The dairy industry has finally been given one big swift kick where they need it most, in the scientific credibility department where top officials have been falsely linking dairy and bone strength for decades. The study, published by the British Medical Journal, found that people don’t get stronger bones by eating dairy products or taking calcium supplements.
What interesting about cow’s milk is that the more people drink, the more likely they are to die or experience a bone fracture and other diseases. The risks are especially pronounced for women.
Taking into account studies from around the world, the systematic review and meta-analysis found that those who took calcium were just as likely to suffer from fractures as those who did not.
Dr Ian Reid from the University of Auckland in New Zealand stated that the focus on treating bone diseases, such as osteoporosis, needs to be elsewhere.
“I think we’ve actually misdirected a whole lot of effort into the use of calcium supplements, in particular in North America, where use has been higher for last 30 years,” he said.
The dairy industy has been hard at work the last 50 years convincing people that pasteurized dairy products such as milk or cheese increases bioavailable calcium levels. This is totally false. The pasteurization process only creates calcium carbonate, which has absolutely no way of entering the cells without a chelating agent. So what the body does is pull the calcium from the bones and other tissues in order to buffer the calcium carbonate in the blood. This process actually causes osteoporosis.
Pasteurized dairy contains too little magnesium needed at the proper ratio to absorb the calcium. Most would agree that a minimum amount of Cal. to Mag Ratio is 2 to 1 and preferably 1 to 1. So milk, at a Cal/Mag ratio of 10 to 1, has a problem. You may put 1200 mg of dairy calcium in your mouth, but you will be lucky to actually absorb a third of it into your system.
Over 99% of the body’s calcium is in the skeleton, where it provides mechanical rigidity. Pasteurized dairy forces a calcium intake lower than normal and the skeleton is used as a reserve to meet needs. Long-term use of skeletal calcium to meet these needs leads to osteoporosis.
Dairy is pushed on Americans from birth yet they have one of the highes risk of osteoporosis in the world. Actually, people from the USA, Canada, Norway, Sweden, Australia, and New Zealand have the highest rates of osteoporosis.
The research investigated putative mechanism by which calcium intake affects bone health namely by increasing bone mineral density (BMD). BMD is a surrogate endpoint for fracture risk that allows biological effects to be explored in randomised controlled trials of modest size.
Following old information
The results from the new study flies in the face of long-held beliefs that calcium makes for stronger, better bones.
For years, US guidelines have advised men and women to take anywhere from 1,000 to 1,200 mg of calcium per day to help prevent fractures and improve bone density.
Reid said this likely lasted for so long due to an overreliance on studies from the 1970s and 1980s.
Now, there are more sophisticated bone density studies, and none have shown the need for anything more than 500mg of calcium per day for bone density health.
Going a step further, the study said too much calcium may cause build ups in the arteries or in the kidneys, which can cause ailments such as heart disease or kidney stones respectively.
“Dietary calcium intake is not associated with risk of fracture, and there is no clinical trial evidence that increasing calcium intake from dietary sources prevents fractures,” the study said.
“Evidence that calcium supplements prevent fractures is weak and inconsistent.”
Methodology of the study
The researchers looked at two studies, finding in one that increasing calcium intake from supplements increases bone density by 1% to 2%, something they said is unlikely to create a meaningful reduction in the risk of fracture.
“This is not a cumulative benefit,” Reid said. “It’s only 1% at any year. It’s a one off small gain. When you look at the fracture data in the large high quality studies carried out in the last 10 to 15 years, we found there is no total benefit to total number of fractures. There may even be an increase. I think we should really be deleting calcium as a significant tissue in management of osteoporosis.”
In another study, researchers found that dietary calcium is not associated with risk of fracture, with no clinical evidence finding that increase in consumption helps prevent fractures.
Professor Karl Michaelsson from Uppsala University in Sweden wrote in an accompanying commentary with the study that the although recommendations point to those over 50 taking calcium, most will not benefit by increasing their intakes.
“The weight of evidence against such mass medication of older people is now compelling, and it is surely time to reconsider these controversial recommendations,” he wrote.
Supplement Quality Key
While some dairy may be useful to help the elderly keep weight on their body as they get older, many low-quality calcium supplements appear to be ineffective for bone health.
Most supplements on the supplement market today contain calcium carbonate which is an inferior form of calcium and manufacturers attach a simple chelating agent like citric acid to make it more absorbable, however the end product is inferior to other calcium supplements such as calcium orotate, which is the only known form of calcium which can effectively penetrate the membranes of cells.
Many of these supplements are increasing the risk of kidney stones and abdominal problems and whose risks are greater than the benefits.
“They’ve been so entrenched and supported by industry for so long that it’s taking a while to turn around,” Reid said.
If you want to supplement for calcium intake you must seek a reputable and balanced calcium/magnesium formula. Researchers examined 21 formulations of calcium carbonate (both natural [i.e., oyster shell] and refined). Four out of seven natural products and four out of 14 refined products, including brand products, had measurable lead content. A research team in California found essentially the same contamination in calcium supplements.
Acid rebound. Calcium carbonate may cause acid rebound: the stomach overcompensates for the high dose of calcium carbonate, which is alkaline, by churning out more acid. For that reason, people with a history of stomach ulcers are advised that they may not tolerate it and may have to switch to calcium citrate.
Constipation. Calcium supplements can have a mild binding effect but by themselves don’t usually cause serious constipation. But if you’re taking another supplement or medication that binds the stool, the addition of calcium supplements could cause a problem.
Too much calcium. Although it doesn’t happen often, some people have taken so much calcium that it causes hypercalcemia, an above-normal level of calcium in the blood since most of the calcium carbonate is not absorbed. Hypercalcemia may cause nausea, vomiting, confusion, and other neurological symptoms.
The type of minerals in the formula determines the absorption levels: Opti-Cal/Mag with Vitamin K2 is a co-enzyme complex, heat-stabled molecules that must be associated with another enzyme for them to perform their function in the body. It is necessary in the utilization of vitamins and minerals for proper delivery to the cell nucleus. One study found that Opti-Cal/Mag complex is 8.79 times more absorbed into the blood than calcium carbonate and 2.97 times more than calcium gluconate.
6 WAYS TO BUILD STRONG BONES
1. Eat calcium rich foods
Eat foods high in calcium. The best food sources are non-pasteurized raw dairy sources such as raw milk/yogurt, as well as bony fish, such as sardines. Leafy green veg such as kale, broccoli and spinach are also rich in calcium. Dried herbs and dried fruits such as figs and currants are also good choices. Seeds such as sesame, chia and flax are also rich sources of calcium. Also, enjoy foods that contain sulfur such as garlic and onions.
2. Food selections/combinations are critical
Try not to eat whole grains and calcium-rich foods at the same time. Whole grains contain a substance that binds with calcium and prevents proper absorption. Some foods that contain compounds such as oxalic or phytic acids, such as sweet potatoes, beans, rhubarb, celery and beets, can also decrease the amount of calcium that’s absorbed when eaten at the same time as calcium-rich foods.
3. Avoid the causes of mineral excretion
Pass on phosphate-containing foods such as soft drinks. Phosphorus causes the body to excrete calcium. Limit or avoid high-protein animal foods. A diet high in protein causes calcium to be excreted from your body. Decrease caffeine consumption. People who smoke have significantly lower bone density, while drinking alcohol can also prevent your bones from absorbing the maximum nutrients from your food.
