This is the second part in our series on the microbial populations we harbour and their effects from brain to bowel.
By far the majority of our companion microbes, weighing an impressive 1.5 kilograms and containing more than 1,000 species, reside in our gut, mostly in the large intestine.
As soon as a baby is born – and perhaps even before – microbes move in. Many are seeded from bacteria in the mother’s birth canal if it’s a vaginal birth or from her skin if it’s a caesarean birth.
An infant’s milky diet fosters a unique set of gut microbes. The infant microbiome gradually changes until, by the time a toddler is three years old, it has morphed into a more diverse ecosystem that is indistinguishable from an adult’s.
Gut communities differ from one person to the next, and are heavily influenced by the food we eat. They are also rapid responders to dietary change, re-configuring for a new diet in just a day or two.
Gut microbes do more than just scavenge from the food we eat. They also harvest energy and synthesise essential nutrients, such as certain B vitamins and folate, for us. Indeed, pregnancy sways a mother’s gut ecosystem towards one that harvests more calories per bite.
Mice raised to be germ-free are skinnier than their germy counterparts, even when they eat more; with no microbes at all, they can’t extract as many calories from their food.
There’s now compelling evidence that tinkering with microbes living in the depths of our bowels could be contributing to our expanding waistlines. Scientists are still figuring out what microbiota changes are most detrimental and how such changes cause weight gain.
Some of the earliest evidence that gut bugs affect weight gain came from farm animals. Since the 1940s, farmers have fattened livestock by feeding them low doses of antibiotics – enough to affect their gut microbiota but not enough to be therapeutic.
Humans, it turns out, aren’t immune to this effect. Taking repeated courses of antibiotics during infancy increases the risk of becoming overweight, at least in childhood, which is a good predictor of obesity in adulthood. The first six months of life are particularly critical. And boys seem to be more susceptible than girls, though why is a mystery.
many strains of so-called ‘good bacteria’ that are available in commercial probiotic concoctions don’t stick around to become long-term members of the gut community
And why infancy is such a crucial time isn’t fully understood either. One suggestion is that it coincides with the time our body decides how many fat-storing adipose cells to lay down to accommodate calories.
It’s not just antibiotics that can make a baby’s microbiota fattening. Birth by caesarean section and being fed formula instead of breast milk also seem to tip the scales towards greater childhood weight gain.
In many cases, antibiotics, caesarean delivery and baby formula can’t be avoided. And an untreated infection or undernourishment can be far more harmful than a potential increase in the risk of being chubbier as a toddler.
Another thing to remember is that even with microbiota disruptions as a child, it’s not a foregone conclusion you’ll end up obese, says Laura Cox, a biologist at the Brigham & Women’s Hospital and Harvard Medical School in Boston in the US who has studied the antibiotic-obesity connection: “The risk of being overweight from microbiota disruption [in early life] is not as big as other risk factors, such as certain genetic factors or eating certain diets or never exercising.”
The situation in adults is murkier.
Scientists are still getting a handle on how disruptive antibiotics – and other chemicals and food additives we encounter daily – might be. Our gut communities tend to bounce back after a dose of antibiotics, but Western gut microbiota are generally less diverse – and perhaps less resilient to disruption – than those of people living more traditional lives. And there’s enormous individual variation.
Mice demonstrate the power of gut microbes to influence weight gain between individuals. In 2006, a research group from Washington University in St Louis took poo from obese mice and transplanted it into the gut of skinny, germ-free mice, which promptly became obese.
It didn’t matter whether the original obese mice were fat from too much healthy chow or from eating a high-fat ‘Western’ diet. Excess calories seemed to be the key factor turning their microbiota into an obesity-causing (or ‘obesogenic’) community.
A single case report from 2015 suggests the same applies to human-to-human poo transplants. A woman who received poo from her overweight daughter to treat severe diarrhoea became obese in the months following the procedure.
So, what makes a microbial ecosystem obesogenic?
