Will a Nicotine Patch Make You Smarter?

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.

Nicotine PatchIn 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

The Art and Science of Nutritional Ketosis

Carbohydrate restricted diets are commonly practiced but seldom taught. As a result, doctors, dietitians, nutritionists, and nurses may have strong opinions about low carbohydrate dieting, but in many if not most cases, these views are not grounded in science.

“The Art and Science of Nutritional Ketosis” was presented by Stephen Phinney, MD, PhD, UC Davis at the University of California on November 16th, 2012. It will inspire you to think more carefully about sugars and starches in your diet, and empower you with essential knowledge to help you achieve long-lasting health and well-being.

 

The Ketogenic Diet – An Overview

A ketogenic diet is based on animal fat sources.

A ketogenic diet is based on animal fat sources.

Ketosis is an often misunderstood subject. Its presence is thought to be equal to starvation or a warning sign of something going wrong in your metabolism. But nothing could be farther from the truth, except if you are an ill-treated type 1 diabetic person.[1] Ketones – contrary to popular belief and myth – are a much needed and essential healing energy source in our cells that comes from the normal metabolism of fat.

The entire body uses ketones in a more safe and effective way that the energy source coming from carbohydrates – sugar AKA glucose. Our bodies will produce ketones if we eat a diet devoid of carbs or a low carb diet (less than 60 grams of carbs per day).[2] By eating a very low carb diet or no carbs at all (like a caveman) we become keto-adapted.

In fact, what is known today as the ketogenic diet was the number one treatment for epilepsy until Big Pharma arrived with its dangerous cocktails of anti-epileptic drugs. It took several decades before we heard again about this diet, thanks in part to a parent who demanded it for his 20-month-old boy with severe seizures. The boy’s father had to find out about the ketogenic diet in a library as it was never mentioned as an option by his neurologist. After only 4 days on the diet, his seizures stopped and never returned.[3] The Charlie Foundation was born after the kid’s name and his successful recovery, but nowadays the ketogenic diet is available to the entire world and it’s spreading by word of mouth thanks to its healing effects.

It is not only used as a healthy lifestyle, it is also used for conditions such as infantile spasms, epilepsy, autism, brain tumors, Alzheimer’s disease, Lou Gehrig’s disease, depression, stroke, head trauma, Parkinson’s disease, migraine, sleep disorders, schizophrenia, anxiety, ADHD, irritability, polycystic ovarian disease, irritable bowel syndrome, gastroesophageal reflux, obesity, cardiovascular disease, acne, type 2 diabetes, tremors, respiratory failure and virtually every neurological problem but also cancer, and conditions were tissues need to recover after a loss of oxygen.[4]

Our body organs and tissues work much better when they use ketones as a source of fuel, including the brain, heart and the core of our kidneys. If you ever had a chance to see a heart working in real time, you might have noticed the thick fatty tissue that surrounds it. In fact, heart surgeons get to see this every day. A happy beating heart is one that is surrounded by layers of healthy fat. Both the heart and the brain run at least 25% more efficiently on ketones than on blood sugar.

Ketones are the ideal fuel for our bodies unlike glucose – which is damaging, less stable, more excitatory and in fact shortens your life span. Ketones are non-glycating, which is to say, they don’t have a caramelizing aging effect on your body. A healthy ketosis also helps starve cancer cells as they are unable to use ketones for fuel, relying on glucose alone for their growth. [5] The energy producing factories of our cells – the mitochondria – work much better on a ketogenic diet as they are able to increase energy levels on a stable, long-burning, efficient, and steady way. Not only that, a ketogenic diet induces epigenetic changes[6] which increases the energetic output of our mitochondria, reduces the production of damaging free radicals, and favors the production of GABA – a major inhibitory brain chemical. GABA has an essential relaxing influence and its favored production by ketosis also reduces the toxic effects of excitatory pathways in our brains. Furthermore, recent data suggests that ketosis alleviates pain other than having an overall anti-inflammatory effect. [7]

The ketogenic diet acts on multiple levels at once, something that no drug has been able to mimic. This is because mitochondria is specifically designed to use fat for energy. When our mitochondria uses fat as an energetic source, its toxic load is decreased, expression of energy producing genes are increased, its energetic output is increased, and the load of inflammatory energetic-end-products is decreased.

The key of these miraculous healing effects relies in the fact that fat metabolism and its generation of ketone bodies (beta-hydroxybutyrate and acetoacetate) by the liver can only occur within the mitochondrion, leaving chemicals within the cell but outside the mitochondria readily available to stimulate powerful anti-inflammatory antioxidants.  The status of our mitochondria is the ultimate key for optimal health and while it is true that some of us might need extra support in the form of nutritional supplementation to heal these much needed energy factories, the diet still remains the ultimate key for a proper balance.

Our modern world’s staple energetic source is sugar which needs to be processed first in the cell soup before it can be passed into the energy factory of the cell- the mitochondrion. Energy sources from fat don’t require this processing; it goes directly into the mitochondria for energetic uses.  That is, it is more complicated to create energy out of sugar than out of fat. As Christian B. Allan, PhD and Wolfgang Lutz, MD said in their book Life Without Bread:

Carbohydrates are not required to obtain energy. Fat supplies more energy than a comparable amount of carbohydrate, and low-carbohydrate diets tend to make your system of producing energy more efficient. Furthermore, many organs prefer fat for energy.