4. Get more Sunlight and Vitamin D
Vitamin D helps the body absorb calcium. Although some is found in oily fish, our main source comes from the effect of sunlight on your skin. It’s estimated that half of us have a deficiency because we don’t get outside enough or because we always use sunblock. It is especially important to maximize sun exposure between May and September to keep vitamin D levels topped up. Just 10 minutes of sunlight a day on bare arms and your face can cut your risk of bone fractures by a third. A half hour exposing your torso is equivalent to roughly 10,000 units of Vitamin D.
5. The right exercise
Another vital way to boost your bones is weight-bearing exercise –basically anything that has you upright and using your body weight. Good choices include squatting, rope skipping, aerobics, plyometrics, dancing or brisk walking. “Research shows that if you don’t exercise you end up weeing out all the calcium you take in instead of storing it in your bones,” warns Professor Dawn Skelton, an aging and health specialist at Glasgow Caledonian University. “Ideally we should aim for 150 minutes of moderate activity per week. “Put simply, the more hours we spend on our feet, the fewer bone breakages we should have in later life.”
6. Avoid Medications and Medical Therapies
Acid-blocking medications used for heartburn and other gastrointestinal conditions can block the absorption of calcium through the stomach walls. Stomach acids break down food during the digestive process, allowing the nutrients to become absorbed into your body. Medications designed to stop acid production or decrease the amount of acids present in your stomach can have a negative effect on calcium.
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“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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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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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 interplay of hormones in the body is crucial in enabling physical intercourse.
ONE of the things that I like to tell my patients is that the brain is the most powerful sex organ of all.
Women – and their partners who come to the clinic with them – are always taken aback by this statement.
Many of them know, of course, that hormones can affect their sexual desires, as well as many of the emotions and sensations related to sex. But few people realise just how central hormones are to every aspect of sexual desire, arousal, intercourse and recovery – never mind the penis or the vagina, it is the hormones that are doing all the work.
And the brain? Well, that’s because the brain is one of the main hormone control centres in the body. Therefore, without the brain, there would be no sex at all!
Let us take a look at how each hormone plays a role in every phase of a woman’s sex life.
Hormones that control desire
Everything to do with sex begins with desire. You start off by being physically attracted to your partner, which is a form of chemical reaction triggered by hormones like catecholamines, dopamine and noradrenaline, as well as some neurotransmitters, which sometimes behave like hormones.
Sexual desire gradually increases with the help of hormones like DHEA (dehydroepiandrosterone) and testosterone (yes, even women have testosterone, as we have previously covered in this column).
Your brain also produces a type of neurotransmitter called serotonin, which activates various areas of the brain to provoke erections of the nipples, clitoris, and penis.
During the foreplay stage of sex, your body also produces specific hormones to arouse sexual desire in your partner. These hormones are called “pheromones”, and they are secreted from the sweat glands in your armpits and your pubic area.
Pheromones produce a subtle sexual fragrance that your partner inhales, and they send a signal to his brain that you are sexually aroused.
When you are aroused, your body produces oestrogens, which stimulates certain neurons in the brain and prompts the release of more pheromones.
You may be wondering why some hormones affect the release of others. Our hormones work in a feedback system, so they are continuously sending signals to one another that say “Produce more!” or “Stop producing!” Again, this happens with two hormones produced in the pituitary gland, LH (luteinising hormone) and FSH (follicle-stimulating hormone), which stimulate the production of more sex hormones like oestrogen and testosterone to further increase desire.
After foreplay, comes…
At this point, the hormones continue on this loop, as physical contact increases. More pheromones are triggered by DHEA and oestrogens, are secreted through the skin and saliva, and further enhance pleasure.
During this stage, several hormones play a role in helping to maintain energy and endurance to prolong intercourse. Cortisol is a hormone that keeps the energy and excitement up, by maintaining a man’s erection for a longer time, and providing energy to the muscles, including the heart, for endurance.
Growth hormones also help to maintain a firmer and more prolonged erection of the penis and clitoris, so that intercourse can last longer.
Other hormones that come into play are vasopressin, which also helps to make the penis and clitoris more erect.
At the peak
As the excitement reaches its climax, the nerves and adrenal glands produce a hormone called noradrenaline, which allows the body to react quickly to unexpected stimulation. Then, the body releases adrenaline, which triggers orgasm and ejaculation.
In a woman, the uterus and vagina muscles contract due to the hormone oxytocin. This same hormone also appears when a woman is breastfeeding, as it is responsible for signaling the milk glands to release milk when the baby suckles. This may explain why breastfeeding produces a pleasant feeling, similar to the after-effects of an orgasm.
In some novels and movies, the female character always complains that her partner falls asleep after sex. Well, women may be relieved to know that there is a perfectly good hormonal reason for this.
After orgasm, the hormone progesterone is released to subdue the levels of desire. This leads to a state of serenity, relaxation, drowsiness and passivity. In fact, as women produce much more progesterone compared to men, this effect is strong in women.
Another hormone with a similar effect is prolactin, which is also produced in greater amounts in women (just like oxytocin, prolactin also plays a role in milk production for breastfeeding mothers, so nursing mums may find their breasts leaking a bit of milk during and after sexual intercourse).
Endorphins, a type of neurotransmitter, will be released to make you feel drowsy, but good. The hormone melatonin is also produced, which causes deep sleep after sex.
Some people feel a little down after they have recovered from the orgasm phase – this may be due to a dramatic drop in all the neurotransmitters and hormones that were involved in intercourse, causing a sudden sadness.
Nutrition for better sex
What does food have to do with sex? Plenty, because certain nutrients in food have a direct effect on hormone levels in the body, and can therefore improve your sex life!
Protein and certain fats (the healthful types) increase the level of sex hormones in the body, which improves libido and erections.
Some people believe that spicy and salty foods act as aphrodisiacs, and there is some truth to this, as they enhance the effects of testosterone, DHEA and cortisol.
Animal protein, which are highest in animal meats, increases adrenal hormones, such as cortisol, oestrogen, progesterone and adrenalin.
As we have already seen above, these hormones all play crucial roles in maintaining sexual desire, excitement and function throughout intercourse.
Fruits are sexy too! They increase the level of the thyroid hormones in your body, which are believed to improve your vivacity, intelligence and reaction rate.
Now you have a better understanding of how hormones work in their subtle ways to affect sexual desire, arousal and pleasure.
If you experience problems with any aspect of your sexual relationship, the cause may lie in your hormones. Talk to your doctor to find out more.
> Datuk Dr Nor Ashikin Mokhtar is a consultant obstetrician & gynaecologist (FRCOG, UK). For further information, visit www.primanora.com. The information provided is for educational and communication purposes only and it should not be construed as personal medical advice. Information published in this article is not intended to replace, supplant or augment a consultation with a health professional regarding the reader’s own medical care. The Star does not give any warranty on accuracy, completeness, functionality, usefulness or other assurances as to the content appearing in this column. The Star disclaims all responsibility for any losses, damage to property or personal injury suffered directly or indirectly from reliance on such information.