According to Cox, there doesn’t seem to be any ‘bad’ microbes that take over in an obese gut community. But along with an overall loss of diversity in the ecosystem, a handful of microbes consistently become less common.
Other studies have focused not just on who’s there, but what they collectively do.
A hallmark of an obesogenic microbiota is a change in the types and amounts of short chain fatty acids microbes pump out after fermenting dietary fibre (and to a lesser extent, protein).
Short chain fatty acids provide up to 10% of calories absorbed when consuming a Western-style diet – and probably more in extremely high-fibre, plant-based diets. But they also act as signalling molecules, dialling up satiety messages in our brain, slowing food movement through our gut and boosting fat cell production.
How do we keep good microbes happy? Unfortunately, cultivating protective microbes with dietary supplements called prebiotics has seen mixed results. When mice are fed a low-fibre diet, their microbial ecosystem becomes less diverse. Simply re-adding fibre to their diet doesn’t fix the problem – once an organism is lost, it may be lost for good. And over generations, the problem is compounded – mothers can’t seed their offspring with gut bacteria they no longer have.
Similarly, in obese women given the fermentable fibre inulin – to boost short chain fatty acid production – weight loss was only modest. And the best responders already harboured particular clusters of beneficial bacteria that could blossom with the added nutrient.
Probiotics – consuming live bacteria to replenishing the gut with microbes that have been lost or are limited in number – has been touted as a possible solution. But scientists are yet to identify microbes that reliably work to reduce weight gain, and many strains of so-called ‘good bacteria’ that are available in commercial probiotic concoctions don’t stick around to become long-term members of the gut community.
The more drastic approach of replacing the entire ecosystem with a poo transplant hasn’t fared much better. In 2012, researchers in the Netherlands transplanted poo from lean donors to people showing early signs of developing type 2 diabetes, a metabolic disorder that frequently accompanies obesity.
Although metabolism improved in the immediate aftermath of the transplant, microbes and metabolism reverted to an unhealthy state within six months.
The lesson seems to be that the best way to foster a healthy, diverse gut community is to feed it right from the get-go – with foods high in fibre, low in fat and not overloaded with calories.
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We are not alone. Our bodies are teeming metropolises of microscopic life – and the microbes that call us home influence everything from bowel to brain.
Over the past decade, technological advances in the lab have allowed us to take a census of our microbial entourage – known as the microbiota – like never before. Instead of seeing only the small fraction of microbes from our skin or poo that blossom on a petri dish, we can now blend, extract and read the genetic essence – the DNA – of all microbes, called the microbiome, to get a better idea of who’s there.
The picture that has emerged is one of staggering complexity. From nostrils to armpits, wisdom teeth to bowels, lungs to vaginas, unique communities of bacteria, fungi, viruses and parasites have got us covered.
“Every single surface of our body is colonised with microbes,” says Laura Cox, a biologist at the Brigham & Women’s Hospital and Harvard Medical School in Boston in the US.
Bacteria alone are as numerous as the cells of our own body. The genes they harbour dwarf our own genetic endowment more than a hundred times over. Together, we work in concert in what some consider a ‘super-organism’ – with our existence as reliant on theirs as theirs is on us.
Gut microbes synthesise vitamins, while those on our skin earn their keep by eating dead cells and transforming oils into natural moisturiser. And microbes everywhere play a role in keeping harmful pathogens at bay.
Families of gut microbes diverged from a common ancestor some 15 million years ago.
On the other side of the ledger, a mother’s milk contains some nutrients useless to her baby, but essential for the early microbial colonisers of her baby’s gut.
The assemblages of species inhabiting each bodily niche represent complex ecosystems that have evolved with us over millennia. The microbes lurking on the doorknob of the public toilet might give us the heebie-jeebies. But those that take up residence on or in us aren’t usually picked up from the environment. They are passed down from generation to generation, and have been for millions of years.
Families of gut microbes living in both us and other apes diverged from a common ancestor some 15 million years ago.