The fact is you get MORE energy per molecule of fat than sugar. How many chronic and autoimmune diseases have an energy deficit component?  How about chronic fatigue?  Fibromyalgia?  Rheumatoid Arthritis?  Multiple Sclerosis? Cancer? Back to Allan and Lutz:

Mitochondria are the power plants of the cell. Because they produce most of the energy in the body, the amount of energy available is based on how well the mitochondria are working. Whenever you think of energy, think of all those mitochondria churning out ATP to make the entire body function correctly. The amount of mitochondria in each cell varies, but up to 50 percent of the total cell volume can be mitochondria. When you get tired, don’t just assume you need more carbohydrates; instead, think in terms of how you can maximize your mitochondrial energy production…

If you could shrink to a small enough size to get inside the mitochondria, what would you discover? The first thing you’d learn is that the mitochondria are primarily designed to use fat for energy!

In short, let fat be thy medicine and medicine be thy fat!

You will think that with all of this information we would see ketogenic diets recommended right and left by our health care providers, but alas, that is not the case. Mainstream nutritionists recommend carbohydrates AKA sugar as the main staple of our diets. The problem with this (and there are several of them) is that in the presence of a high carb diet we are unable to produce ketones from the metabolism of fats, thus, depriving ours bodies from much healing ketone production.  The fact that we live in a world which uses glucose as a primary fuel means that we eat a very non healing food in more ways than one.

I have been doing the low carb diet for about a week and a half now and I must say, I am really starting to feel amazing!!!  The first few days my head hurt, I felt lethargic, and my legs felt so heavy. But after I got past that, I have so much energy. I don’t get tired anymore around 3pm. The best part is, I am not constantly thinking and obsessing about food. I feel a real sense of inner calm. My skin looks better, my hair looks better too. I have been having bacon and eggs for breakfast, a pork chop or other piece of meat for lunch, and usually some pork and sometimes some green beans for dinner. I have also lost some weight!  Woo hoo!!! -Angela, United States. Sott.net forum.

 

We have been on a ketogenic diet for nearly three million years and it has made us human. It was the lifestyle in which our brains got nurtured and evolved. But not anymore, unless we all make an effort to reclaim this lost wisdom. Nowadays the human brain is not only shrinking, but brain atrophy is the norm as we age and get plagued with diseases such as Alzheimer’s disease, Parkinson’s disease, senile dementia and so forth.

In the mean time new research is starting to elucidate the key role of our mitochondria in the regulation of the cell cycle – the vital process by which a single celled fertilized egg develops into a mature organism, as well as the process by which hair, skin, blood cells, and some internal organs are renewed. In the complicated and highly choreographed events surrounding cell-cycle progression, mitochondria are not simple bystanders merely producing energy but instead are full-fledged participants.[8] Given the significant amount of energy needed to make all the nutrients required for cell division, it makes sense that some coordination existed. This long ignored and overlooked connection between the mitochondria and the cell cycle is something that is worthy of considerable more attention as we understand the role of diet in our bodies. We’ll have to take a closer look to this subject of ketosis, as it really holds the key to unlock our transformational pathways that will lead us to an outstanding healthy living.

Mitochondrial Dysfunction

Mitochondria are best known as the powerhouses of our cells since they produce the cell’s energy. But they also lead the genetic orchestra which regulates how every cell ages, divides, and dies. They help dictate which genes are switched on or off in every single cell of our organism. They also provide the fuel needed to make new brain connections, repair and regenerate our bodies.

Whether we are housewives, sportsmen or labor people, energy is a topic that concerns us all, every day and in every way. Our well being, behavior and ability to perform the tasks in front of us to do is our individual measure of energy. But how we derive energy from the foods that we eat?

There are many man-made myths surrounding energy production in the body and which foods supply energy. Mainstream science says that carbohydrates are what mitochondria use as fuel for energy production. This process is called oxidative metabolism because oxygen is consumed in the process. The energy produced by mitochondria is stored in a chemical “battery”, a unique molecule called adenosine triphosphate (ATP). Energy-packed ATP can then be transported throughout the cell, releasing energy on demand of specific enzymes. In addition to the fuel they produce, mitochondria also create a by-product related to oxygen called reactive oxygen species (ROS), commonly known as free radicals. But what we are not told is that mitochondria were specifically designed to use fat for energy, not carbohydrate.

Source: Christian B. Allan, PhD and Wolfgang Lutz, MD, Life Without Bread.There are several very complicated steps in making ATP within mitochondria, but a look at 5 major parts of ATP production will be all that you need to know in order to understand how energy is created within our mitochondria and why fats are the key to optimize their function. Don’t get focused on specific names, just try to see the whole picture.Step 1 – Transportation of Food-Based Fuel Source into the MitochondriaFuel must first get into the mitochondria where all the action happens. Fuel can come from carbs or it can come from fats. Fatty acids are the chemical name for fat, and medium and large sized fatty acids get into the mitochondria completely intact with the help of L-carnitine. Think of L-carnitine as a subway train that transports fatty acids into the mitochondria. L-carnitine (from the Greek word carnis means meat or flesh) is chiefly found in animal products.Fuel coming from carbs needs to get broken down first outside the mitochondria and the product of this breakdown (pyruvate) is the one who gets transported inside the mitochondria, or it can be used to produce energy in a very inefficient way outside the mitochondria through anaerobic metabolism which produces ATP when oxygen is not present.