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Drugs that combat aging may be available within five years, following landmark work led by an Australian researcher.
The work, published in the March 8 issue of Science, finally proves that a single anti-ageing enzyme in the body can be targeted, with the potential to prevent age-related diseases and extend lifespans.
The paper shows all of the 117 drugs tested work on the single enzyme through a common mechanism. This means that a whole new class of anti-ageing drugs is now viable, which could ultimately prevent cancer, Alzheimer’s disease and type 2 diabetes.
“Ultimately, these drugs would treat one disease, but unlike drugs of today, they would prevent 20 others,” says the lead author of the paper, Professor David Sinclair, from UNSW Medicine, who is based at Harvard University. “In effect, they would slow aging.”
The target enzyme, SIRT1, is switched on naturally by calorie restriction and exercise, but it can also be enhanced through activators. The most common naturally-occurring activator is resveratrol, which is found in small quantities in red wine, but synthetic activators with much stronger activity are already being developed.
Although research surrounding resveratrol has been going for a decade, until now the basic science had been contested. Despite this, there have already been promising results in some trials with implications for cancer, cardiovascular disease and cardiac failure, type 2 diabetes, Alzheimer’s and Parkinson’s diseases, fatty liver disease, cataracts, osteoporosis, muscle wasting, sleep disorders and inflammatory diseases such as psoriasis, arthritis and colitis (inflammatory bowel disease).
“In the history of pharmaceuticals, there has never been a drug that tweaks an enzyme to make it run faster,” says Professor Sinclair, a geneticist with the Department of Pharmacology at UNSW.
The technology was sold to pharmaceutical giant GlaxoSmithKline in 2008[i]. Four thousand synthetic activators, which are 100 times as potent as a single glass of red wine, have been developed – the best three are in human trials.
“Our drugs can mimic the benefits of diet and exercise, but there is no impact on weight,” says Professor Sinclair, who suggests the first therapeutic to be marketed will be for diabetes.
There have been limited trials in people with type 2 diabetes and the skin inflammatory disease, psoriasis. There were benefits to the metabolism in the first group and a reduction in skin redness in the second.
The drugs can be administered orally, or topically. So far, there have been no drugs developed targeting ageing skin, but one major skin care range has developed a crème with resveratrol in it.
While any drug would be strictly prescribed for certain conditions, Professor Sinclair suggests that one day, they could be taken orally as a preventative. This would be in much the same way as statin drugs are commonly prescribed to prevent, instead of simply treating, cardiovascular disease.
In animal models, overweight mice given synthetic resveratrol were able to run twice as far as slim mice and they lived 15 per cent longer.
“Now we are looking at whether there are benefits for those who are already healthy. Things there are also looking promising,” says Professor Sinclair, who also heads the Lowy Cancer Research Centre’s Laboratory for Ageing Research at UNSW.
“We’re finding that aging isn’t the irreversible affliction that we thought it was,” he says. “Some of us could live to 150, but we won’t get there without more research.”
Media contact: Susi Hamilton, UNSW Media Office, +61 422 934 024, firstname.lastname@example.org
[i] Professor Sinclair formed a started up company Sirtris to develop the anti-ageing technology. This was subsequently sold to GlaxoSmithKline (GSK). Professor Sinclair is now a scientific advisor to GSK. Several other authors on the paper work for GSK or an affiliated company.
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It seems so intuitive: People with diabetes should inject insulin. In the case of people with type 1 diabetes, in which the pancreas doesn’t produce insulin, that’s probably true. However, modern doctors routinely give insulin to people with type 2 diabetes simply because it reduces blood sugar levels.
The reality, though, is that type 2 diabetics who take insulin injections die at more than double the rate of those given non-insulin treatment!
The study, Mortality and Other Important Diabetes-Related Outcomes With Insulin vs Other Antihyperglycemic Therapies in Type 2 Diabetes, investigated 84,622 primary care patients with type 2 diabetes from 2000 to 2010 and compared the results of these treatments:
- Metformin monotherapy
- Sulfonylurea monotherapy
- Insulin monotherapy
- Metformin plus Sulfonylurea combination therapy
- Insulin plus Metformin combination therapy
These groups were compared for risks of certain severe adverse events: cardiac, cancer, and mortality. A primary outcome was defined as any one of these events occurring, but each such event was counted only once and only if it was the first adverse result. Any one of these events happening at any time, plus microvascular complications, counted as a secondary outcome. The results were dramatic.
Those on Metformin therapy had the lowest death rates, so that group was used as the reference.
In terms of primary outcome – that is, consideration of first adverse events only:
- Sulfonylurea therapy resulted in patients being 1.4 times more likely to suffer one of these outcomes.
- A combination of Metformin and Insulin resulted in 1.3 times greater risk.
- Insulin therapy alone resulted in 1.8 times greater risk.
- Those considered to be at greater risk because of glycosylated hemoglobin had as much as 2.2 times greater risk with Insulin therapy alone.
When considering any of these events happening, whether they were the first event or a subsequent one, the results were even more dramatic:
- Insulin monotherapy resulted in:
- 2.0 times more myocardial infarctions.
- 1.7 time more major adverse cardiac events
- 1.4 time more strokes
- 3.5 times more renal complications
- 2.1 time more neuropathy
- 1.2 times more eye complications
- 1.4 times more cancer
- 2.2 times more deaths
Modern medicine’s hubris allows it to make claims that simply are not supported. Based on those unsupported claims, thousands—and in the case of diabetes, millions—of people are placed on drugs and regimens that have never been demonstrated to have any beneficial effect. The result is that the general public becomes a mass of guinea pigs for medical experimentation—experimentation that isn’t even documented and analyzed!
The use of insulin in type 2 diabetics is only one example, but it’s been clearly demonstrated again and again with disasters like Vioxx.
Redirection to Markers
The method by which these treatments are justified is a little redirection away from what really counts. What matters is whether lives are improved and lengthened. But drugs are rarely tested on that basis. The excuse generally given is that it would take too long. But if that were a valid explanation, then surely we’d see the regulating agencies keeping careful and formal oversight over the experiences of all new drugs for the first few years of use. That, though, simply doesn’t happen.
Instead of looking at the outcomes that matter, substitutes are used. They’re called markers, which are intermediate results that are assumed to be indicative of benefit. In the case of insulin, the marker is blood sugar level. Insulin is required to transport glucose (blood sugar) into cells so that they can produce energy. Thus, insulin reduces blood sugar levels. If artificial pharmaceutical insulin brings blood sugar to more “normal” levels, then the treatment is considered successful.
As this study has demonstrated, markers are simply not a valid way to determine effectiveness of a treatment. In type 2 diabetes, the problem isn’t a lack of ability to produce insulin; neither is it high blood glucose. The problem is the cells’ ability to utilize insulin to transport glucose from blood into cells.
The problem is that cells’ ability to use insulin has deteriorated. So, how can it be beneficial to give more insulin when cells are unable to utilize what’s already there? Clearly, that’s counterproductive.
Yet, that’s precisely what doctors do! They give insulin to replace insulin, when a lack of insulin isn’t the problem! It should come as no surprise that the real concerns of anyone being treated for diabetes are not answered by insulin treatment.
