended nutrients from five helpings a day of fruits or vegetables you might have to eat four or five more conventionally grown strawberries or two or three more baby carrots to get the same amount of vitamins, minerals, or antioxidants as provided by organic fruits and vegetables. But I’m not sure the evidence supports even that weak position.
History of the term “organic”
The term ‘organic’ as a descriptor for certain sustainable agriculture systems appears to have been used first by Lord Northbourn in his book Look to the Land (1940).
“Northbourn used the term to describe farming systems that focused on the farm as a dynamic, living, balanced, organic whole, or an organism.”* T
he term ‘organic’ was first widely used in the U.S. by J. I. Rodale, founder of Rodale Press, in the 1950s. “Rodale failed to convince scientists of the validity of his approach because of his reliance on what were perceived to be outrageous unscientific claims of organic farming’s benefits.”*
The USDA standards for organic food state:
Organic food is produced without using most conventional pesticides; fertilizers made with synthetic ingredients or sewage sludge; bioengineering; or ionizing radiation.
These standards capture the essence of the organic mythology:
Conventional pesticides should be avoided.
Synthetic fertilizers should be avoided.
Food should not be genetically altered.
Food should not be subjected to ionizing radiation.
The bit about sewage sludge is there because some organic farmers follow the “law of return” as proposed by Sir Albert Howard (1873-1947), a founder and pioneer of the organic movement. He advocated recycling all organic waste materials, including sewage sludge, in farmland compost. The practice of adding human and animal feces to the soil is an ancient practice found in many cultures even today.
The fact that these cultures developed their practices without benefit of modern knowledge of such things as bacteria or heavy metals is trumped by the romantic notion that farm life was idyllic in those times and places when life expectancy was half that of today.
Rudolf Steiner, the founder of a set of superstitious agricultural practices known as biodynamics, also advocated using manure as fertilizer but it had to be prepared according to a magical formula based on his belief that cosmic forces entered animals through their horns. Steiner also romanticized farming. Commenting on some peasants stirring up manure, he said:
“I have always had the opinion … that [the peasants’] alleged stupidity or foolishness is wisdom before God [sic], that is to say, before the Spirit. I have always considered what the peasants and farmers thought about their things far wiser than what the scientists were thinking.”*
Steiner gave lectures on farming, but did no scientific research to test his ideas.
A central concept of these lectures was to “individualize” the farm by bringing no or few outside materials onto the farm, but producing all needed materials such as manure and animal feed from within what he called the “farm organism.”
Other aspects of biodynamic farming inspired by Steiner’s lectures include timing activities such as planting in relation to the movement patterns of the moon and planets and applying “preparations,” which consist of natural materials which have been processed in specific ways, to soil, compost piles, and plants with the intention of engaging non-physical beings and elemental forces. Steiner, in his lectures, encouraged his listeners to verify his suggestions scientifically, as he had not yet done.*
Steiner opposed the use of synthetic fertilizers and pesticides, not on scientific grounds but on spiritual grounds. He claimed there were “spiritual shortcomings in the whole chemical approach to farming.”* He had a mystical idea of the farm as an organism, “a closed self-nourishing system.”*
KaiserScience 