Step 2 – Fuel is Converted into Acetyl-CoA

When pyruvate – the product of breaking down carbs – enters the mitochondria, it first must be converted into acetyl-CoA by an enzymatic reaction.

Fatty acids that are already inside the mitochondria are broken down directly into acetyl-CoA in what is called beta-oxidation.

Acetyl-CoA is the starting point of the next step in the production of ATP inside the mitochondria.

Step 3 – Oxidation of Acetyl-CoA and the Krebs Cycle

The Krebs cycle (AKA tricarboxylic acid cycle or citric acid cycle) is the one that oxidizes the acetyl-CoA, removing thus electrons from acetyl-CoA and producing carbon dioxide as a by-product in the presence of oxygen inside the mitochondria.

Step 4 – Electrons Are Transported Through the Respiratory Chain

The electrons obtained from acetyl-CoA – which ultimately came from carbs or fats – are shuttled through many molecules as part of the electron transport chain inside the mitochondria. Some molecules are proteins, others are cofactors molecules. One of these cofactors is an important substance found mainly in animal foods and it is called coenzyme Q-10. Without it, mitochondrial energy production would be minimal. This is the same coenzyme Q10 that statins drug block producing crippling effects on people’s health. Step 4 is also where water is produced when oxygen accepts the electrons.

Step 5 – Oxidative phosphorylation

As electrons travel down the electron transport chain, they cause electrical fluctuations (or chemical gradients) between the inner and outer membrane in the mitochondria. These chemical gradients are the driving forces that produce ATP in what is called oxidative phosphorylation. Then the ATP is transported outside the mitochondria for the cell to use as energy for any of its thousands of biochemical reactions.

But why is fat better than carbs?

If there were no mitochondria, then fat metabolism for energy would be limited and not very efficient. But nature provided us during our evolution with mitochondria that specifically uses fat for energy. Fat is the fueled that animals use to travel great distances, hunt, work, and play since fat gives more packed-energy ATPs than carbs. Biochemically, it makes sense that if we are higher mammals who have mitochondria, then we need to eat fat.  Whereas carb metabolism yields 36 ATP molecules from a glucose molecule, a fat metabolism yields 48 ATP molecules from a fatty acid molecule inside the mitochondria. Fat supplies more energy for the same amount of food compared to carbs. But not only that, the burning of fat by the mitochondria – beta oxidation – produces ketone bodies that stabilizes overexcitation and oxidative stress in the brain related to all its diseases, it also causes epigenetic changes that produce healthy and energetic mitochondria and decreasing the overproduction of damaging and inflammatory free radicals among many other things!

 

Mitochondria regulate cellular suicide, AKA apoptosis, so that old and dysfunctional cells which need to die will do so, leaving space for new ones to come into the scene. But when mitochondria function becomes impaired and send signals that tell normal cells to die, things go wrong. For instance, the destruction of brain cells leads to every single neurodegenerative condition known including Alzheimer’s disease, Parkinson’s disease and so forth. Mitochondrial dysfunction has wide-ranging implications, as the health of the mitochondria intimately affects every single cell, tissue and organ within your body.

The catalysts for this destruction is usually uncontrolled free radical production which cause oxidative damage to tissues, fat, proteins, DNA; causing them to rust. This damage, called oxidative stress, is at the basis of oxidized cholesterol, stiff arteries (rusty pipes) and brain damage. Oxidative stress is a key player in dementia as well as autism.

We produce our own anti-oxidants to keep a check on free radical production, but these systems are easily overwhelmed by a toxic environment and a high carb diet, in other words, by today’s lifestyle and diet.

Mitochondria also have interesting characteristics which differentiate them from all other structural parts of our cells. For instance, they have their own DNA (referred as mtDNA) which is separate from the widely known DNA in the nucleus (referred as n-DNA),. Mitochondrial DNA comes for the most part from the mother line, which is why mitochondria is also considered as your feminine life force. This mtDNA is arranged in a ring configuration and it lacks a protective protein surrounding, leaving its genetic code vulnerable to free radical damage. If you don’t eat enough animal fats, you can’t build a functional mitochondrial membrane which will keep it healthy and prevent them from dying.

If you have any kind of inflammation from anywhere in your body, you damage your mitochondria. The loss of function or death of mitochondria is present in pretty much every disease. Dietary and environmental factors lead to oxidative stress and thus to mitochondrial injury as the final common pathway of diseases or illnesses.

Autism, ADHD, Parkinson’s, depression, anxiety, bipolar disease, brain aging are all linked with mitochondrial dysfunction from oxidative stress. Mitochondrial dysfunction contributes to congestive heart failure, type 2 diabetes, autoimmune disorders, aging, cancer, and other diseases.

Whereas the nDNA provides the information your cells need to code for proteins that control metabolism, repair, and structural integrity of your body, it is the mtDNA which directs the production and utilization of your life energy. A cell can still commit suicide (apoptosis) even when it has no nucleus nor nDNA.

Because of their energetic role, the cells of tissues and organs which require more energy to function are richer in mitochondrial numbers. Cells in our brains, muscles, heart, kidney and liver contain thousands of mitochondria, comprising up to 40% of the cell’s mass. According to Prof. Enzo Nisoli, a human adult possesses more than ten million billion mitochondria, making up a full 10% of the total body weight.[9] Each cell contains hundreds of mitochondria and thousands of mtDNA.

