“Our results clearly show that there is a link between infections of herpes simplex virus and the risk of developing Alzheimer’s disease. This also means that we have new opportunities to develop treatment forms to stop the disease,” says Hugo Lövheim, associate professor at the Department of Community Medicine and Rehabilitation, Geriatric Medicine, Umeå University, who is one of the researchers behind the study.
Alzheimer’s disease is the most common among the dementia diseases. In recent years research has increasingly indicated that there is a possible connection between infection with a common herpes virus, herpes simplex virus type 1, and Alzheimer’s disease. A majority of the population carries this virus. After the first infection the body carries the virus throughout your lifetime, and it can reactivate now and then and cause typical mouth ulcer. The hypothesis which links the herpes virus and Alzheimer’s disease is based on that a weakened immune system among the elderly creates opportunities for the virus to spread further to the brain. There this can in turn start the process which results in Alzheimer’s disease.
Hugo Lövheim and Fredrik Elgh, professor at the Department of Virology, have now confirmed this link in two large epidemiological studies. In one study, which is based on the Betula project, a study on aging, memory and dementia, the researchers show that a reactivated herpes infection doubled the risk of developing Alzheimer’s disease. This study had 3,432 participants who were followed for 11.3 years on average. In another study, samples donated to the Medical Biobank at Umeå University from 360 people with Alzheimer’s disease were examined and as many matched people who had not developed dementia. The samples were taken on average 9.6 years before diagnosis. This study showed an approximately doubled risk of developing Alzheimer’s disease if the person was a carrier of the herpes virus.
“Something which makes this hypothesis very interesting is that now herpes infection can in principle be treated with antiviral agents. Therefore within a few years we hope to be able to start studies in which we will also try treating patients to prevent the development of Alzheimer’s disease,” says Hugo Lövheim.
- Hugo Lövheim, Jonathan Gilthorpe, Anders Johansson, Sture Eriksson, Göran Hallmans, Fredrik Elgh. Herpes simplex infection and the risk of Alzheimer’s disease—A nested case-control study. Alzheimer’s & Dementia, 2014; DOI: 10.1016/j.jalz.2014.07.157
- Hugo Lövheim, Jonathan Gilthorpe, Rolf Adolfsson, Lars-Göran Nilsson, Fredrik Elgh. Reactivated herpes simplex infection increases the risk of Alzheimer’s disease. Alzheimer’s & Dementia, 2014; DOI: 10.1016/j.jalz.2014.04.522
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There is an 18 percent chance that a case of the Ebola virus will reach the United States by the end of September, according to a study published on Tuesday in PLOS Currents: Outbreaks.
Despite restrictions reducing travel in and out of the infected countries by 80 percent, the study, which analyzes global flight patterns, suggests that a case of Ebola in the United States is becoming increasingly harder to avoid. It also lists the chance of the virus reaching the United Kingdom as between 25 percent and 28 percent.
The analysis warns that if the current West African outbreak is not contained the likelihood of the virus reaching Europe and the United States will “increase consistently.”
The study lists just a 5 percent chance of Ebola occurring in the United States today, suggesting that the disease is far from contained to countries in West Africa. According to numbers obtained by the World Health Organization, there have been an estimated 3,685 cases and 1,841 deaths from the virus since the outbreak began.
Although two Americans — Dr. Kent Brantley and Nancy Writebol — have been treated for Ebola in the United States, both of them contracted the disease while working in Liberia. Doctors suggested that better medical care contributed to their eventual recovery.
A third infected American working in Liberia, Dr. Richard A. Sacra, is on his way to the United States for treatment.
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Dr. Taya Varteresian, a board certified psychiatrist working for the Veterans Administration, is the lead publisher in an article in the journal Current Psychiatry Reports titled: “Natural products and supplements for geriatric depression and cognitive disorders: an evaluation of the research.”
According to the abstract, more and more elderly people are starting to use “Complementary and Alternative Medicine (CAM) for late-life mood and cognitive disorders.” This obviously concerns psychiatrists, since their main remedies for “cognitive disorders” are powerful anti-psychotic drugs. They are not trained in natural supplements, therefore they apparently felt the need to educate other psychiatrists about the “side effects and indications for various natural products” so that psychiatrists could “protect their patients.”
Unfortunately, the patients probably need protection against the powerful arsenal of psychiatric drugs more than they do against harmless natural supplements and foods!