As this study has demonstrated, forcing insulin into the body actually results in worse outcomes. How many decades has this treatment been in vogue? All that time it’s been justified because it reduces blood sugar. But the effects that count—quality of life and longevity—haven’t been considered.
There’s one lesson to be learned here: Health isn’t found in pharmaceutical drugs, not even old tried-and-true drugs.
- Mortality and Other Important Diabetes-Related Outcomes With Insulin vs Other Antihyperglycemic Therapies in Type 2 Diabetes, Journal of Clinical Endocrinology & Metabolism, Craig J. Currie, Chris D. Poole, Marc Evans, John R. Peters and Christopher Ll. Morgan; doi:10.1210/jc.2012-3042
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Sunlight is well-known to provide us vitamin D, but did you know that it kills pain, keeps us alert at night, burns fat and more…
Our biological connection and dependence to the sun is so profound, that the very variation in human skin color from African, melanin-saturated dark skin, to the relatively melanin de-pigmented, Caucasian lighter-skin, is a byproduct of the offspring of our last common ancestor from Africa (as determined by mitochondrial DNA) migrating towards sunlight-impoverished higher latitudes, which began approximately 60,000 years ago. In order to compensate for the lower availability of sunlight, the body rapidly adjusted, essentially requiring the removal of the natural “sunscreen” melanin from the skin, which interferes with vitamin D production; vitamin D, of course, is involved in the regulation of over 2,000 genes, and therefore is more like a hormone, without which our entire genetic infrastructure becomes destabilized.
While the health benefits of vitamin D are well-documented (GreenMedInfo.com has identified over 200 health conditions that may benefit from optimizing vitamin D levels: Vitamin D Health Benefits page, and Henry Lahore’s Vitamin D Wiki has far more), the therapeutic properties of sunlight are only now being explored in greater depth by the research community.
Below are detailed five noteworthy properties of sunlight exposure:
1) Sunlight Has Pain-Killing (Analgesic) Properties: A 2005 study published in the journal Psychosomatic Medicine titled, “The effect of sunlight on postoperative analgesic medication use: a prospective study of patients undergoing spinal surgery,” analyzed patients staying on the bright side of the hospital unit who were exposed to 46% higher-intensity sunlight on average. The patients exposed to an increased intensity of sunlight experienced less perceived stress, marginally less, took 22% less analgesic medication per hour, and had 21% less pain medication costs. [i]
2) Sunlight Burns Fat: A 2011 study published in The Journal of Investigative Dermatology revealed a remarkable fact of metabolism: The exposure of human skin to UV light results in increased subcutaneous fat metabolism. While subcutaneous fat, unlike visceral fat, is not considered a risk factor for cardiovascular disease, it is known that a deficiency of one of sunlight’s best known beneficial byproducts, vitamin D, is associated with greater visceral fat.[ii] Also, there is a solid body of research showing that vitamin D deficiency is linked to obesity, with 9 such studies on our obesity research page.
One of them, titled “Association of plasma vitamin D levels with adiposity in Hispanic and African Americans,” and which was published in the journal Anticancer Research in 2005, found that vitamin D levels were inversely associated with adiposity in Hispanics and African-Americans, including abdominal obesity.[iii] The point? Exposure to UVB radiation, which is most abundant two hours on either side of solar noon and responsible for producing vitamin D, may be an essential strategy in burning fat, the natural way.
3) Sunlight via Solar Cycles May Directly Regulate Human Lifespan: Published in 2010 in the journal Medical Hypotheses and titled, “The effect of solar cycles on human lifespan in the 50 United states: variation in light affects the human genome,” researchers review the possibility that solar cycles directly affect the human genome. According to the researchers:
In the current study we report that those persons conceived and likely born during the peaks (MAX approximately 3 years) of approximately 11-year solar cycles lived an average 1.7 years less than those conceived and likely born during non-peaks (MIN approximately 8 years). Increased energy at solar MAX, albeit relatively a small 0.1% increase from MIN, apparently modifies the human genome/epigenome and engenders changes that predispose to various diseases, thereby shortening lifespan. It is likely that same energy increases beneficial variety in the genome which may enhance adaptability in a changing environment.
Sunlight exposure, therefore, may directly affect the length of our life, and may even accelerate genetic changes that may confer a survival advantage.[iv]
4) Daytime Sunlight Exposure Improves Evening Alertness: A 2012 study published in the journal Behavioral Neuroscience titled, “Effects of prior light exposure on early evening performance, subjective sleepiness, and hormonal secretion,” found that subjects felt significantly more alert at the beginning of the evening after being exposed to 6 hours of mainly daylight exposure, whereas they became sleepier at the end of the evening after artificial light exposure.[v]
5) Sunlight May Convert To Metabolic Energy: If a novel hypothesis published in 2008 in the Journal of Alternative and Complementary Medicine is correct,[vi] a longstanding assumption that animals are incapable of utilizing light energy directly is now called into question. In other words, our skin may contain the equivalent of melanin “solar-panels,” and it may be possible to “ingest” energy, as plants do, directly from the Sun.
Melanin has a diverse set of roles in various organisms. From the ink of the octopus, to the melanin-based protective colorings of bacteria and fungi, melanin offers protection against a variety of threats: from predators and similar biochemical threats (host defenses against invading organisms), UV light, and other chemical stresses (i.e. heavy metals and oxidizing agents). Commonly overlooked, however, is melanin’s ability to convert gamma and ultraviolet radiation into metabolic energy within living systems.
Single-celled fungi, for instance, have been observed thriving within the collapsed nuclear reactor at Chernobyl, Ukraine, using gamma radiation as a source of energy. Albino fungi, without melanin, were studied to be incapable of using gamma radiation in this way, proving that gamma rays initiate a yet-unknown process of energy production within exposed melanin.
Vertebrate animals may also convert light directly into metabolic energy through the help of melanin. In a review titled, “Melanin directly converts light for vertebrate metabolic use: heuristic thoughts on birds, Icarus and dark human skin,” Geoffrey Goodman and Dani Bercovich offer a thought-provoking reflection on the topic, the abstract of which is well worth reading in its entirety:
Pigments serve many visually obvious animal functions (e.g. hair, skin, eyes, feathers, scales). One is ‘melanin’, unusual in an absorption across the UV-visual spectrum which is controversial. Any polymer or macro-structure of melanin monomers is ‘melanin’. Its roles derive from complex structural and physical-chemical properties e.g. semiconductor, stable radical, conductor, free radical scavenger, charge-transfer.
Clinicians and researchers are well acquainted with melanin in skin and ocular pathologies and now increasingly are with internal, melanized, pathology-associated sites not obviously subject to light radiation (e.g. brain, cochlea). At both types of sites some findings puzzle: positive and negative neuromelanin effects in Parkinsons; unexpected melanocyte action in the cochlea, in deafness; melanin reduces DNA damage, but can promote melanoma; in melanotic cells, mitochondrial number was 83% less, respiration down 30%, but development similar to normal amelanotic cells.
A little known, avian anatomical conundrum may help resolve melanin paradoxes. One of many unique adaptations to flight, the pecten, strange intra-ocular organ with unresolved function(s), is much enlarged and heavily melanized in birds fighting gravity, hypoxia, thirst and hunger during long-distance, frequently sub-zero, non-stop migration. The pecten may help cope with energy and nutrient needs under extreme conditions, by a marginal but critical, melanin-initiated conversion of light to metabolic energy, coupled to local metabolite recycling.