Since mtDNA is less protected than nDNA because it has no “protein” coating (histones), it is exquisitely vulnerable to injury by destabilizing molecules such as neurotoxic pesticides, herbicides, excitotoxins, heavy metals and volatile chemicals among others. This tips off the balance of free radical production to the extreme which then leads to oxidative stress damaging our mitochondria and its DNA. As a result we get overexcitation of cells and inflammation which is at the root of Parkinson’s disease and other diseases, but also mood problems and behavior problems.

Enough energy means a happy and healthy life. It also reflects in our brains with focused and sharp thinking. Lack of energy means mood problems, dementia, and slowed mental function among others. Mitochondria are intricately linked to the ability of the prefrontal cortex –our brain’s captain- to come fully online. Brain cells are loaded in mitochondria that produce the necessary energy to learn and memorize, and fire neurons harmoniously.

The sirtuin family of genes works by protecting and improving the health and function of your mitochondria.[10] They are positively influenced by a diet that is non-glycating, i.e. a low carb diet as opposed to a high carb diet which induces mitochondrial dysfunction and formation of reactive oxygen species.

Another thing that contributes to mitochondrial dysfunction is latent viral infection such as the ones of the herpes family. As I mentioned in On Viral “Junk” DNA, a DNA Enhancing Ketogenic Diet, and Cometary Kicks, most, if not all of your “junk” DNA has viral-like properties. If a pathogenic virus takes hold of our DNA or RNA, it could lead to disease or cancer.

Herpes simplex virus is a widespread human pathogen and it goes right after our mitochondrial DNA. Herpes simplex virus establishes its latency in sensory neurons, a type of cell that is highly sensitive to the pathological effects of mt DNA damage.[11] A latent viral infection might be driving the brain cell loss in neurodegenerative diseases such as Alzheimer’s disease.[12] As I speculated in Heart attacks, CFS, herpes virus infection and the vagus nerve , a latent herpes virus infection might drive more diseases than we would like to admit.

Members of the herpes virus family (i.e. cytomegalovirus and Epstein-Barr virus which most people have as latent infections!), can go after our mitochondrial DNA, causing neurodegenerative diseases by mitochondrial dysfunction. But a ketogenic diet is the one thing that would help stabilize mtDNA since mitochondria runs the best on fat fuel. As it happens, Alzheimer’s disease is the one condition where a ketogenic diet has its most potential healing effect.[4]

The role of mitochondrial dysfunction in our “modern” age maladies is a staggering one. Optimal energetic sources are essential if we are to heal from chronic ailments. It is our mitochondria which lies at the interface between the fuel from foods that come from our environment and our bodies’ energy demands. And it is a metabolism based on fat fuel, a ketone metabolism, the one which signals epigenetic changes that maximizes energetic output within our mitochondria and help us heal.

I am incredulous at how my body is responding.  I think I am totally carb intolerant.  I’ve struggled with extreme fatigue/exhaustion for so many years, even with improved sleep in a dark room that I can’t tell you how wonderful it is to wake up in the morning, get out of bed and not long to crawl back in, going through the day by will mostly.  Also chronic long-standing intestinal issues are finally resolving.  A couple of people at work have made comments to the effect that I’m a “different woman”, calmer, no more hyperness under pressure, stress seems to roll off of my back as well.  I’ve lost a little weight and although I don’t weigh myself, my clothes are definitely looser.  I’ve had the round middle for so many years I was resigned to struggling to bend over to pull my shoes on!  -Bluefyre, 56 years old, United States. Sott.net forum

 

Ketosis – Closer Look

The presence of ketones in the blood and urine, a condition known as ketosis, has always been regarded as a negative situation, related to starvation. While it is true that ketones are produced during fasting, ketones are also produced in times of plenty, but not plenty of carbohydrates since a carb metabolism suppresses ketosis. In the absence of most carbs in the diet, ketones will form from fat to supply for energy. This is true even if lots of fats and enough protein are eaten, something that is hardly a starvation condition.

As we already saw, a ketogenic diet has been proved useful in a number of diseases, especially neurological ones. Strictly speaking, a ketogenic diet is a high fat diet in which carbohydrates are either completely eliminated or nearly eliminated so that the body has the very bare minimum sources of glucose. That makes fats (fatty acids) a mandatory energetic fuel source for both the brain and other organs and tissues. If you are carb intake is high, you’ll end up storing both the fat and the carbs in your fat tissue thanks to the hormone insulin. A ketogenic diet is not a high protein diet, which as it happens, can also stimulate insulin. It is basically a diet where you rely primarily on animal foods and especially their fats.

I recently had my annual blood work done (cholesterol, etc.) During the review, my doctor said that everything looked great! He then encouraged me to continue on my great ‘low fat, high fruit and veggie diet’ that I must be following! I just smiled. Next visit I’m going to tell him about my real ‘diet’. Lol  -1984, United States. Sott.net forum.

 

Among the by-products of fat burning metabolism are the so called ketone bodies – acetoacetate, β-hydroxybutyrate and acetone – which are produced for the most part by the liver. When our bodies are running primarily on fats, large amounts of acetyl-CoA are produced which exceed the capacity of the Krebs cycle, leading to the making of these three ketone bodies within liver mitochondria. Our levels of ketone bodies in our blood go up and the brain readily uses them for energetic purposes. Ketone bodies cross the blood brain barrier very readily. Their solubility also makes them easily transportable by the blood to other organs and tissues. When ketone bodies are used as energy, they release acetyl-CoA which then goes to the Krebs cycle again to produce energy.