This is particularly true regarding anti-psychotic drugs prescribed to veterans, where the rate of suicide is far above the rate among the general population. More service members die by suicide than in combat, with 22 veterans killing themselves every single day. Obviously our pharma-based mental health system is not helping veterans, as suicide is a side effect of many anti-psychotic drugs.
So what are these dangerous supplements and “CAM products” that the field of psychiatry feels the need to warn fellow doctors about? According to the abstract they are: “omega-3 fatty acids, ginkgo biloba, SAMe, St John’s wort, B vitamins and vitamin D, huperzine, caprylidene, and coconut oil.” If these supplements are bringing about positive changes in the lives of elderly folks, it is not surprising that they are competing with Big Pharma drugs, which have a multitude of side effects, and little or no effect on cognitive diseases like Alzheimer’s. Unfortunately, Medicare and insurance companies will cover the toxic drugs, which the medical system admits kill over 100,000 people a year (not including suicides or other secondary deaths), but they will not cover natural products that have few or no side effects, but are often far more effective.
If this list is indicative of natural remedies that are effective and present competition to Big Pharma, it might be well worth the time to do your own research into each one rather than trust a doctor who has been trained by Big Pharma-funded psychiatrists to advise you on natural supplements and foods. The largest criminal convictions in modern times are against the pharmaceutical companies selling these powerful drugs through the pseudo-science of psychiatry, often through deception and “off label” prescriptions for conditions the drugs were never tested against. (See: Pharmaceutical companies now among largest corporate criminals in the world: no better than white-collar drug dealers.) Their list of “dangerous” natural products might be unwittingly tipping you off to the most successful natural products to combat mental disease.
We have often reported here at Health Impact News on the testimonials of families who have successfully incorporated coconut oil and a high-fat diet into the lives of seniors suffering from mental illness with great success. (See: New Alzheimer’s Drugs Continue to Fail Where Coconut Oil Shines)
Don’t be fooled by dire warnings made against natural products such as coconut oil by Big Pharma and Big Pharma-funded mainstream media. The scare tactics usually look like this:
1. There is no science to support health claims of natural products like coconut oil.
FALSE. There are plenty of scientific studies regarding coconut oil, the high-fat ketogenic diet, and natural supplements. It is true that rigorous and costly studies as are spent by drug companies to get their products FDA approved will seldom be funded or conducted on natural products. This is because they cannot be patented to obtain a return on such an investment as the lucrative FDA-approved products can provide. However, natural products also do not need such extensive research, since they are not toxic and they are not killing people like pharmaceutical products are. Coconut oil, for example, has been nourishing billions of people around the world for thousands of years.
2. Natural products like coconut oil are dangerous because they are not regulated or approved by the FDA.
FALSE. Just the opposite is true. Nobody is dying from toxic side effects of natural foods and supplements (because there are none), but over 100,000 people a year die from prescription drugs.
There is actually one claim made against natural supplements that is generally true: their interaction with prescription drugs is unknown and potentially dangerous. However, this is true because pharmaceutical drugs are inherently dangerous, even without interactions with other products.
Of course we would disagree with the medical community’s suggested solution regarding potential dangerous drug interactions, which would be to forgo natural treatments in favor of “approved” drugs. Instead, one might want to skip the “approved” drugs and try the natural products first.
But that would put a lot of people out of business, wouldn’t it? If people found natural products to be more effective for mental illness, they might never return to the toxic drugs. It is not likely that Big Pharma will allow that to happen.
Natural products and supplements for geriatric depression and cognitive disorders: an evaluation of the research. Curr Psychiatry Rep. 2014 Aug;16(8):456.
Source: Brian Shilhavy Health Impact News Editor
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Britain’s “obesity epidemic” is mainly caused by the fact that its population are lazy slobs and not because they eat too much, a shock new study called The Fat Lie has found.
The only reason the study – produced by Christopher Snowdon of the Institute of Economic Affairs (IEA) – is shocking is because it contradicts one of the great received ideas of our politically correct times: that fatties are the hapless victims of the rapacious and bullying food and drink industry which pressures them into eating and drinking far too much fat and sugar.
What Snowdon’s research clearly shows that this claim is nonsense. Yes, it is indeed true that British people are getting porkier. Since 2002 the average body weight of English adults has increased by two kilograms, contributing to Britain’s unenviable status as the fattest country in Europe.