And bacterial strains from Africa and America diverged 1.7 million years ago, around the time early humans made their first forays out of Africa. If you wanted to, you could trace the history of human migrations around the globe using our microbiome.
Our microbes continue to evolve with us, and in response to our modern lifestyles. People living in industrialised societies have less diverse microbial communities than people in places such as Malawi.
Microbiome composition ebbs and flows depending on the food we supply and the various chemicals and drugs we send their way. Not surprisingly, the fluctuations in our microbial residents have clear implications for our health – from immune responses to how we think and act.
Tomorrow, we’ll explore how gut microbes tinker with our metabolism.
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Study co-authored by a UCSB researcher reveals Latinos age slower, neutralizing higher health risks of obesity and diabetes
A new paper co-authored by a UC Santa Barbara researcher reveals that Latinos age at a slower rate than other ethnic groups. The findings, published in the current issue of Genome Biology, may one day help scientists understand how to slow the aging process for everyone.
“Latinos live longer than Caucasians, despite experiencing higher rates of diabetes and other diseases. Scientists refer to this as the ‘Hispanic paradox,’ ” said lead author Steve Horvath, a professor of human genetics at the David Geffen School of Medicine at UCLA. “Our study helps explain this by demonstrating that Latinos age more slowly at the molecular level.”
According to the Centers for Disease Control and Prevention, Latinos in the United States live an average of three years longer than Caucasians, with a life expectancy of 82 versus 79. At any age, healthy Latino adults face a 30 percent lower risk of death than other racial groups, according to a 2013 study in the American Journal of Public Health.
The UCLA team used several biomarkers, including an “epigenetic clock” developed by Horvath in 2013, to track an epigenetic shift in the genome that’s linked to aging. Epigenetics is the study of changes to the DNA molecule that influence which genes are active but don’t alter the DNA sequence.
“Our findings show that ethnic disparities in health risk are not just due to socioeconomic differences, which we adjust for in the analyses,” explained co-author Michael Gurven, a UCSB professor of anthropology. “The epigenetic analyses show biological differences in aging-related processes — but in a novel way — in how the genome is maintained and expressed through methylation, rather than conventional differences in genetic alleles.”
Horvath and his colleagues analyzed 18 sets of data on DNA samples from nearly 6,000 people. The participants represented seven ethnicities: two African groups, African-Americans, Caucasians, East Asians, Latinos and an indigenous people called the Tsimane, who are genetically related to Latinos. The Tsimane live in Bolivia.
When the scientists examined the DNA from blood — which reveals the health of a person’s immune system — they were struck by differences linked to ethnicity. In particular, the scientists noticed that, after accounting for differences in cell composition, the blood of Latinos and the Tsimane aged more slowly than that of other groups.
According to Horvath, the UCLA research points to an epigenetic explanation for Latinos’ longer life spans. For example, the biological clock measured Latino women’s age as 2.4 years younger than non-Latino women of the same age after menopause.
“We suspect that Latinos’ slower aging rate helps neutralize their higher health risks, particularly those related to obesity and inflammation,” said Horvath, who is also a professor of biostatistics at the UCLA Fielding School of Public Health. “Our findings strongly suggest that genetic or environmental factors linked to ethnicity may influence how quickly a person ages and how long they live.” Gurven added “Epigenetic aging measures are fascinating because they subsume many environmental and psychosocial factors we know matter in life. One hypothesis to explain the Hispanic paradox emphasizes the strong family ties and social support found in many Hispanic families. Such a social support network may leave its biological signature in the epigenome.”
The Tsimane aged even more slowly than Latinos. The biological clock calculated the age of their blood as two years younger than Latinos and four years younger than Caucasians. This possibly reflects the group’s minimal signs of heart disease, diabetes, hypertension, or obesity, the researchers said.
“Despite frequent infections, the Tsimane people show very little evidence of the chronic diseases that commonly afflict modern society,” Gurven said. “Our findings provide an interesting molecular explanation for their robust health.”