In children who were treated with the ketogenic diet to treat their epilepsy, it was seen that they become seizure-free even long after the diet ended, meaning that not only did the diet proved to be protective, but also it modified the activity of the disease , something that no drug has been able to do.[13] In Alzheimer’s disease, as levels of ketone bodies rise, memory improves. People’s starved brains finally receive the much needed fats they need! In fact, every single neurological disease is improved on the ketogenic diet.

The benefits of a ketogenic diet can be seen as fast as one week, developing gradually over a period of 3 weeks. There are several changes in gene expression involving metabolism, growth, development, and homeostasis among others.

The hippocampus is a region in your brain that is very vulnerable to stress which makes it lose its brain cells. The hippocampus has to do with memory, learning, and emotion. As it happens, a ketogenic diet promotes the codification of genes which creates mitochondria in the hippocampus, making more energy available. A larger mitochondrial load and more energy means more reserve to withstand much more stress.[14]

In some animal models, there is a 50% increase in the total number of mitochondria in the hippocampus, resulting in more brain ATP.[15] Other animal studies show how communication between brain cells in the hippocampus would remain smooth for 60% longer when exposed to a stressful stimulus compared to their counterparts who didn’t had a ketogenic diet.[16] This is very important since too much stress can damage the hippocampus and its capacity to retrieve information, making you “absent-minded” or “brain-scattered”, as well as affecting the ability of your prefrontal cortex to think and manage behavior.

A ketogenic diet also increases levels of the calming neurotransmitter – GABA which then serves to calm down the overexcitation which is at the base of major neurodegenerative diseases, but also anxiety and other mood problems. A ketogenic diet also increases antioxidant pathways that level the excess production of free radicals from a toxic environment. It also enhances anti-inflammatory pathways.

Ketosis also cleans our cells from proteins that act like “debris” and which contribute to aging by disrupting a proper functioning of the cell.[17] It basically does this by what is known as autophagy which preserves the health of cells and tissues by replacing outdated and damaged cellular components with fresh ones. This prevents degenerative diseases, aging, cancer, and protects you against microbial infections.A ketogenic diet not only rejuvenates you, it also makes a person much less susceptible to viruses and bacterial infections.[18] This is very relevant due to the increasing number of weird viral and bacterial infections that seem to be incoming from our upper atmosphere[19] (for more information see New Light on the Black Death: The Viral and Cosmic Connection), or due to high levels of radiation that creates more pathogenic strains (see Detoxify or Die: Natural Radiation Protection Therapies for Coping With the Fallout of the Fukushima Nuclear Meltdown). Either or, we are more vulnerable than ever due to the state of our mitochondria. But we can prepare for the worst with ketosis.

Ketone-enhanced autophagy is very important because autophagy can target viruses and bacteria that grow inside cells which are very problematical.[20] Intracellular viruses and bacteria can lead to severe mitochondrial dysfunction and ketosis remains by far our best chance against them.

fig 1 ket rev.pptxKetone bodies production through intermittent fasting and the ketogenic diet is the most promising treatment for mitochondrial dysfunction.[21] The longevity benefits seen caloric restriction research is due to the fact that our bodies shift to a fat burning metabolism within our mitochondria. With a ketogenic diet, we go into a fat burning metabolism without restricting our caloric intake.

Ketosis deals effectively with all the problems of a diet rich in carbs – the one recommended by mainstream science: anxiety, food cravings, irritability, tremors, and mood problems among others. It is a crime to discourage the consumption of a high fat diet considering that a ketogenic diet shrinks tumors on human and animal models, and enhances our brain’s resiliency against stress and toxicity.

In addition to increasing the production of our body’s natural valium – GABA – the increased production of acetyl-CoA generated from the ketone bodies also drives the Krebs cycle to increase mitochondrial NADH (reduced nicotinamide adenine nucleotide) which our body uses in over 450 vital biochemical reactions – including the cell signaling and assisting of the ongoing DNA repair. Because the ketone body beta-hydroxybutyrate is more energy rich than pyruvate, it produces more ATP. Ketosis also enhances the production of important anti-oxidants that deal with toxic elements from our environments, including glutathione.

Mitochondria from the hippocampus of ketogenic diet-fed animals are also resistant to mtDNA damage and are much less likely to commit cell suicide –apoptosis- at inappropriate times.

As Douglas C. Wallace, PhD, Director of the Center for Mitochondrial and Epigenomic Medicine says, “the ketogenic diet may act at multiple levels: It may decrease excitatory neuronal activity, increase the expression of bioenergetic genes, increase mitochondrial biogenesis and oxidative energy production, and increase mitochondrial NADPH production, thus decreasing mitochondrial oxidative stress.”[21]

Keto-adaptation results in marked changes in how we construct and maintain optimum membrane (“mem-brain”) composition, not only because of the healthy fats we provide through the diet, but also because of less free radical production and inflammatory mediators, along with more production of anti-oxidants. It is really the ideal balanced state.