But what is rarely mentioned by health campaigners is that this rise in obesity over three decades has coincided with a steady fall in average sugar and fat consumption.
Fat consumption has fallen from 111 grammes per day in 1974 to 81 grammes per day in 2012.
Sugar consumption has fallen by 16 percent since 1992.
Total calorie consumption has fallen from 2534 calories per person per day in 1974 to 1990 in 2012 – a decrease of 21.5 per cent.
Yet obesity has gone on rising. Why? Because, as Snowdon explains, obesity is a simple function of repeatedly eating more calories than you burn off. And people are taking much less physical exercise than they used to. Britons are walking less (from 255 miles per year in 1976 to 179 miles in 2010) and cycling less (from 51 miles per year in 1976 to 42 miles in 2010). At work, 63 per cent never climb stairs; while 40 per cent never walk. Outside work, 63 per cent report spending less than ten minutes a day walking, while 53 per cent claim to do no sports or exercise at all.
This is worth keeping in mind next time you read some shrill lobby group – such as Action on Sugar – demanding that the government does more to rein in the food and drink industry or pushes for a ban on supersize portions in fast food outlets or higher taxes on fizzy drinks.
The reason these lobbyists get away with such drivel is because they find a ready audience among the panic junkies at places like Mumsnet and in much of the mainstream media which thrives on public health scare stories.
And the reason they find a ready audience in government is because there are few things a minister on the make enjoys more than being seen to clamp down on some greedy industry or other.
With most departmental budgets being cut, ministers can no longer make a name for themselves by spending their way into public favour. But what they can do – because notionally it’s “cost-free”, though of course it’s not really – is introduce more regulations in the name of public health and safety. It has happened to the tobacco industry. Now it is happening to the food and drink industry.
This is why reports like Christopher Snowdon’s are so unusual and refreshing. They’re one of our few remaining toeholds on reality in a world which finds it more convenient to fall for the cultural Marxist lie that nobody is responsible for their own problems and that it’s the government’s job to sort them out.
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So far this Sunlight Series has discussed exactly what sunlight is, how it is produced, how it interacts with Earth’s atmosphere, what reaches the surface, and an initial look at what happens when it hits your skin. The last post focused on how UV-B radiation creates vitamin D in your skin, and how ample vitamin D levels are extremely important for optimal human health. Sunlight has other benefits too, such as nitric oxide production and the control of circadian rhythms. Clearly, for optimal health, human beings require sunlight, yet most health advice cautions against intense sunlight.
Almost everybody who is fair-skinned (or even darker skinned) has likely at some point in his or her life received a painful sunburn. It is understandable that many people believe sunlight is dangerous as extreme sunburns are indeed painful and can lead to skin cancers. Sunlight exposure can be a factor in the development of a skin cancer, but the process is misunderstood. There are three main types of skin cancer, with only one, melanoma, being a real threat to survival. Generally speaking, one can increase one’s resistance to being sunburned, and significantly lower any chance of developing a skin cancer, particularly melanoma, all the while reaping ample vitamin D levels and helping to prevent the development of all cancers. This will be discussed in a later post.
For this post, let’s take a look first at what a sunburn is, followed by the different types of skin cancer.
What is a Sunburn?
In a similar way that UV-B radiation is able to turn 7-dehydrocholesterol into vitamin D3 (as explained in the previous post), UV-B radiation is intense enough to cause changes in other molecules as well. UV-B radiation is able to break molecules apart in your skin cells, including DNA, which causes a cascade of reactions.
If enough skin cells are damaged, the body’s immune system will react with inflammation in the form of increased blood flow causing redness and swelling. Pain receptors at the site of damage will also be activated. The skin then needs to be repaired, and one way of doing that is replacing the skin, which the sunburned-individual will experience as peeling. Skin damage also leads to the formation of melanin, which causes the oft-desired tan colour. Individuals with naturally darker skin have naturally higher concentrations of melanin even without UV-B induced production. Melanin also acts as a photoprotectant (protects against sunlight), and when sufficiently concentrated, can disperse up to 99.9% of UV-B radiation. Once enough melanin is produced (either through genetics or UV-B exposure), sunburns, including damage to DNA, become very unlikely.
Conventional medicine believes that unrecognized errors in the DNA repair process are the cause of all cancers in general, and the errors resulting from UV radiation exposure are the cause of skin cancers. It is hypothesized that if DNA is not repaired properly, then mutant DNA can proliferate, which if left unchecked can result in tumours. The work of Dr. Seyfried makes an opposing case that it is damage to mitochondria, and not DNA that causes cancer. Either way, with regard to skin cancer, UV-radiation is almost always implicated as the cause. The below case argues that this is illogical.