In another finding, the researchers learned that men’s blood and brain tissue ages faster than women’s from the same ethnic groups. The discovery could explain why women have a higher life expectancy than men.
The research was supported by grants from the National Heart, Lung and Blood Institute and the National Institute on Aging.
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“Dr. Hyman, I’m so confused about coffee,” writes this week’s house call. “One day I read that it’s so bad for me and the next it’s good for me. Why all the conflicting information?”
Let’s face it: Americans love their coffee, which is the number one source of antioxidants in our diet – which actually makes me kind of sad!
In a recent animal study, researchers saw improvements in non-alcoholic fatty liver disease (NAFLD) and cholesterol when mice consumed coffee and fat together. (More on that combo in a minute.) They also found coffee can help reduce gut permeability or leaky gut.
On the other hand, coffee can become highly addictive, altering stress hormones while making you feel simultaneously wired and tired.
So I understand the confusion. It feels like one day we see studies that support coffee and the next day we see 10 reasons why coffee is bad. So let’s uncover the truth about this aromatic beverage that most of us love.
When to Avoid Coffee
Before jumping to conclusions, remember those blurred lines aren’t entirely about coffee itself. It also depends on the person drinking the coffee. The way you respond to coffee is often determined by genetics that affect caffeine metabolism. For one person, a cup could have them bouncing off the walls, while another person can have a triple espresso at dinner and fall fast asleep easily.
In other words, everyone is different and we all experience coffee’s effects differently. One patient complained about fatigue, restlessness and heart palpitations. Obviously, in that situation, I recommended avoiding coffee.
Likewise, if you suffer from adrenal fatigue, coffee could easily become dangerous. Some individuals might also be sensitive to coffee beans, meaning their bodies can’t tolerate them and they create unpleasant symptoms.
Sometimes, too, I find patients substitute coffee for real food. Never ignore your hunger and eat regularly to prevent low blood sugar levels. Keep protein on hand and snack on a handful of nuts or seeds like almonds, pecans, walnuts or pumpkin seeds.
I had one patient who drank 12 cups of coffee a day yet constantly fell asleep at his desk. This person could barely function and couldn’t understand why he felt so exhausted. The truth is he wasn’t sleeping well at night due to all the caffeine but he was too exhausted to realize it. He wasn’t getting the proper rest his body desperately needed at the right time.
So we tapered him off coffee, and he began to sleep soundly at night, rather than nodding off at his desk during the day.
If you fall into those categories, coffee probably isn’t for you.
Regardless, I recommend treating coffee like any other potential toxic trigger and eliminate it for at least three weeks, especially if you’re addicted and can’t seem to function without coffee or if you drink multiple cups a day.
If you need coffee every day to feel motivated or even function, you have a coffee addiction. If you have withdrawal symptoms and headaches from stopping coffee or feel like you can’t live without it, you are biologically addicted to it. There’s also a big chance your stress hormones are out of whack and need resetting.
How to Quit Coffee
The best way to wean off coffee is switching from drinking multiple cups to just one cup and eventually half a cup. You might also switch to green tea or herbal teas and warm lemon water.
As with any detox plan, drink adequate amounts of water and get plenty of rest during this time. I also suggest regular exercise to stabilize energy levels. Should you get irritable or have difficulty sleeping, supplement with 200 to 500 mg of magnesium citrate before bed.
My favorite detoxification rituals include a sauna, meditation and yoga. I provide powerful techniques to relax and combat stress on my website.
If you can handle it, remove coffee from your diet for three weeks and add it back in slowly. Be attentive to how you feel once you reintroduce coffee. Pay attention to your energy levels, symptoms (like anxiety or jittery feelings) or changes in digestion.
In other words, monitor how you personally respond to coffee. You are your own best doctor here.
It’s perfectly fine if you realize coffee just does not work for you. Other health-friendly beverages include green tea or non-coffee-based lattes using reishi powder and other powerful herbs.