Moreover, you might want to keep in mind this excerpt from Human Brain Evolution: The Influence of Freshwater and Marine Food Resources[22]:

There are two key advantages to having ketone bodies as the main alternative fuel to glucose for the human brain. First, humans normally have significant body fat stores, so there is an abundant supply of fatty acids to make ketones. Second, using ketones to meet part of the brain’s energy requirement when food availability is intermittent frees up some glucose for other uses and greatly reduces both the risk of detrimental muscle breakdown during glucose synthesis, as well as compromised function of other cells dependent on glucose, that is, red blood cells. One interesting attribute of ketone uptake by the brain is that it is four to five times faster in newborns and infants than in adults. Hence, in a sense, the efficient use of ketones by the infant brain means that it arguably has a better fuel reserve than the adult brain. Although the role of ketones as a fuel reserve is important, in infants, they are more than just a reserve brain fuel – they are also the main substrate for brain lipid synthesis.

I have hypothesized that evolution of a greater capacity to make ketones coevolved with human brain expansion. This increasing capacity was directly linked to evolving fatty acid reserves in body fat stores during fetal and neonatal development. To both expand brain size and increase its sophistication so remarkably would have required a reliable and copious energy supply for a very long period of time, probably at least a million, if not two million, years. Initially, and up to a point, the energy needs of a somewhat larger hominin brain could be met by glucose and short – term glucose reserves such as glycogen and glucose synthesis from amino acids. As hominins slowly began to evolve larger brains after having acquired a more secure and abundant food supply, further brain expansion would have depended on evolving significant fat stores and having reliable and rapid access to the fuel in those fat stores. Fat stores were necessary but were still not sufficient without a coincident increase in the capacity for ketogenesis. This unique combination of outstanding fuel store in body fat as well as rapid and abundant availability of ketones as a brain fuel that could seamlessly replace glucose was the key fuel reserve for expanding the hominin brain, a reserve that was apparently not available to other land – based mammals, including nonhuman primates.

It is indisputable that a ketogenic diet has protective effects in our brains. With all the evidence of its efficacy in mitochondrial dysfunction, it can be applied for all of us living in a highly stressful and toxic environment. Ketone bodies are healing bodies that helped us evolve and nowadays our mitochondria are always busted in some way or another since the odds in this toxic world are against us. Obviously, there are going to be people with such damaged mtDNA or with mutations they were born with, who can’t modify their systems (i.e. defects on L-carnitine metabolism), but even in some of those cases, they can halt or slow down further damage. Our healthy ancestors never had to deal with the levels of toxicity that we live nowadays and nevertheless, they ate optimally. Considering our current time and environment, the least we can do is eat optimally for our physiology.

The way to have healing ketone bodies circulating in our blood stream is to do a high fat, restricted carb and moderated protein diet. Coupled with intermittent fasting which will enhance the production of ketone bodies, and resistance training which will create mitochondria with healthier mtDNA, we can beat the odds against us.

What is considered nowadays a “normal diet” is actually an aberration based on the corruption of science which benefits Big Agra and Big Pharma. If we would go back in time to the days before the modern diet became normalized by corporative and agricultural interests, we will find that ketosis was the normal metabolic state. Today’s human metabolic state is aberrant. It is time to change that.

Source: health-matrix.net

References

[1] A research member of sott.net’s forum has diabetes type 1 and is doing the ketogenic diet. On normal circumstances, diabetics (including type I) report amazing results on a low-carbohydrate diet. See Dr. Bernstein’s Diabetics Solution by Richard K. Bernstein, MD (Little, Brown and Company: 2007).

[2] It varies among each person, but the general range is between 0 and 70 grams of carbs plus moderate intake of protein, between 0.8 and 1.5 grams of protein per kg of ideal body weight. Pregnant women and children should not have their protein restricted.

[3] Ketogenic diets in seizure control and neurologic disorders by Eric Kossoff, MD, Johns Hopkins Hospital, Baltimore, Maryland. The Art and Science of Low Carbohydrate Living by Jeff S. Volek, PhD, Rd and Stephen D. Phinney, MD, PhD. Beyond Obesity, LLC , 2011.

[4]A Paoli, A Rubini, J S Volek and K A Grimaldi. Beyond weight loss: a review of the therapeutic uses of very-low-carbohydrate (ketogenic) diets. European Journal of Clinical Nutrition (2013) 67, 789–796

[5] Rainer J Klement, Ulrike Kämmerer. Is there a role for carbohydrate restriction in the treatment and prevention of cancer? Nutr Metab (Lond). Oct 26, 2011; 8: 75.

[6] If the genetic code is the hardware for life, the epigenetic code is software that determines how the hardware behaves.

[7] David N. Ruskin and Susan A. Masino, The Nervous System and Metabolic Dysregulation: Emerging Evidence Converges on Ketogenic Diet Therapy. Front Neurosci. 2012; 6: 33.

[8] Finkel T, Hwang PM. The Krebs cycle meets the cell cycle: mitochondria and the G1-S transition. Proc Natl Acad Sci U S A. 2009 Jul 21;106(29):11825-6.

[9] Matthews C.M. Nurturing your divine feminine. Proc (Bayl Univ Med Cent). 2011 July; 24(3): 248.

[10] Hipkiss AR. Energy metabolism, altered proteins, sirtuins and ageing: converging mechanisms? Biogerontology. 2008 Feb;9(1):49-55.

[11] Saffran HA, Pare JM, Corcoran JA, et al. Herpes simplex virus eliminates host mitochondrial DNA. EMBO Rep. 2007 Feb;8(2):188-93.