There are three main types of skin cancer: basal cell carcinoma, squamous cell carcinoma, and melanoma. The entire category of skin cancers comprises the most common type of cancer in the US, with more than 3.5 million cases in over 2.0 million people being diagnosed annually. 80% of these 3.5 million cases are of the basal cell carcinoma variety, close to 20% are of the squamous cell carcinoma variety, and less than 1% of all skin cancer cases are life-threatening melanoma. It is estimated that all cancers (not just skin) will be responsible for 580,350 deaths in the US in 2013, of which 12,650 (2%) are the result of melanoma.
The post on ozone depletion vs. global dimming explained that despite anthropogenic emissions decreasing the concentration of UV-blocking ozone in the stratosphere, the overall amount of sunlight (and accompanying UV radiation) hitting Earth’s surface at has decreased due to global dimming. In addition, it is estimated by the EPA that Americans (and presumably citizens of other developed countries) spend a whopping 90% of their time indoors. From these combined effects, although there has been an overall decrease in average sun and UV exposure, melanoma rates in the UK more than quadrupled from 1975-2010, with similar dramatic increases in the US as well.
How can UV radiation be the cause of melanoma if UV exposure is decreasing while melanoma rates are skyrocketing? It is the aim of this author to prove that sunlight and UV radiation is not the sole cause of skin cancer and that it has a myriad of health benefits, and that exposure should be encouraged.
First, let’s take a look at the three types of skin cancer.
Basal Cell Carcinoma:
Basal cell carcinoma (BCC), by far the most common type of skin cancer, is rarely fatal (fatal in less than 0.1% of diagnosed cases) although it can be disfiguring if its growth is left unchecked. Basal cells are the inner layer of the epidermis. Current thought has BCC generally associated with chronic ultraviolet exposure with a list of other contributing factors such as inflammatory skin conditions and complications resulting from burns, scars, and infections. Fair-skinned caucasians are the most likely to develop BCC. It is more prevalent amongst older people with a history of intense sun exposure. Although most tumors grow on sun-exposed areas of the body, BCC tumors arise on non-exposed parts of the body (the nether regions…), indicating that UV exposure is not always a factor. A photo of a BCC tumour is shown below.
Squamous Cell Carcinoma:
Squamous cell carcinoma (SCC), the second most common type of skin cancer, is also rarely fatal (fatal in less than 0.5% of diagnosed cases), but can also be disfiguring in serious cases. Squamous cells are the outer layer of the epidermis. As with BCC, UV exposure gets most of the blame for causing SCC, and fair skinned individuals are most at risk. Most of these tumours are on sun-exposed parts of the body, but again, these do pop up in non-exposed areas as well, implying that UV exposure is not the only factor in tumour development. An image of a SCC tumour is below:
Melanoma is by far the least common skin cancer, but also by far the most deadly (death in 12.4% of cases). Melanoma is a cancer of the melanocytes, which are responsible for producing melanin (tan pigment). Once again, Caucasians are the most at risk. Treatment is usually surgical removal, and if the tumour returns, then chemo- and radiation-therapy is pursued. Although UV-radiation is generally implicated as the causative factor, one study found that up to 75% of melanoma tumours occur on relatively unexposed body sites. This observation has lead many researchers to hypothesize that when a certain area of the body is usually unexposed and is infrequently exposed to high doses of UV-radiation, that the skin is not “prepared” (ie: tanned) for the radiation assault and thus is more damaged which leads to skin cancer. However, there are exceptional cases where melanoma develops on areas that are almost never exposed to sunlight, including the male scrotum and urethra. The urethra is definitely one area where the sun don’t ever shine. A photo of a melanoma tumour is below.
Based on the information presented above, the following conclusions can be made:
- UV exposure can be a factor in the development of skin cancer, especially amongst caucasians, but skin cancer also develops in areas of the body that are not exposed to sunlight.
- The vast majority of skin cancer cases are not life threatening.
- Despite the average amount of UV-exposure decreasing in developed countries, rates of skin cancer, including melanoma, are skyrocketing. UV radiation cannot explain the massive increase in skin cancer rates.