If you find you can occasionally tolerate coffee, avoid adding milk and sugar. These two culprits do more damage than the actual coffee.
Alternately, add fat to your coffee. Once people taste the creamy, frothy goodness of fat blended with coffee, they don’t miss milk at all. You’ve probably heard of Bulletproof® Coffee, which blends MCT oil and a bit of grass-fed butter or ghee with high-quality, organic coffee. If you are a vegan, try adding 1 tablespoon of cashew butter for the creamy texture.
This delicious beverage keeps me satiated for hours, cuts cravings and keeps my brain extremely sharp. You can also drink this before exercise for steady energy levels without coffee’s crash.
Here is a version of my friend Dave Asprey’s Bulletproof Coffee:
In a blender, add:
- 2 cups of hot coffee (regular or decaf), ideally fresh brewed with organic beans
- 2 tablespoons of grass-fed butter or ghee
- 2 tablespoons of organic coconut oil or 2 Tablespoons of MCT oil
- ½ teaspoon of organic cinnamon (optional) or 1 teaspoon of organic cocoa powder for a mocha
Blend until creamy. For best results, I suggest using a metal mesh filter in your drip coffee maker or a French press.
Note: Always be very careful when pureeing hot liquids in a blender. The heat from the liquid can cause the pressure in the blender to build up under the lid, and when the blender is turned on, the top can blow off and your hot soup will go everywhere. Keep the lid vented by removing the small window insert from the middle of the blender lid; hold a towel over the open window to prevent splattering. Always start on the lowest speed possible.
The bottom line is that much no one-size-fits-all approach exists for diet and lifestyle, and that includes your coffee intake.
One person may be able to enjoy raw, cruciferous vegetables while another needs to avoid them because of digestive issues. This same thing applies to coffee. For some people it works; others, not so much.
If you’re a coffee drinker, have you ever felt like you’ve over-relied on this popular beverage? If you temporarily gave it up, how did it affect you? Comment below or on my Facebook page. And be sure to submit your questions to drhyman.com.
Wishing you health and happiness,
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Like the flawed Frontline documentary, like New York state’s attorney general, US Attorney General Loretta Lynch is spreading gross misinformation about dietary supplements. Action Alert!
Last week, Attorney General Lynch released a video for National Consumer Protection Week about supplements. Excuse us, but since when is the US attorney general an expert on this subject? Since she obviously isn’t, she must be relying on distortions and untruths she has been fed by other agencies of the government such as the FDA and Centers for Disease Control.
For instance, Ms. Lynch warns consumers against “ingesting substances whose safety and efficacy are not guaranteed” by FDA study. As we pointed out in our response to PBS, pharmaceutical drugs are also not studied by the FDA. The agency relies on industry studies to determine if new drugs can come to market. No independent review is done to check the industry’s results, which has led to all kinds of manipulation and sometimes disastrous outcomes (see the examples of Vioxx and Avandia). And after approval is granted, the actual medicine itself is never tested, even though it may be manufactured in Chinese plants or other faraway locales.
FDA approval is certainly no guarantor of safety. Consider that pharmaceutical drugs, when properly prescribed, cause an estimated 1.9 million hospitalizations and 128,000 deaths each year. And that’s just in hospitals—deaths outside hospitals would add considerably to this total if they were recorded. In stark contrast, dietary supplements caused zero deaths in 2013, the last year reported.
Ms. Lynch also charges that supplements “endanger public health” by containing harmful ingredients. The supplement industry—like all industries—has some bad actors. But supplements that contain unsafe ingredients are already “adulterated” which means that the FDA has a responsibility to remove them and prosecute the makers. Nor does Ms. Lynch mention that supplement companies must follow stringent guidelines known as current good manufacturing practices (cGMPs) intended to ensure the safety and quality of dietary supplements. In other words, supplements are federally regulated.