[12] Porcellini E, Carbone I, et al. Alzheimer’s disease gene signature says: beware of brain viral infections. Immun Ageing. 2010 Dec 14;7:16.

[13] Gasior M, Rogawski MA, Hartman AL. Neuroprotective and disease-modifying effects of the ketogenic diet. Behav Pharmacol. 2006 Sep;17(5-6):431-9.

[14] Maalouf M, Rho JM, Mattson MP. The neuroprotective properties of calorie restriction, the ketogenic diet, and ketone bodies. Brain Res Rev. 2009 Mar;59(2):293-315.

[15] Nylen K, Velazquez JL. The effects of a ketogenic diet on ATP concentrations and the number of hippocampal mitochondria in Aldh5a1(-/-) mice. Biochim Biophys Acta. 2009 Mar;1790(3):208-12.

[16] Bough K. Energy metabolism as part of the anticonvulsant mechanism of the ketogenic diet. Epilepsia. 2008 Nov;49 Suppl 8:91-3.

[17] Finn PF, Dice JF. Ketone bodies stimulate chaperone-mediated autophagy. J Biol Chem. 2005 Jul 8;280(27):25864-70.

[18] Yuk JM, Yoshimori T, Jo EK. Autophagy and bacterial infectious diseases. Exp Mol Med. 2012 Feb 29;44(2):99-108.

[19] Chandra Wickramasinghe, Milton Wainwright & Jayant Narlika. SARS – a clue to its origins? The Lancet, vol. 361, May 23, 2003, pp 1832.

[20] Yordy B, Iwasaki A. Autophagy in the control and pathogenesis of viral infection. Curr Opin Virol. 2011 Sep;1(3):196-203.

[21] Douglas C. Wallace, Weiwei Fan, and Vincent Procaccio. Mitochondrial Energetics and Therapeutics Annu Rev Pathol. 2010; 5: 297–348.

[22] Stephen Cunnane, Kathlyn Stewart.Human Brain Evolution: The Influence of Freshwater and Marine Food Resources. June 2010, Wiley-Blackwell.

Breeding the Nutrition Out of Our Food

WE like the idea that food can be the answer to our ills, that if we eat nutritious foods we won’t need medicine or supplements. We have valued this notion for a long, long time. The Greek physician Hippocrates proclaimed nearly 2,500 years ago: “Let food be thy medicine and medicine be thy food.” Today, medical experts concur. If we heap our plates with fresh fruits and vegetables, they tell us, we will come closer to optimum health.

Noma Bar

Noma Bar

This health directive needs to be revised. If we want to get maximum health benefits from fruits and vegetables, we must choose the right varieties. Studies published within the past 15 years show that much of our produce is relatively low in phytonutrients, which are the compounds with the potential to reduce the risk of four of our modern scourges: cancer, cardiovascular disease, diabetes and dementia. The loss of these beneficial nutrients did not begin 50 or 100 years ago, as many assume. Unwittingly, we have been stripping phytonutrients from our diet since we stopped foraging for wild plants some 10,000 years ago and became farmers.

These insights have been made possible by new technology that has allowed researchers to compare the phytonutrient content of wild plants with the produce in our supermarkets. The results are startling.

Wild dandelions, once a springtime treat for Native Americans, have seven times more phytonutrients than spinach, which we consider a “superfood.” A purple potato native to Peru has 28 times more cancer-fighting anthocyanins than common russet potatoes. One species of apple has a staggering 100 times more phytonutrients than the Golden Delicious displayed in our supermarkets.

Were the people who foraged for these wild foods healthier than we are today? They did not live nearly as long as we do, but growing evidence suggests that they were much less likely to die from degenerative diseases, even the minority who lived 70 years and more. The primary cause of death for most adults, according to anthropologists, was injury and infections.

Each fruit and vegetable in our stores has a unique history of nutrient loss, I’ve discovered, but there are two common themes. Throughout the ages, our farming ancestors have chosen the least bitter plants to grow in their gardens. It is now known that many of the most beneficial phytonutrients have a bitter, sour or astringent taste. Second, early farmers favored plants that were relatively low in fiber and high in sugar, starch and oil. These energy-dense plants were pleasurable to eat and provided the calories needed to fuel a strenuous lifestyle. The more palatable our fruits and vegetables became, however, the less advantageous they were for our health.

The sweet corn that we serve at summer dinners illustrates both of these trends. The wild ancestor of our present-day corn is a grassy plant called teosinte. It is hard to see the family resemblance. Teosinte is a bushy plant with short spikes of grain instead of ears, and each spike has only 5 to 12 kernels. The kernels are encased in shells so dense you’d need a hammer to crack them open. Once you extract the kernels, you wonder why you bothered. The dry tidbit of food is a lot of starch and little sugar. Teosinte has 10 times more protein than the corn we eat today, but it was not soft or sweet enough to tempt our ancestors.

Nutritional Weaklings in the Supermarket

Nutritional Weaklings in the Supermarket

Over several thousand years, teosinte underwent several spontaneous mutations. Nature’s rewriting of the genome freed the kernels of their cases and turned a spike of grain into a cob with kernels of many colors. Our ancestors decided that this transformed corn was tasty enough to plant in their gardens. By the 1400s, corn was central to the diet of people living throughout Mexico and the Americas.