There are strategies to increase your skin’s resistance to the damage incurred by sunlight exposure through dietary and exposure habits. These will be discussed in the next post, where these practices will be outlined with the intention of educating on how to reap all the disease preventing benefits of sunlight exposure, while minimizing damage. Sounds like a win-win, and it is indeed possible.
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- Male brains are more strongly affected by pollution than female brains
- Pollution exposure could cause memory and learning problems in people
- It causes ‘rampant’ inflammation throughout the brain
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Back home in New Jersey, I read through dozens of human and animal studies published over the past five years showing that nicotine—freed of its noxious host, tobacco, and delivered instead by chewing gum or transdermal patch—may prove to be a weirdly, improbably effective cognitive enhancer and treatment for relieving or preventing a variety of neurological disorders, including Parkinson’s, mild cognitive impairment, ADHD, Tourette’s, and schizophrenia. Plus it has long been associated with weight loss. With few known safety risks.
Nicotine? Yes, nicotine.
In fact—and this is where the irony gets mad deep—the one purpose for which nicotine patches have proven futile is the very same one for which they are approved by the Food and Drug Administration, sold by pharmacies over the counter, bought by consumers, and covered by many state Medicaid programs: quitting smoking. In January 2012, a six-year follow-up study of 787 adults who had recently quit smoking found that those who used nicotine replacement therapy in the form of a patch, gum, inhaler, or nasal spray had the same long-term relapse rate as those who did not use the products. Heavy smokers who tried to quit without the benefit of counseling were actually twice as likely to relapse if they used a nicotine replacement product.
“I understand that smoking is bad,” said Maryka Quik, director of the Neurodegenerative Diseases Program at SRI International, a nonprofit research institute based in California’s Silicon Valley. “My father died of lung cancer. I totally get it.”
Yet for years Quik has endured the skepticism and downright hostility of many of her fellow neuroscientists as she has published some three dozen studies revealing the actions of nicotine within the mammalian brain.
“The whole problem with nicotine is that it happens to be found in cigarettes,” she told me. “People can’t disassociate the two in their mind, nicotine and smoking. It’s not the general public that annoys me, it’s the scientists. When I tell them about the studies, they should say, ‘Wow.’ But they say, ‘Oh well, that might be true, but I don’t see the point.’ It’s not even ignorance. It’s their preconceived ideas and inflexibility.”
I met Quik at the annual meeting of the Society for Neuroscience held in Washington, D.C. Amid thousands of studies presented in a cavernous exhibition hall, the title of hers jumped out: “Nicotine Reduces L-dopa-Induced Dyskinesias by Acting at 2 Nicotinic Receptors.”
“A huge literature says that smoking protects against Parkinson’s,”she said. “It started as a chance observation, which is frequently the most interesting kind.”
The first hint of nicotine’s possible benefits, I learned, came from a study published in 1966 by Harold Kahn, an epidemiologist at the National Institutes of Health. Using health-insurance data on 293,658 veterans who had served in the U.S. military between 1917 and 1940, he found the kinds of associations between smoking and mortality that even by the mid-1960s had become well known. At any given age, cigarette smokers were eleven times more likely to have died of lung cancer as were nonsmokers and twelve times more likely to have died of emphysema. Cancers of the mouth, pharynx, esophagus, larynx—blah, blah, blah. But amid the lineup of usual suspects, one oddball jumped out: Parkinson’s disease. Strangely enough, death due to the neurodegenerative disorder, marked by loss of dopamine-producing neurons in the midbrain, occurred at least three times more often in nonsmokers than in smokers.
What was it about tobacco that ravages the heart, lungs, teeth, and skin but somehow guards against a disease of the brain? Over the course of the 1970s, neuroscientists like Quik learned that the nicotine molecule fits into receptors for the neurotransmitter acetylcholine like a key into a lock. By managing to slip through doors marked “Acetylcholine Only,” nicotine revealed a special family of acetylcholine receptors hitherto unknown.
And what a family. Nicotinic receptors turn out to have the extraordinary capacity to moderate other families of receptors, quieting or amplifying their functioning. According to psychopharmacologist Paul Newhouse, director of the Center for Cognitive Medicine at Vanderbilt University School of Medicine in Nashville, “Nicotinic receptors in the brain appear to work by regulating other receptor systems. If you’re sleepy, nicotine tends to make you more alert. If you’re anxious, it tends to calm you.”