Similarly in Central Africa, reduction in body hair and melanin increase may also have lead to ‘photomelanometabolism’ which, though small scale/ unit body area, in total may have enabled a sharply increased development of the energy-hungry cortex and enhanced human survival generally. Animal inability to utilize light energy directly has been traditionally assumed. Melanin and the pecten may have unexpected lessons also for human physiology and medicine.
- [i] Jeffrey M Walch, Bruce S Rabin, Richard Day, Jessica N Williams, Krissy Choi, James D Kang. The effect of sunlight on postoperative analgesic medication use: a prospective study of patients undergoing spinal surgery. Psychosom Med. 2005 Jan-Feb;67(1):156-63. PMID: 15673638
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Metazene – Niacinamide Gel
Acne vulgaris — or common acne — isn’t just a cosmetic issue: it’s a serious medical problem often leading to permanent skin damage and scarring, and emotional distress with a lifelong psychological impact. Contrary to popular belief attributing it to hygiene, stress, or diet, acne is actually caused by a bacterium, Propionibacterium acnes, feeding on skin oils. When the body dispatches immune cells to deal with the infection the result is irritation, swelling, and, sometimes, nodules or cysts. While acne primarily affects teenagers — and virtually all of them report having acne at some point — it plagues many adults well into their thirties or even forties!
Whether it be short- or long-term, acne can lead to substantial, permanent skin damage with few viable treatment options beyond cosmetic surgery — including dermabrasion, collagen injections, and grafts. As many as forty percent of acne sufferers seek medical treatment at least once. Traditional treatments include benzoyl peroxide creams, oral antibiotics (clindamycin, erythromycin, and tetracycline), and isotretinoin or retinoic-acid products (Accutane™, Roaccutane ™, and Retin-A™).
Benzoyl peroxide is hard on the skin and can cause irritation. Oral antibiotics are troublesome because of bacterial resistance, digestive upset, discolored teeth or skin, sun sensitivity, and interference with other medications. Isotretinoin compounds cause severe health problems, ranging from skin disorders, sun sensitivity, and nausea to vision irregularities, serious birth defects, depression, and even suicide. Side effects and poor results cause many acne sufferers to abandon traditional approaches. There is, however, a safe and effective alternative treatment: Lifelink’s Metazene, a Vitamin B-3 derivative.
Vitamin B-3, or niacinamide, is a potent topical anti-inflammatory. In clinical trials for acne, niacinamide gels proved superior to antibiotics without their side effects, which is why they are used worldwide. When a niacinamide gel is prescribed by a physician in the United States, however, federal law requires that it be made only by a specialized compounding pharmacy, often at considerable expense. Lifelink’s Metazene is the only niacinamide gel available in the United States that is made to pharmaceutical standards and sold over the counter without a prescription. Because Metazene is not compounded one tube at a time, it costs a fraction of what physicians and pharmacies charge.
Some people report amazing results using only Metazene. Others find it dramatically improves the results of traditional acne treatments, often with the added benefit of reducing the dosages for prescription drugs. We cannot, of course, guarantee that Metazene will work for you. What we can guarantee is that unless you try it, you will never know.
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About 16 percent of Americans between the ages of 14 and 49 are infected with genital herpes, making it one of the most common sexually transmitted diseases, U.S. health officials said on Tuesday.
Black women had the highest rate of infection at 48 percent and women were nearly twice likely as men to be infected, according to an analysis by the U.S. Centers for Disease Control and Prevention.
About 21 percent of women were infected with genital herpes, compared to only 11.5 percent of men, while 39 percent of blacks were infected compared to about 12 percent for whites, the CDC said.
There is no cure for genital herpes, or herpes simplex virus type 2 (HSV-2), which can cause recurrent and painful genital sores and also increases the likelihood of acquiring and transmitting the AIDS virus. It is related to herpes simplex virus 1, or oral herpes, which causes cold sores.
Several drugs are available to treat herpes symptoms and outbreaks, including acyclovir, which is available generically or under the Zovirax brand name, and valacyclovir, known generically as Valtrex — both made by GlaxoSmithKline PLC . Ganciclovir, sold as Zirgan, is made by privately-held Sirion Therapeutics, Inc.
The CDC estimates that more than 80 percent of people with genital herpes do not know they are infected.
“The message is herpes is quite common. The symptoms can be often very innocuous,” Dr. John Douglas of the CDC said in a teleconference.
“Because herpes is so prevalent it becomes … a really important reason to use condoms on a consistent and correct basis with all of your partners,” Douglas said.
Douglas said the increased rate of infection in blacks is not do to increased risk behavior but likely due to biological factors that make women more susceptible as well as the higher rate of infection within black communities.
The CDC estimates that there are 19 million new sexually transmitted disease infections every year in the United States, costing the health care system about $16 billion annually.
For information on using dietary BHT as a treatment for Herpes see:
Download the latest eBook on BHT here
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Aging, diabetes, toast, and roast beef all have something in common: crosslinking.
To a chemist, this means that sugars – from carbohydrates, starches, and natural sources – have reacted with cellular components like amino acids, fats, proteins, and DNA.
To a chef, it means that the Maillard reaction (See article in this issue) has browned a roast or caramelized onions.
To a doctor, it means that your arteries, organs, and cells have been hardened or damaged, causing cardiovascular disease, neurological disorders, vision loss, kidney problems, and chronic inflammation.
To you, it means premature aging, diabetes, and lowered quality of life.
Joined at the Hip
The basis of crosslinking is what chemists call intermolecular bonding. This means that molecules bond to other molecules. (Bonding inside the same molecule is called cyclization.)
Crosslinking is very useful: leather is tanned (crosslinked) skin, paint is cured (crosslinked) polymer films, plastics are polymerized (crosslinked) oils, and tires are made from vulcanized (crosslinked) rubber. Many of the natural products that we enjoy – fibers, wool, fur, and feathers, to name just a few – depend upon crosslinking.
Nearly anything can crosslink, which creates both opportunities and problems for the body.
A Double-Edged Sword
Crosslinking is a lot like Janus, the two-faced Roman god of doorways. With it we age, but without it we can’t live at all. Consider collagen, a critical protein in connective tissue, tendons, ligaments, cartilage, skin, bone, and even the cornea of the eye.
Crosslinked collagen is hard, which creates a host of problems: skin deterioration (wrinkles, sagging, stiffness), connective tissue rigidity (often misdiagnosed as arthritis), bone problems, organ stiffening (heart problems, bladder incontinence, lung issues), etc. But collagen is an example of the two faces of crosslinking; while unwanted bonds destroy collagen, they are also crucial for connective tissue strength. Without this web of interlocking we’d fall apart.
Our hair and fingernails are a type of crosslinked protein called keratin. (Hair straightener and depilatories rely on breaking crosslinks.)
Any solution to the crosslinking problem must target the unwanted type causing damage, while leaving the remainder alone. This is not always so easy to do, and considering how crosslinking originates will explain why.
Literally Tied Up in Knots
Consider a strand of protein as a flexible piece of rope. Imagine two adjacent strands of rope (protein) fixed only at the ends, such that each has total freedom to bend and move, independent of the other.
