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
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The human papillomavirus (HPV) vaccine is given to prevent the risk of cancer associated with HPV and is typically administered between the ages of eight and 26. Opponents argue that not only is the vaccine risky, but it is of no value.
The HPV vaccine effects are said to last for only about five years.
In a Health Impact News Daily Post dated today, Dr. Mark Flannery states that, “The problem with this vaccine is this: Even though it’s estimated 60 percent of women have the HPV virus, only 1-2 percent of the total population gets cervical cancer, and most of those women get the cancer in their 50s. If the vaccine only works for five years, is administered up to age 26, and yet most cases of cervical cancer happen to women in their 50s, the benefits of the Gardasil vaccine are questionable given the severe consequences it can cause.”
In Dr. Flannery’s practice, he has worked with a number of people injured by the Gardasil vaccine for HPV and, according to SaneVax, Inc., as of 2013 more than 32,000 people have reported adverse affects to the Gardasil vaccine, more than 145 have died, over 1,000 are permanently disabled, and more than 6,400 have yet to recover. Dr. Flannery writes, “The evidence shows HPV rarely proceeds to cancer and that very few women with HPV develop cervical cancer, as other risk factors are involved.”
More than 30 to 40 types of HPV are typically transmitted through sexual contact and infect the anogenital region. Some sexually transmitted HPV types may cause genital warts. PositiveSingles, a trusted online dating site for people with HPV, Syphilis and other STDs in the Unted States, United Kingdom, Canada, Australia and Europe has information on the latest treatments for sexually transmitted infections as well as locations where someone with HPV or another STD can receive appropriate health care or find the support they need.
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Carbohydrate restricted diets are commonly practiced but seldom taught. As a result, doctors, dietitians, nutritionists, and nurses may have strong opinions about low carbohydrate dieting, but in many if not most cases, these views are not grounded in science.
“The Art and Science of Nutritional Ketosis” was presented by Stephen Phinney, MD, PhD, UC Davis at the University of California on November 16th, 2012. It will inspire you to think more carefully about sugars and starches in your diet, and empower you with essential knowledge to help you achieve long-lasting health and well-being.
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It might seem too good to be true, but dark chocolate is good for you and scientists now know why. Dark chocolate helps restore flexibility to arteries while also preventing white blood cells from sticking to the walls of blood vessels. Both arterial stiffness and white blood cell adhesion are known factors that play a significant role in atherosclerosis. What’s more, the scientists also found that increasing the flavanol content of dark chocolate did not change this effect. This discovery was published in the March 2014 issue of The FASEB Journal.
“We provide a more complete picture of the impact of chocolate consumption in vascular health and show that increasing flavanol content has no added beneficial effect on vascular health,” said Diederik Esser, Ph.D., a researcher involved in the work from the Top Institute Food and Nutrition and Wageningen University, Division of Human Nutrition in Wageningen, The Netherlands. “However, this increased flavanol content clearly affected taste and thereby the motivation to eat these chocolates. So the dark side of chocolate is a healthy one.”
To make this discovery, Esser and colleagues analyzed 44 middle-aged overweight men over two periods of four weeks as they consumed 70 grams of chocolate per day. Study participants received either specially produced dark chocolate with high flavanol content or chocolate that was regularly produced. Both chocolates had a similar cocoa mass content. Before and after both intervention periods, researchers performed a variety of measurements that are important indicators of vascular health. During the study, participants were advised to refrain from certain energy dense food products to prevent weight gain. Scientists also evaluated the sensory properties of the high flavanol chocolate and the regular chocolate and collected the motivation scores of the participants to eat these chocolates during the intervention.
“The effect that dark chocolate has on our bodies is encouraging not only because it allows us to indulge with less guilt, but also because it could lead the way to therapies that do the same thing as dark chocolate but with better and more consistent results,” said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal. “Until the ‘dark chocolate drug’ is developed, however, we’ll just have to make do with what nature has given us!”