The primary neurotransmitter that nicotine nudges is dopamine, which plays an important role in modulating attention, reward-seeking behaviors, drug addictions, and movement. And therein lies the answer to the mystery of why nicotine could prevent a movement disorder like Parkinson’s disease, due to its effects on dopamine.
To put the drug to the test, Quik treated rhesus monkeys with Parkinson’s with nicotine. After eight weeks, she reported in a landmark 2007 paper in the Annals of Neurology, the monkeys had half as many tremors and tics. Even more remarkably, in monkeys already receiving L-dopa, the standard drug for Parkinson’s, nicotine reduced their dyskinesias by an additional one-third. Studies of nicotine in humans with Parkinson’s are now under way, supported by the Michael J. Fox Foundation.
Other research suggests the drug may protect against the early stages of Alzheimer’s disease. A study involving sixty-seven people with mild cognitive impairment, in which memory is slightly impaired but decision-making and other cognitive abilities remain within normal levels, found “significant nicotine-associated improvements in attention, memory, and psychomotor speed,” with excellent safety and tolerability.
“What we saw was consistent with prior studies showing that nicotinic stimulation in the short run can improve memory, attention, and speed,” said Newhouse, who led the study.
As Newhouse sees it, “Obviously the results of small studies often aren’t replicated in larger studies, but at least nicotine certainly looks safe. And we’ve seen absolutely no withdrawal symptoms. There doesn’t seem to be any abuse liability whatsoever in taking nicotine by patch in nonsmokers. That’s reassuring.”
That’s not reassuring: it’s totally bizarre. Nicotine has routinely been described in news accounts as among the most addictive substances known. As the New York Times Magazine famously put it in 1987, “nicotine is as addictive as heroin, cocaine or amphetamines, and for most people more addictive than alcohol.”
But that’s just wrong. Tobacco may well be as addictive as heroin, crack, alcohol, and Cherry Garcia combined into one giant crazy sundae. But as laboratory scientists know, getting mice or other animals hooked on nicotine all by its lonesome is dauntingly difficult. As a 2007 paper in the journal Neuropharmacology put it, “Tobacco use has one of the highest rates of addiction of any abused drug. Paradoxically, in animal models, nicotine appears to be a weak reinforcer.”
That same study, like many others, found that other ingredients in tobacco smoke are necessary to amp up nicotine’s addictiveness. Those other chemical ingredients—things like acetaldehyde, anabasine, nornicotine, anatabine, cotinine, and myosmine—help to keep people hooked on tobacco. On its own, nicotine isn’t enough.
But what about nicotine as a cognitive enhancer for people without Alzheimer’s, Parkinson’s or any other brain disease?
“To my knowledge, nicotine is the most reliable cognitive enhancer that we currently have, bizarrely,” said Jennifer Rusted, professor of experimental psychology at Sussex University in Britain when we spoke. “The cognitive-enhancing effects of nicotine in a normal population are more robust than you get with any other agent. With Provigil, for instance, the evidence for cognitive benefits is nowhere near as strong as it is for nicotine.”
In the past six years, researchers from Spain, Germany, Switzerland, and Denmark—not to mention Paul Newhouse in Vermont—have published over a dozen studies showing that in animals and humans alike, nicotine administration temporarily improves visual attention and working memory. In Britain, Rusted has published a series of studies showing that nicotine increases something called prospective memory, the ability to remember and implement a prior intention. When your mother asks you to pick up a jar of pickles while you’re at the grocery store, she’s saddling you with a prospective memory challenge.
“We’ve demonstrated that you can get an effect from nicotine on prospective memory,” Rusted said. “It’s a small effect, maybe a 15 percent improvement. It’s not something that’s going to have a massive impact in a healthy young individual. But we think it’s doing it by allowing you to redeploy your attention more rapidly, switching from an ongoing task to the target. It’s a matter of cognitive control, shutting out irrelevant stimuli and improving your attention on what’s relevant.”
Of course, all the physicians and neuroscientists I interviewed were unanimous in discouraging people from using a nicotine patch for anything other than its FDA-approved purpose, as an aid to quit smoking, until large studies involving hundreds of people establish the true range of benefits and risks (even though studies find it doesn’t work for that purpose). But with so many studies showing that it’s safe, and so many suggesting it might well be the most effective cognitive enhancer now on the market, I decided to ignore not only their advice but the advice of my personal physician.
I added a nicotine patch to my list [of things to try to become smarter.]
Source: Scientific American