As more and more horizontal pieces of twine are tied from one rope to the other, the flexibility of movement declines until the two have become somewhat rigid. As the joining twine contracts, as it often does in crosslinked molecules, the ropes pull together simplifying adding new crosslinks.
This is exactly what happens in the body, as proteins and other molecules bind together. This changes their shapes, and thus their biological properties, preventing normal functioning.
Chemists call changes like these ‘denaturing’, since the original properties of the molecule have been altered. This isn’t always bad; cooking a steak denatures the proteins, making them far more digestible, and much tastier, too.
The idea that crosslinking causes aging is hardly a new one; back in 1941, Dr. Johan Bjorksten, a Wisconsin chemist, first proposed that undesirable bonding gradually damages proteins, fats, DNA, vitamins, etc.
These damaged molecules bind together into sticky tangles; over time, these blobs grow and wrap around other molecules, growing and posing more and more of a problem.
Leather, Hectographs, & Aging
Bjorksten came to his discovery because of his background in leather chemistry and his work on hectograph films, which were used to duplicate pages prior to the invention of the photocopier.
This wet process, which dates back to the late 19th century, uses a gelatin film to transfer ink to paper, much like a printing press. It was good for about fifty copies of the same sheet. (Remember this the next time you use fast, inexpensive, and dry copier technology.)
The problem plaguing Bjorksten was how to stop the gelatin films from hardening with age and use. He quickly identified the culprit as protein crosslinking, and noticed that the hard gelatin films were remarkably similar to damaged skin. He concluded that the same chemical processes must be at work in both cases and that inhibiting crosslinking would prevent any human diseases and disorders, and thus extend life.
Cracking Bonds With Enzymes
Bjorksten began taking vitamin E, the only anti-crosslinking agent available to him, and began searching for a means to crack the strong bonds with proteins.
The first approach used soil bacteria a rich source of raw material for pharmaceuticals fed crosslinked protein, exclusively. (Many antibiotics, like the potent streptomycin, originated with bacteria from dirt.)
The bacteria that survived would, of necessity, produce enzymes capable of breaking protein bonds. Bjorksten felt that these enzymes could then be used in humans.
The Real World Intrudes
Facing him were two big problems: science and funding. Every single enzyme he found that could break protein crosslinks was so toxic it couldn’t be used in lab animals, let alone humans. Beyond science, however, the debate over extending human lifespan was as contentious as today’s debates over stem cell research, and this made funding his work controversial.
Bjorksten also contributed to the controversy, including a proposal that the United States Department of Defense fund development of a “rapid-aging spray” to be used against enemy soldiers during wartime. The military’s reaction was, needless to say, not enthusiastic.
Running out of money and deciding the search for enzymes was hopeless, at least in any time frame that would benefit him – both of Bjorksten’s parents died from Alzheimer’s Disease, which exhibits a great deal of crosslinking – he abandoned breakers for other approaches.
Cracking Bonds With Chelation
Moving into chelation agents like Ethylenediaminetetracetic acid (EDTA), Bjorksten reasoned that if these compounds can break bonds with metals that they would prevent, or even break down, the protein tangles in the body.
There is evidence that copper and iron catalyze reactions between sugars and proteins, particularly in cataracts and Alzheimer’s disease, Johan Bjorksten and that eliminating excess metalions may slow crosslinking. This is, of course, a topic so big it needs to be covered in its own article.
A Theory Now Accepted as Fact
Bjorksten’s work on the ‘crosslinking theory of aging’ provides an explanation for aging and diabetes making perfect sense; the body’s proteins do harden over time. One example is the leathery skin of cowboys and habitual beach goers. His theory is accepted today as a crucial component in aging and disease, especially diabetes.
Origins of the Ties That Bind
Crosslinking is caused by such diverse factors as: inter-molecular bonding (metabolic by-products), ultraviolet light (sun, tanning salons), ozone (pollution), acetaldehyde (alcohol, cigarette smoke, pollution), ketones (diabetics, high-protein/low-carb diets), metal ions (lead, cadmium, mercury, copper, iron, aluminum), x-rays, and free radicals (normal metabolism, rancid or overheated oils and fats).
It wasn’t until 1965, however, that one of the leading culprits in crosslinking and aging was identified: sugar bonding to protein via the “maillard reaction”. (See the article in this issue.) This is why diabetics age prematurely and why otherwise healthy people need to protect themselves from even typical blood-sugar levels.
Other types of crosslinking, such as between proteins, lipids (fats) or involving metals like copper and iron, are very important as well. So are the sulfur-sulfur (disulfide) bonds made between the sulfur bearing amino acids in proteins. Sugar, however, seems to be the leading cause of damage and aging, even in non-diabetics.
Increases in blood-sugar happen after consuming starches and carbohydrates – these are broken down into simple sugars – as well as fruits and vegetables which also contain sugars and carbohydrates.
The problem is that sugar is a biochemical straight jacket: before it can be broken down and metabolized it locks up molecules needed for routine cellular function and creates toxic compounds.
Marrying Sugar to Protein
The overall process is very simple, but sounds a little complicated because of terminology. All you really need to know is in the next two paragraphs.
It all begins when sugar oxidizes, giving it a reactive carbon-oxygen (carbonyl) group that binds to proteins in a process called glycation. These glycated, or sugared, proteins eventually form stable, long-lived, and highly damaging Advanced Glycation End-products (AGE). This is the key phrase to remember, because the crosslinking theory of aging is basically all about AGEs.
Similar results occur when fats and proteins bond together. Reactions between proteins, sugars, and fats explain why sautÃ©ed food is tastier than steamed, and why sauces are made from browned bones (reacted proteins, fats, and sugars), roasted vegetables (caramelized carbohydrates and natural sugars), and butter (fat). (See the article on the “Maillard Reaction”.)
How Sweet It Isn’t
Arteries and the fine capillaries in the retina and kidney are particularly vulnerable to sugar protein reactions because, unlike other cells, they cannot break down some forms of sugar like sorbitol. These then attack the proteins in the blood-vessel walls, leading to damage and AGEs.
Artery-clogging plaque is nothing more than globs of crosslinked AGEs made from a variety of material sugars, proteins, lipids and fats like cholesterol, metals, fibrin, etc.
You’re Showing Your AGE
Over time, AGEs crosslink the inside of your body like a browned roast, causing diseases like cardiovascular hardening and heart attacks, retinal deterioration, cataracts, glaucoma, peripheral nerve damage, kidney failure, osteoarthritis, stroke, scleroderma, and atherosclerosis.
Once a long-lived protein, such as those in the eye s lens or the collagen in skin and joint cartilage, is damaged it usually remains so. This is why levels of the AGE product pentosidine in the joint cartilage of an eighty-year old have been measured as being over thirty times those of a twenty-year old.
Implicated in many diseases, AGEs are known to activate a variety of inflammatory cytokines, or messenger molecules, including tumor necrosis factor alpha (TNF-a) and interleukin, even in otherwise healthy people.
Stop Doing That Right Now!
A variety of prescription drugs and nutritional supplements with anti-crosslinking effects are readily available. (See “Which of the Crosslinking Inhibitors and Breakers Are Right For You” in this blog.)