Finally, Ms. Lynch says that many supplements “falsely claim to cure illness and disease.” As a student of the law, Ms. Lynch must be aware that the FTC and FDA regulate what can be said on supplement labels. By law, supplements cannot make disease claims—only drugs can. Any supplement that does make such claims is therefore breaking the law. We don’t agree with this law, but if it isn’t being followed why doesn’t the government simply enforce the law. In past years, FDA memos have indicated that sometimes the agency does not enforce the law on purpose, in the hopes that an ensuing scandal will lead to even more federal control over supplements. The cost of this would in turn drive their cost sky high and largely eliminate them as competition for drugs.
No, Ms. Lynch, supplements are regulated, are safe, and are effective. Just the opposite of what you suggested. You are not a doctor or scientist. But as the top law enforcement official of the country, you can at least get your law right.
Action Alert! Write to Attorney General Loretta Lynch and urge her to correct the misinformation she spread to consumers about dietary supplements. Please send your message immediately.
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The “standard”, if you have ever had a cardiac “event” or coronary artery disease, is to immediately place you on a statin (for the rest of your life) and, in most cases (exception: if you have ulcer issues) low-dose aspirin as a low-level anticoagulant.
Here’s the problem: It doesn’t work because it’s not targeting where the actual issue resides.
This has now been known since 2004, when this study published; the study itself was initiated in 1999. 304 patients with a history of coronary artery disease were tested and baselined. Only those with normal glucose levels were accepted into the study; clinical diabetes was an exclusionary factor. 202 of the 304 were excluded at baseline for this reason, leaving the study authors with 102 patients.
The results ought to wake you up; they’re here in this table.
The CVE+ entries are for those who had a second cardiac event during the three years of the study, the CVE- entries are for those who did not. ALL of the CVE+ entries had elevated (by double on average) insulin levels despite both groups having normal blood glucose.
Further, those who had a second event had no material difference in cholesterol levels compared to those who did not. In other words “management” of cholesterol levels was not protective. Finally, there was a material difference in statin use — in the negative sense, in that a greater percentage of those who had an event were taking a statin (and a nitrate!) than those who didn’t, and even worse, aspirin wasn’t protective either.
One cautionary note: All of these results are associative, as they must be in such a study. Even though the divergence in insulin levels was ridiculous between the two groups that does not prove causation.
But remember — while associations can provide strong evidence of a connection they are just as valuable, if not more-so, in disproving said connections. In this case it appears that both statins and aspirin are worthless when it comes to preventing a second CAD event.
Further, since all of the participants had normal glucose levels there is no intervention that targets “diabetes management” which helps in this case. Indeed the study showed that “management” of diabetes symptoms (specifically, blood glucose levels) that allows high insulin to persist may actually potentiate — that is, cause — the second heart attack and CAD event.
There is no medicine for the condition of high insulin — that is, “insulin resistance.” We can and do treat the symptom that it (eventually) produces, that is, high blood glucose, but the cause of the high glucose remains unaddressed.
There is, however, a means to improve your insulin sensitivity — that is, to move yourself either from that second column to the first one or at least get closer to it: Get all of the vegetable oils and carbohydrates (that is, grains and starches including breads, cereals and similar), with the exception of green vegetables and modest amounts of fruit, out of your diet.
Again — this study has been out since 2004. Why hasn’t your doctor — and especially, if you have one, your cardiologist — told you?
Further, if you’ve got evidence of CAD in your medical history why hasn’t your insulin sensitivity (NOT just cholesterol and glucose tolerance) been tested and monitored? Is it because there is no pill for it and that the actual means of improvement available to us require admitting that the so-called “standard recommendations” for what to eat, especially for those with heart disease, are exactly backward?
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The World Health Organization (WHO) just announced that red meat is “probably carcinogenic to humans.”
Yep–Right up there with glyphosate, cigarettes, alcohol and asbestos.
——–> insert facepalm <——–
This announcement is absurdly misguided and largely based upon the notoriously two least reliable forms of science we have:
1) Observational studies driven by…
2) Food questionnaires
(By the way, what did YOU have for lunch on Thursday of last week/month year?)