When European colonists first arrived in North America, they came upon what they called “Indian corn.” John Winthrop Jr., governor of the colony of Connecticut in the mid-1600s, observed that American Indians grew “corne with great variety of colours,” citing “red, yellow, blew, olive colour, and greenish, and some very black and some of intermediate degrees.” A few centuries later, we would learn that black, red and blue corn is rich in anthocyanins. Anthocyanins have the potential to fight cancer, calm inflammation, lower cholesterol and blood pressure, protect the aging brain, and reduce the risk of obesity, diabetes and cardiovascular disease.

EUROPEAN settlers were content with this colorful corn until the summer of 1779 when they found something more delectable — a yellow variety with sweeter and more tender kernels. This unusual variety came to light that year after George Washington ordered a scorched-earth campaign against Iroquois tribes. While the militia was destroying the food caches of the Iroquois and burning their crops, soldiers came across a field of extra-sweet yellow corn. According to one account, a lieutenant named Richard Bagnal took home some seeds to share with others. Our old-fashioned sweet corn is a direct descendant of these spoils of war.

Up until this time, nature had been the primary change agent in remaking corn. Farmers began to play a more active role in the 19th century. In 1836, Noyes Darling, a onetime mayor of New Haven, and a gentleman farmer, was the first to use scientific methods to breed a new variety of corn. His goal was to create a sweet, all-white variety that was “fit for boiling” by mid-July.

He succeeded, noting with pride that he had rid sweet corn of “the disadvantage of being yellow.”

The disadvantage of being yellow, we now know, had been an advantage to human health. Corn with deep yellow kernels, including the yellow corn available in our grocery stores, has nearly 60 times more beta-carotene than white corn, valuable because it turns to Vitamin A in the body, which helps vision and the immune system.

SUPERSWEET corn, which now outsells all other kinds of corn, was derived from spontaneous mutations that were selected for their high sugar content. In 1959, a geneticist named John Laughnan was studying a handful of mutant kernels and popped a few into his mouth. He was startled by their intense sweetness. Lab tests showed that they were up to 10 times sweeter than ordinary sweet corn.

Mr. Laughnan was not a plant breeder, but he realized at once that this mutant corn would revolutionize the sweet corn industry. He became an entrepreneur overnight and spent years developing commercial varieties of supersweet corn. His first hybrids began to be sold in 1961.

Within one generation, the new extra sugary varieties eclipsed old-fashioned sweet corn in the marketplace. Build a sweeter fruit or vegetable — by any means — and we will come. Today, most of the fresh corn in our supermarkets is extra-sweet. The kernels are either white, pale yellow, or a combination of the two. The sweetest varieties approach 40 percent sugar, bringing new meaning to the words “candy corn.” Only a handful of farmers in the United States specialize in multicolored Indian corn, and it is generally sold for seasonal decorations, not food.

We’ve reduced the nutrients and increased the sugar and starch content of hundreds of other fruits and vegetables. How can we begin to recoup the losses?

Here are some suggestions to get you started. Select corn with deep yellow kernels. To recapture the lost anthocyanins and beta-carotene, cook with blue, red or purple cornmeal, which is available in some supermarkets and on the Internet. Make a stack of blue cornmeal pancakes for Sunday breakfast and top with maple syrup.

In the lettuce section, look for arugula. Arugula, also called salad rocket, is very similar to its wild ancestor. Some varieties were domesticated as recently as the 1970s, thousands of years after most fruits and vegetables had come under our sway. The greens are rich in cancer-fighting compounds called glucosinolates and higher in antioxidant activity than many green lettuces.

Scallions, or green onions, are jewels of nutrition hiding in plain sight. They resemble wild onions and are just as good for you. Remarkably, they have more than five times more phytonutrients than many common onions do. The green portions of scallions are more nutritious than the white bulbs, so use the entire plant. Herbs are wild plants incognito. We’ve long valued them for their intense flavors and aroma, which is why they’ve not been given a flavor makeover. Because we’ve left them well enough alone, their phytonutrient content has remained intact.

Experiment with using large quantities of mild-tasting fresh herbs. Add one cup of mixed chopped Italian parsley and basil to a pound of ground grass-fed beef or poultry to make “herb-burgers.” Herbs bring back missing phytonutrients and a touch of wild flavor as well.

The United States Department of Agriculture exerts far more effort developing disease-resistant fruits and vegetables than creating new varieties to enhance the disease resistance of consumers. In fact, I’ve interviewed U.S.D.A. plant breeders who have spent a decade or more developing a new variety of pear or carrot without once measuring its nutritional content.

We can’t increase the health benefits of our produce if we don’t know which nutrients it contains. Ultimately, we need more than an admonition to eat a greater quantity of fruits and vegetables: we need more fruits and vegetables that have the nutrients we require for optimum health.

http://www.nytimes.com

Anti-aging drug breakthrough

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, susi.hamilton@unsw.edu.au

[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.

Insulin Doubles Death Rate in Type 2 Diabetics: Study

Enough-with-Insulin-by-Jeff-Fillmore

Enough with Insulin! by Jeff Fillmore

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

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

Medical Hubris

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.

Invalid Markers

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.


Resources

GaiaHealthHeidi Stevenson is Allopathy’s Gadfly. She’s an iatrogenic survivor whose prior career in computer science, research, and writing was lost as a result. She has turned her skills towards exposing the modern medical scam and the politics surrounding it, along with providing information about the effectiveness of much alternative medicine, without which she would not be here today acting as Allopathy’s Gadfly. Find her work on GaiaHealth.com