Nearly a thousand such compounds are known, but many of them, as Bjorksten discovered a long time ago, are completely unsuitable for use in the body.
Crosslinking inhibitors – available as both prescription and supplements – typically interfere with the binding of the carbonyl groups (just a carbon-oxygen bond) on sugars to amino acids and other molecules. Some inhibitors are sacrificial, binding to an active site on the sugar before it can disrupt an amino acid in a protein.
The aptly-named crosslinking breakers crack the bond between the sugar and the protein, undoing some of the damage and allowing repair. This is more difficult, and many of the breakers target bonds – like those giving cartilage its strength – that must remain untouched.
Breaking Sugar’s Hammerlock
Supplement-based compounds are known to break existing AGE bonds without serious side effects. Prescription drug breakers are still relatively new, however, and have limited safety histories. Until their long-term, and even short term, effects are well known and understood, supplements are generally a safe, effective, and very affordable alternative.
Toast, roasts, and caramelized onions can be delicious, but you certainly don’t want the same reactions occurring in your body. So, if you have diabetes or just want to put the brakes on your age-related deterioration, you’ll definitely want to add crosslinking inhibitors and breakers to your supplement list. Before your body gets tied up in knots!
For a more information on Aging & Diabetes see:
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Heart disease and cancer can be easily branded as the two most notorious and common killers in the United States. However, there are other causes of death which are less common with the nation as a whole but are actually much more typical in specific states.
A new color-coded map has been created by the CDC in order to categorize the most likely causes of death for each of the 50 U.S. states.
According to Francis Boscoe, a research scientist at New York State Cancer Registry the most distinctive causes of death in majority of cases is not so surprising. In several northern states, including Maine, North Dakota, South Dakota and Wyoming the flu is considered as the most distinctive cause of death. In Alaska and Idaho the most distinctive causes of death is considered to be plane crashes or boat accidents. In mining states such as Pennsylvania, West Virginia and Kentucky pneumoconiosis, a group of lung diseases caused by inhaling dusts, are branded as the most distinctive causes of death.
There were however, some unexpected findings. In New Jersey, Sepsis is categorized as the most distinctive cause of death and deaths by legal intervention. Surprisingly the most distinctive cause of death in New Mexico, Nevada and Oregon is that caused by law enforcement officers, excluding legal executions.
In order to determine the most distinctive causes of death for each individual state, the researchers from the Centers for Disease Control and Prevention initiated a list of 113 causes of death.
Then, the researchers began determining the estimate of death from each cause, for each state and divided this by the rate of death from that particular cause in the United States as a whole. This theory allowed the researchers to observe which of the states had higher rates of death from certain causes than the rest of the United States.
In Alaska, for instance the rate of death for plane crashes and boat accidents was about 4 deaths per 100,000 people; whereas the national rate is 0.6 deaths per 100,000 people. This essentially proves beyond reasonable doubt that deaths from plane crashes or boat accidents are seven times more likely in Alaska than entire United States. According to Boscoe, this “distinctive” cause of death makes sense, since some parts of Alaska are accessible only by boat or plane.
In Florida, HIV was identified as the most distinctive cause of death, where about 15,000 people died from the disease. But in numerous cases, the most distinctive cause of death was still quite uncommon. Although Syphilis caused only 22 deaths in Louisiana, it is considered as the most distinctive cause of death in that particular state.
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Recent studies in chronobiology have indicated that melatonin supplements can help treat circadian sleep disorders as well as a variety of sleep-related issues. However, not all melatonin supplements are created equal. The way melatonin supplements are metabolized can have a huge effect on physiological levels and effects of this hormone.
Melatonin and the Circadian Rhythm
Melatonin, also known as the “mother hormone of chronobiology”, is a hormone made in the pineal gland due to cues from the suprachiasmatic nucleus of the hypothalamus, which regulates the circadian rhythm. When the retinas stop sensing as much blue wavelength light, the suprachiasmatic nucleus senses this and induces the pineal gland to begin making melatonin. When early morning light is sensed by the retinas, melatonin production is ceased and hormones associated with wakefulness are made instead. This cycle helps to create a circadian rhythm, or 24-hour sleep-wake cycle.
Melatonin has a very short half-life, of about thirty minutes. Because it breaks down so quickly, it must be made continuously throughout the night in order to sustain restful sleep. In people with a healthy circadian rhythm, melatonin levels rise rapidly after dark and plateau throughout the night until early morning. These high levels are essential not just for falling asleep, but for sleeping deeply and restfully. Melatonin levels then drop sharply in the early morning to allow people to wake up in response to increasing light levels.
Melatonin Supplements and Sleep
Studies in circadian biology have shown how important melatonin levels are to maintaining a natural human sleep-wake pattern. In fact, studies have found that many sleep disorders improve significantly with melatonin supplementation. However, some people find that melatonin doesn’t work as dramatically as they expected. They may assume that melatonin is not a useful treatment for their sleep issues when in fact, they could be simply taking the wrong kind of melatonin supplement.
The most common types of melatonin supplements are fast release and slow release. Fast release melatonin causes a sharp spike in melatonin levels that drops off after an hour. People who use this type of melatonin supplement may find that they are immediately sleepy but have trouble remaining asleep or do not get high quality sleep. Slow-release melatonin, on the other hand, takes hours to build up to sleep-inducing levels and then does not wear off in the early morning. People who take slow release melatonin may have trouble falling asleep due to low melatonin levels, followed by difficulty waking up because the levels are unnaturally high.
Timed-Release Melatonin: A Better Option for Maintaining Natural Circadian Rhythms Timed-release melatonin is a supplement that is formulated to be released in amounts that mimic healthy, natural melatonin levels. It is metabolized so that levels rise sharply after the supplement is taken and then remain at a high plateau for several hours. Levels then drop sharply to allow for waking. This mimics the healthy, normal circadian rhythm cycles that are linked to restful sleep.
Research in chronobiology has shown that maintaining melatonin cycles is important not just to restful sleep but to overall health. For this reason, an increasing number of health experts are recommending timed-release melatonin as the ideal melatonin supplement. It more closely correlates to the natural levels of melatonin in a healthy brain. Maintaining a healthy circadian rhythm is important to health, so timed-release melatonin supplements are usually the best option.
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Depression and chronic pain are two common conditions that are also associated with poor sleep quality. While it is often thought that the sleep issues are secondary to these conditions, a new study conducted by researchers from the University of Alabama indicates that depression and pain due to osteoarthritis could be the result of poor sleep quality instead of the other way around.
Prior research has shown that people with hip and knee osteoarthritis (OA) are more likely to have insomnia, daytime sleepiness, and depression, than those without OA. The obvious relationship is that the arthritis pain affects sleep and makes people depressed. However, a 2012 study published in the journal SLEEP looked at sleep quality in people who were in chronic pain, including those with osteoarthritis and researchers found:
- The amount of pain that people were in before they went to bed had little to do with how well they slept.
- A person’s sleep quality predicted how much pain they were in the next day. People who slept poorly had more pain the following day.
Other studies have shown that poor sleep quality can trigger inflammatory pathways that make arthritis pain worse, and poor sleep also make people more sensitive to the feeling of pain from any cause.