This is all fully based on the idea of “guilt by weak association” and any rational person knows that association is NOT causation.
UGH–Back to the nutritional Dark Ages we go…
The WHO seems to be mostly citing evidence from research based on observational studies and food questionnaires published in the Archives of Internal Medicine in 2012, which included an analysis of “two prospective cohort studies.” Similar in its failures to the ill-conceived and embarrassingly poor 2011 World Cancer Research Fund “Meta-analysis”—also entirely based upon observational studies and questionnaires— ZERO distinction was made between feedlot meat and 100% grass-fed meat (a potentially huge distinction), and no real effort was made to distinguish the effect of the red meat from whatever else people happened to be eating. What did they include as “red meat?” McDonald’s hamburgers, pizza, hot dogs, tacos, bologna, nitrate-laced bacon and feedlot meat (GMO-fed and God knows what else). Although they did graciously concede that red meat is “only slightly less hazardous than preserved meats.” And red meat consumption was not separated in any way from whatever else anyone was eating or doing to their health (alcohol intake, sugar consumption, grains, etc. or other lifestyle factors). And since 97% of all meat production is commercial feedlot-based, grass-fed meat likely didn’t even factor into these results at all.
Suspiciously, too, the Archives of Internal Medicine study used what is called relative risk to show their results. “Relative risk” is frequently used to make things look far worse than they are—rather than what is called absolute risk, which really tells it like it is (but might make your results look less dramatic and, well, boring and meaningless).
It is a significant fact that cancer has been consistently reported to be extremely rare to even non-existent in red meat-eating, hunter-gatherer societies., What in particular has characterized the difference between even Neolithic hunter-gatherer diets and the modern-day Western diet causing us so much trouble now? Data from 229 hunter-gatherer societies included in the Revised Ethnographic Atlas indicate that hunter-gatherer diets differ from typical Western ones in basically two aspects: first, a strong reliance on animal foods (45-65% of energy or E%) and second, the consumption of low-GI [glycemic index] plant foods such as fibrous vegetables, some fruits, nuts and seeds. But we also need to take the quality of the foods they had available to them into account and the very, very different nutrient/fatty acid profile between feedlot meat and 100% naturally grass-fed meat/wild game. Grain fed meats are predominated by potentially inflammatory omega-6 content (while being nearly devoid of healthy omega-3’s), versus 100% grass-fed and finished meat (and wild game) which supplies a high percentage of highly anti-inflammatory omega-3 fatty acids (EPA/DHA). Omega-3’s have additionally shown some significant anti-cancer benefits.  
Quality counts for a LOT and we all need to start taking that seriously. Deadly seriously.
In spite of the WHO declaration, other research has shown no meaningful link between diets higher in dietary animal fat and increased cancer risk., With respect to colon cancer, alone, there are many, many more (and better designed) studies finding little to no significant association with red meat and cancer than those that do, some even showing an actual lowered risk!              
With respect to Paleo—at least the form of Paleo I personally recommend and the form adopted by The Paleo Way, bases its meat consumption overall on two very distinct recommendations:
- Red meat should only come from 100% pasture fed and finished animals. NO feedlot and/or commercial processed meat!
- I recommend meat/protein in general to be consumed in strict moderation—no more than about 1 gram per kg of ideal body weight (i.e., approximating the weight of a person’s lean tissue mass)
Excessive protein from any source is potentially bad by virtue of 1) its up-regulation of proliferative mTOR pathways 2) its increase of IGF-1, which increases non-specific cellular proliferation and 3) the excess presence of glutamine and 4) protein in excess of what we need in order to meet our basic requirements is readily (up to 40% or so) converted to sugar and used the same way. –And SUGAR (not red meat) is cancer’s #1 most essential metabolic fuel.