To better examine the relationship between OA, pain, and depression, 367 patients with OA of the knee from a variety of sources were recruited to participate in a trial. The participants completed a detailed questionnaire that identified overall health, depression, pain, joint function, and sleep quality. One-year follow-up was available for 288 patients.
Analysis of the data collected from the questionnaires indicated that comparing the initial baseline with 1-year follow-up data, sleep disturbance at baseline was linked with increased depression and further loss of joint function, but interestingly not more pain.
Since the questionnaire used in the study was not specifically designed to identify the exact sleep issues in OA patients, further research is needed to more fully pinpoint what is abnormal about OA patients’ sleep. Nonetheless, the conclusion from the study is the disturbance in sleep definitely precedes the depression, loss of joint function, and likely increased pain associated with OA. Hence, the takeaway message is that improving sleep quality is a key goal in preventing the progression of OA as well as the associated depression.
Early on in my clinical practice, I realized that improving my patient’s ability to get a good night’s sleep was usually the quickest way to help them feel better in every way. Over the years I have used a number of natural products that can help to improve sleep quality. The specific product that I now recommend as a first step is the one that I developed: Tranquil Sleep from Natural Factors. This formula provides the combination of melatonin (3 mg), 5-HTP (30 mg), and L-theanine (200 mg) in a great tasting chewable tablet or soft-gelatin capsule. These three ingredients work together to decrease the time required to get to sleep and to decrease the number of nighttime awakenings. Here is a brief description of each ingredient as it relates to improving sleep quality. If you don’t use Tranquil Sleep, you can get the same effect by combining them on your own
Melatonin is the most popular natural aid for improving sleep quality. Supplementation with melatonin has been shown in several studies to be very effective in helping induce and maintain sleep in both children and adults and in both people with normal sleep patterns and those with insomnia. Typical dosage is 3 mg at bedtime.
5-HTP (5-Hydroxytryptophan) is converted in the brain to serotonin – an important initiator of sleep. It is one step closer to serotonin than l-tryptophan and has shown more consistent results in promoting and maintaining sleep, even though used at lower dosages. One of the key benefits of 5-HTP is its ability to increase REM sleep (typically by about 25%) while increasing deep sleep stages 3 and 4 without lengthening total sleep time. Recommended dosage for improving sleep quality in combination with melatonin is 25 to 50 mg at bedtime.
L-Theanine is a unique amino acid found in green tea. Clinical studies have demonstrated that L-theanine reduces stress, improves the quality of sleep, diminishes the symptoms of the premenstrual syndrome, heightens mental acuity and reduces negative side effects of caffeine. It is an excellent support agent to melatonin and 5-HTP. Recommended dosage is 200 mg at bedtime.
Parmelee PA, Tighe CA, Dautovich ND. Sleep disturbance in Osteoarthritis: Linkages with pain, disability and depressive symptoms. Arthritis Care Res. 2014 Oct 6. doi: 10.1002/acr.22459. [Epub ahead of print]
Dr. Michael Murray
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Contrary to News Headlines, Robin Williams Was on Drugs at the Time of His Death—Antidepressant Drugs
If news headlines were to be believed about the autopsy findings of beloved actor/comedian Robin Williams, who tragically committed suicide nearly two months ago, no drugs were found in his system at the time of his death, as evidenced by headlines from USA Today, NBC News, the BBC and others proclaiming “no alcohol or drugs” were found. These headlines couldn’t be more wrong.
The medical examiner’s report cites an antidepressant drug was in Williams’ system at the time of his death. The particular antidepressant, Mirtazapine, (also known as Remeron) carries 10 international drug regulatory warnings on causing suicidal ideation.
According to the autopsy results, not only was Williams under the influence of antidepressant drugs, but the powerful antipsychotic Seroquel was also found at the scene and appears to have been recently taken by Williams. While toxicology tests apparently were negative for the antipsychotic Seroquel, the fact remains that a bottle of Seroquel prescribed to Williams on August 4th, just seven days prior to Williams’ suicide, was missing 8 pills. The Seroquel instructions advise to take one pill per day as needed. Side effects associated with Seroquel include psychosis, paranoid reactions, delusions, depersonalization and suicide attempt.
The question that has to be asked is why the press continues to promote the idea that no drugs were found in Williams’ system? At what point did mind-altering psychiatric drugs, which have side effects rivaling those of heroin or crack cocaine, stop being called drugs? And for those in the press who did “mention” the fact that Williams was found to have antidepressants in his system, the acknowledgement seems to promote the fact that “therapeutic concentrations” of prescription psychiatric drugs “improved his condition and kept him active until his death.”
This is a highly misleading take on the events leading to Williams tragic suicide, especially in light of the fact that not only was Williams receiving mental health “treatment,” he was under the supervision of a psychiatrist, was not abusing illegal drugs and had not “fallen off the wagon.”
The facts regarding antidepressant drugs are these:
- Food and Drug Administration’s Medwatch Adverse Drug Reports include 470,000 adverse reactions for psychiatric drugs between 2004-2012. The FDA admits only 1% of side effects are ever reported to them, so the actual number of reported side effects is assuredly much higher.
- Mirtazapine (also known as Remeron) carries the Food and Drug Administration’s (FDA) “Black box” warning for suicidality.
- There are ten warnings of suicide associated with Mirtazapine alone and suicide is among the top 2 side effects reported to the FDA on this particular antidepressant
- The FDA’s MedWatch drug adverse event reporting system recorded 411 attempted and completed suicides associated with the antidepressant Mirtazapine alone (and the FDA estimates only 1% of side effects are ever reported to them)
- 90,000 emergency room visits are attributed to psychiatric drugs each year in the U.S.
- 23,755 suicides are attributed to psychiatric drugs each year in the U.S. alone.
- In addition to suicidal ideation, documented side effects of antidepressants by international drug regulatory agencies include hallucinations, delusions, worsening depression, depersonalization, mania, psychosis, self-harm.
Given the above data, one can only wonder why Williams’ psychiatric drug use has effectively been dismissed by reporting organizations. A careful review of Williams’ psychiatric “non-drug” use paints a very different tragic story.
What was found in Williams’ system were prescription psychiatric drugs with side effects that not only rival illegal street drugs, but also carry the FDA’s “Black box” warnings—the federal agency’s most serious warnings—about increased thoughts of suicide.
The fact is that two of the drugs Williams had been prescribed list suicidal thoughts as possible side effects. The Seroquel he was prescribed (and appears to have taken in the week prior to his suicide), and the antidepressant that was still in his system at the time of his suicide. Moreover, considering the FDA’s Medwatch drug adverse event reporting system recorded 411 attempted and completed suicides associated with the antidepressant Mirtazapine alone (and the FDA estimates only 1% of side effects are ever reported to them), it becomes even more bizarre that the world’s press ignore even the possibility that these drugs could be involved in Williams’ suicide.
The much-loved comedian’s death is a great loss, but the tragedy is further compounded by the mainstream press glossing over the serious and well-known association between suicide and the psychiatric drugs Williams was taking. If only the sentiments from one of Williams’ finest roles in Awakenings had been taken literally in his personal life: “The human spirit is more powerful than any drug and that is what needs to be nourished: with work, play, friendship, family. These are the things that matter.”