With respect to the benefits of exclusively grass-fed meat (over feedlot meat), a particular form of fat that has been more recently lauded for its anti-cancer benefits is one exclusively found in the fat of animals fed on nothing but natural pasture.     In fact, CLA may be one of the most broadly beneficial and potent cancer-fighting substances in our diet. It is somewhat uniquely able to (in very small amounts) block all three stages of cancer: 1) initiation 2) growth/promotion and 3) metastasis. Most “anticancer nutrients” are typically helpful in only one of these areas. To date, beneficial effects of natural CLA from animal fat have been found in cancers of the breast, prostate, colon and skin. In animal studies, as little as one half of one percent CLA in the diet of experimental animals reduced tumor burden by more than 50 percent. As if this wasn’t exciting enough, there is more direct evidence that CLA may reduce cancer risk in humans. In a Finnish study, women who had the highest levels of CLA in their diet had a 60 percent lower risk of breast cancer than those having the lowest levels. Switching from grain-fed to exclusively grass-fed meat literally places women in this lowest risk category!
Additionally, French researchers measured CLA levels in the breast tissues of 360 women and found that the women with the most CLA had the lowest risk of cancer. In fact, the women with the most CLA had a staggering 74% lower risk of breast cancer than the women with the least CLA.  In yet another study, human breast cancer cells were incubated in milk fat high in CLA or in an isolated form of CLA without any milk fat. The high CLA milk fat decreased cancer growth by 90 percent but the isolated CLA decreased it by only 60 percent. When the cells were incubated in the omega-6 fat, linoleic acid, found most abundantly in grain and grain-fed animals, cancer cell growth increased by 25 percent! Other women with the most CLA in their diets were also shown to have a 60% reduction overall in the incidence of breast cancer.
Other studies have additionally shown breast cancer and even colon cancer preventative benefits.    In keeping with this, CLA additionally exerts potent anti-inflammatory effects. The inherent stability of CLA also seems to maintain itself even when meat is cooked., One study pointed out the following, “Of the vast number of naturally occurring substances that have been demonstrated to have anticarcinogenic activity in experimental models, all but a handful of them are of plant origin. Conjugated linoleic acid is unique because it is present in food from animal sources, and its anticancer efficacy is expressed at concentrations close to human consumption levels.” CLA is highly abundant, too, in wild game. The implication here is that naturally occurring CLA in animal fat has always played an important role in our diets and may possibly even be a contributing factor to the near-zero incidence of cancer found in hunter-gatherer populations. For all you Aussies out there, one study reported unusually high levels of CLA in (of all things) kangaroo meat!
ONLY CLA from the fat of wild game and fully pastured animals has the real anticancer health benefits you want. Even though synthetic CLA is sold in capsules in health food stores, it lacks the beneficial form found exclusively in grass-fed meats and may even have potentially adverse effects. But I digress…
According to a research collaboration between Clemson University and the USDA in 2009, in addition to cancer-fighting CLA, fully pastured meat contains the following additional, potentially anti-cancer benefits:
- Higher in beta-carotene
- Higher in vitamin E (alpha-tocopherol)
- Higher in the B-vitamins thiamin and riboflavin and B12
- Higher in the minerals calcium, magnesium, and potassium
- Higher in total omega-3’s  
- A healthier ratio of (inflammatory) omega-6 to anti-inflammatory omega-3 fatty acids (1.65 vs. 4.84)
- Higher in trans-vaccenic acid (TVA–which can be transformed into CLA)
Also, lamb/sheep fed exclusively on pasture vs. grain contains twice as much lutein (closely related to beta-carotene but more easily absorbed), which has shown possible preventative benefits with respect to both colon and breast cancer (while additionally reducing the risk of macular degeneration).
So…in a nutshell, this WHO declaration will not change the recommendations I have been making all along. 100% grass-fed and finished meat (not just red meat, by the way) consumed in moderate amounts along with quality, organic fibrous plant-based foods has been and will continue to be among my foundational recommendations for optimal health.
~ Nora Gedgaudas, CNS, CNT, BCHN
“Red meat is NOT bad for you. Now blue-green meat, THAT’S bad for you!”
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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: