From ScienceDaily.com

In youth with attention deficit hyperactivity disorder (ADHD), the brain matures in a normal pattern but is delayed three years in some regions, on average, compared to youth without the disorder, an imaging study by researchers at the National Institutes of Health’s (NIH) National Institute of Mental Health (NIMH) has revealed. The delay in ADHD was most prominent in regions at the front of the brain’s outer mantle (cortex), important for the ability to control thinking, attention and planning. Otherwise, both groups showed a similar back-to-front wave of brain maturation with different areas peaking in thickness at different times.

“Finding a normal pattern of cortex maturation, albeit delayed, in children with ADHD should be reassuring to families and could help to explain why many youth eventually seem to grow out of the disorder,” explained Philip Shaw, M.D., NIMH Child Psychiatry Branch, who led research team.

Previous brain imaging studies failed to detect the developmental lag because they focused on the size of the relatively large lobes of the brain. The sharp differences emerged only after a new image analysis technique allowed the researchers to pinpoint the thickening and thinning of thousands of cortex sites in hundreds of children and teens, with and without the disorder.

“If you’re just looking at the lobes, you have only four measures instead of 40,000,” explained Shaw. “You don’t pick up the focal, regional changes where this delay is most marked.”

Among 223 youth with ADHD, half of 40,000 cortex sites attained peak thickness at an average age of 10.5, compared to age 7.5 in a matched group of youth without the disorder.

Shaw, Judith Rapoport, M.D., of the NIMH Child Psychiatry Branch, Alan Evans, M.D., of McGill University, and colleagues report on their magnetic resonance imaging (MRI) study during the week of November 12, 2007, in the online edition of the Proceedings of the National Academy of Sciences.

The researchers scanned most of the 446 participants — ranging from preschoolers to young adults — at least twice at about three-year intervals. They focused on the age when cortex thickening during childhood gives way to thinning following puberty, as unused neural connections are pruned for optimal efficiency during the teen years.

In both ADHD and control groups, sensory processing and motor control areas at the back and top of the brain peaked in thickness earlier in childhood, while the frontal cortex areas responsible for higher-order executive control functions peaked later, during the teen years. These frontal areas support the ability to suppress inappropriate actions and thoughts, focus attention, remember things from moment to moment, work for reward, and control movement — functions often disturbed in people with ADHD.

Circuitry in the frontal and temporal (at the side of the brain) areas that integrate information from the sensory areas with the higher-order functions showed the greatest maturational delay in youth with ADHD. For example, one of the last areas to mature, the middle of the prefrontal cortex, lagged five years in those with the disorder.

The motor cortex emerged as the only area that matured faster than normal in the youth with ADHD, in contrast to the late-maturing frontal cortex areas that direct it. This mismatch might account for the restlessness and fidgety symptoms common among those with the disorder, the researchers suggested.

They also noted that the delayed pattern of maturation observed in ADHD is the opposite of that seen in other developmental brain disorders like autism, in which the volume of brain structures peak at a much earlier-than-normal age.

The findings support the theory that ADHD results from a delay in cortex maturation. In future studies, the researchers hope to find genetic underpinnings of the delay and ways of boosting processes of recovery from the disorder.

“Brain imaging is still not ready for use as a diagnostic tool in ADHD,” noted Shaw. “Although the delay in cortex development was marked, it could only be detected when a very large number of children with the disorder were included. It is not yet possible to detect such delay from the brain scans of just one individual. The diagnosis of ADHD remains clinical, based on taking a history from the child, the family and teachers.”

Also participating in the research were: Kristen Eskstrand, Wendy Sharp, Jonathan Blumenthal, Dede Greenstein, Liv Clasen, and Jay Giedd, M.D., NIMH.

The National Institute of Mental Health (NIMH) mission is to reduce the burden of mental and behavioral disorders through research on mind, brain, and behavior.

So why are we giving our kids drugs to deal with this problem?

Like Vitamin D you will start to hear a lot more about K2 and its benefits.

The following video demonstrates results from treatment of Parkinson’s disease with intravenous glutathione. This needs to be public knowledge as any doctor can make this happen.

Glutathione Video – April 2010
David Perlmutter, MD

Glutathione! say it three times and don't forget it. Watch the video.

High-Fructose Corn Syrup vs. Sugar

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By Victoria Stein Apr 26th 2010 4:00PM

Categories: Healthy Living, Healthy Eating

Is high-fructose corn syrup worse for you than sugar? Researchers at Princeton University think so. But the American Medical Association and most dietitians say no. AOL Health contributor and nutritionist Victoria Stein examines the issue.

Before we delve into the debate, let's review some basic chemistry. Sugar and HFCS have the same chemical structure. The main difference is that HFCS is manufactured from corn syrup (primarily glucose), which undergoes enzymatic processing to increase the fructose content and is then mixed with glucose. Pure sugar is also composed of glucose and fructose but in marginally different concentrations. Both are calorie dense (with about 16 per teaspoon) with no nutrients.

Thanks to corn subsidies, HFCS has become a cheap alternative to sugar and is often added to processed foods and soft drinks -- substances that offer little nutritional value and, when consumed in excess, contribute to weight gain. But whether HFCS has distinct adverse health effects is less obvious.

Critics believe HFCS plays a direct role in obesity by disrupting normal metabolic functions. According to a recently published Princeton study, rats fed a diet rich in HFCS accumulated more belly fat and had higher levels of circulating triglycerides (i.e., fat) -- both of which are factors in metabolic syndrome, a precursor to heart disease -- than their sugar-fed peers. However, a number of nutrition experts dispute these findings, suggesting that the data produced inconsistent results. Previous studies have shown that fructose is metabolized differently than glucose and excessive amounts of fructose interfere with appetite-regulating hormones and lead to increased fat accumulation. But HFCS is not any higher in fructose than table sugar -- both are about 50 percent glucose and 50 percent fructose. And an excess of either is unhealthy.

The HFCS Image Makeover
HFCS has become the latest health villain, and consumers have begun to demand that manufacturers remove it from popular processed foods. Starbucks has eliminated HFCS and trans fats from all of its products, and PepsiCo introduced a "throwback" version of Pepsi and Mountain Dew that replaced HFCS with sugar.

Meanwhile, the Corn Refiners Association is busy trying to give HFCS an image makeover. In 2008, the CRA launched a multimillion-dollar media campaign with the goal of destigmatizing and educating consumers about HFCS.

The ads all play upon a similar theme: one character scolding another for using HFCS but unable to come up with a reason why. After the first character trips over his words for a few seconds, the other jumps in to correct him: "What do they say? That it's made from corn, nutritionally the same as sugar, and fine in moderation".

Audrae Erickson, president of the Corn Refiners Association, wants to help consumers make informed decisions.

"It's always been calories in, calories out, and singling out any one ingredient or food or beverage in our overall diet only misleads consumers," she says. "If we single out any element of the food supply and say if you just stop consuming this -- whatever this is -- it suggests to people that they'll get skinny. We all know that's very misleading and not helpful."

How HFCS and Sugar Can Hurt Your Health
What we do know is that as excessive sugar intake (in any form) increases, so does risk of diabetes and heart disease. We also know that liquids do not register the same way as solid food, and people rarely compensate for those extra calories by eating less. As people drink more sugar-sweetened beverages, they gain more weight and, as a result, are at a greater risk of developing diabetes and heart disease.

Sugar-sweetened beverages are the main source of added sugar and the leading source of calories in our diet. When added to drinks, all sweeteners -- including natural ones like brown sugar, sugar in the raw, agave syrup and honey -- contribute empty calories. Since 1980, calorie intake has increased by an average of 150 to 300 calories per day with about half of those calories coming from liquids -- sugar-sweetened beverages in particular. During the same period, there has been no change in physical activity levels. Simply put, Americans are eating more and exercising the same.

The American Heart Association recommends Americans limit their sugar intake to half of their discretionary calorie allowance -- about 100 calories per day for women and 150 calories per day for men (or about five and nine teaspoons respectively). To put that in perspective, one 12-ounce can of Pepsi contains 150 calories and about eight teaspoons of added sugar. But it's worth noting that the same amount of orange juice has 165 calories and more than eight teaspoons of sugar, albeit in its natural form. If you're looking to add vitamins and minerals, the OJ is the smarter choice, but if weight maintenance is your goal, you should steer clear of both. When it comes to energy, it's unlikely that your body registers natural sugar any differently than table sugar or HFCS.

Marion Nestle, NYU professor of nutrition and author of "Food Politics" and "What to Eat", agrees that it's a matter of too many calories, rather than one particular food.

"The public now puts HFCS in the same category as trans fats: poison (it's not; it's just sugars)," says Nestle. "Biochemically, it is about the same as table sugar (both have about the same amount of fructose and calories), but it [HFCS] is in everything and Americans eat a lot of it -- nearly 60 pounds per capita in 2006, just a bit less than pounds of table sugar. HFCS is not a poison, but eating less of any kind of sugar is a good idea these days."

The American Medical Association agrees. In 2008, the organization issued a statement maintaining that HFCS does not contribute more to obesity than other sweeteners.

The Verdict
As a dietitian, I shun foods and drinks with HCFS because I don't think anything manufactured in a lab belongs on our dinner plate. But whether the body differentiates between HFCS and sugar is unclear. While the jury is still out on what (if anything) HFCS does to us, it's always best to eat foods that are as close to their natural form as possible.

Bottom line: Eat less high-fructose corn syrup and, while you're at it, cut back on the sugar, too.

More on Healthy Eating:
Healthy Vending Machine Snacks

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From ScienceDaily.com:

Mirror neurons, many say, are what make us human. They are the cells in the brain that fire not only when we perform a particular action but also when we watch someone else perform that same action.

Neuroscientists believe this “mirroring” is the mechanism by which we can “read” the minds of others and empathize with them. It’s how we “feel” someone’s pain, how we discern a grimace from a grin, a smirk from a smile.

Problem was, there was no proof that mirror neurons existed — only suspicion and indirect evidence. Now, reporting in the April edition of the journal Current Biology, Dr. Itzhak Fried, a UCLA professor of neurosurgery and of psychiatry and biobehavioral sciences, Roy Mukamel, a postdoctoral fellow in Fried’s lab, and their colleagues have for the first time made a direct recording of mirror neurons in the human brain.

The researchers recorded both single cells and multiple-cell activity, not only in motor regions of the brain where mirror neurons were thought to exist but also in regions involved in vision and in memory.

Further, they showed that specific subsets of mirror cells increased their activity during the execution of an action but decreased their activity when an action was only being observed.

“We hypothesize that the decreased activity from the cells when observing an action may be to inhibit the observer from automatically performing that same action,” said Mukamel, the study’s lead author. “Furthermore, this subset of mirror neurons may help us distinguish the actions of other people from our own actions.”

The researchers drew their data directly from the brains of 21 patients who were being treated at Ronald Reagan UCLA Medical Center for intractable epilepsy. The patients had been implanted with intracranial depth electrodes to identify seizure foci for potential surgical treatment. Electrode location was based solely on clinical criteria; the researchers, with the patients’ consent, used the same electrodes to “piggyback” their research.

The experiment included three parts: facial expressions, grasping and a control experiment. Activity from a total of 1,177 neurons in the 21 patients was recorded as the patients both observed and performed grasping actions and facial gestures. In the observation phase, the patients observed various actions presented on a laptop computer. In the activity phase, the subjects were asked to perform an action based on a visually presented word. In the control task, the same words were presented and the patients were instructed not to execute the action.

The researchers found that the neurons fired or showed their greatest activity both when the individual performed a task and when they observed a task. The mirror neurons making the responses were located in the medial frontal cortex and medial temporal cortex, two neural systems where mirroring responses at the single-cell level had not been previously recorded, not even in monkeys.

This new finding demonstrates that mirror neurons are located in more areas of the human brain than previously thought. Given that different brain areas implement different functions — in this case, the medial frontal cortex for movement selection and the medial temporal cortex for memory — the finding also suggests that mirror neurons provide a complex and rich mirroring of the actions of other people.

Because mirror neurons fire both when an individual performs an action and when one watches another individual perform that same action, it’s thought this “mirroring” is the neural mechanism by which the actions, intentions and emotions of other people can be automatically understood.

“The study suggests that the distribution of these unique cells linking the activity of the self with that of others is wider than previously believed,” said Fried, the study’s senior author and director of the UCLA Epilepsy Surgery Program.

“It’s also suspected that dysfunction of these mirror cells might be involved in disorders such as autism, where the clinical signs can include difficulties with verbal and nonverbal communication, imitation and having empathy for others,” Mukamel said. “So gaining a better understanding of the mirror neuron system might help devise strategies for treatment of this disorder.”

Other authors on the study included Arne D. Ekstrom, Jonas Kaplan and Marco Iacoboni, all of UCLA. The project was supported by the National Center for Research Resources, a component of the National Institutes of Health (NIH). The authors report no conflict of interest.

Mirror neurons explain why you can watch an athlete do a certain movement and than go replicate it. Some people may have more of these neurons which makes it easier for them to learn by watching others.

From Dr. Perlmutter,
Please read the following story – very compelling information from a flight surgeon:

My Statin Story

When I first wrote of my personal side effects of Lipitor, my words were focused purely on transient global amnesia (TGA). This is because, in 1999, shortly after this drug was started by my doctors at Johnson Space Center as part of my annual astronaut physical, this is what I experienced.

A year later, they re-started me on the same statin, Lipitor, at half the previous dose, saying that my first 6-hour episode of TGA was only a coincidence. Two months later, I again experienced TGA. For twelve hours I was a thirteen-year-old high school student who knew my subjects, teachers and every kid in my class (according to my worried wife) but with no memory for my entire adult life. I laughed when they told me I was married with children and a doctor. I could not have doctored a mouse and certainly had no children. I was thirteen! Fifty-six years of rich and fulfilled adult life had vanished from my mind as if it had never occurred.

After recovery and several years of research on statin drug side effects I considered myself to be lucky to have had only TGA, for when it is over, you are back to normal. Not so for most of the other statin victims in my bulging repository with their persistent neuromuscular problems, short term memory loss and ALS and Parkinsonism-like reactions.

But now, having read thousands of reports from statin-damaged people, I wonder what the true effect of a statin really has been on my body? For suddenly, in two and one-half years, I have grown old, with weakness and easy fatigability, my coordination is terrible and my reactions are slow.

Back in 1999 when Lipitor was first started, I lived on the side of a mountain. Climbing that mountain was a normal, daily exercise event for me, as was cutting and splitting my own wood and doing odd jobs for my neighbors. No job was too great, from cutting up an aged maple tree downed by unusual winds to replacement of a concrete porch floor cracked by frost. Doctor though I was in the past, handy-man I was in my present retired state. Seemingly, I thrived on physical activity and work and it had always been that way from my early life on a dairy farm – the work ethic of being born and raised during the depression years, I suppose.

By 2003 I had noted the gradual onset of unusual tiredness, easy fatigability and weakness. Cutting and splitting my own wood now required surprising effort. Then it seemed my low back and legs ached uncomfortably after only minimal exercise as if they had been strained excessively. I experienced no discomfort during sleep or recumbency, only after activity. My flowerbeds went untended.

Yes, I was older but these were not what one usually expects with age. Change was evident on a scale of months not years. This was most definitely not the usual aging process. Trust me, after 32 years of family medicine I knew that and as a doctor I had checked my vitals from time to time curiously searching for clues. This was not heart or lung, I deduced. And my annual physicals were always normal. This was some non-specific muscle weakness problem.

X-rays showed moderate degenerative changes throughout my lumbar spine with some narrowing. Other imaging studies showed mild to moderate spinal stenosis. Response to steroids was positive. Although the surgeon admitted he had seen far worse imaging studies, surgical decompression was done with titanium rod stabilization.

Six months post surgery I realized my post-surgical recovery was going backward again rather than forward with increasing weakness and discomfort in low back and legs with the addition of awareness of in-coordination. Walking a straight line, which most of us do without thought, now began to require some concentration.

Then came my never to be forgotten first episode of food aspiration. While enjoying a spinach salad with pecans during Christmas dinner with friends, an entire pecan half, well lubricated with olive oil, slid down through my larynx into my right lung. This is one of the hallmarks of ALS and of course I had been dwelling on this possibility because of my repository of reports from statin damaged victims.

In just three years I had gone from a physically fit to a doddering old man wondering how all this could have happened so fast. I was slow to recognize the truth for initially I was convinced that my problem was mechanical and fixable by surgery.

Then in my repository of statin victims tales I read of case after case of statin associated fatigability, muscle weakness with progressive disability and began to understand why I might never get better. An ALS-like condition was my suspected diagnosis, I thought, hidden by the reality of mild to moderate spinal stenosis.

The X-ray evidence of degenerative change was probably about normal for my age of 76 and unusual history of physical activity. My initial tiredness, weakness, in-coordination and leg aches and all that has followed were somehow triggered by my exposure to statins, just like the hundreds of other cases in my files.

My total time on Lipitor was no more than five months at 5-10 mg dosing, low by today’s standards. I had joined the ranks of thousands of other people whose physiology had been seriously compromised by statins.
Research evidence about the more serious side effects of statin drugs began to flood the internet. Statin induced mevalonate blockade with the consequences of CoQ10 and dolichol inhibition now was documented by research rather than just suspected.

Then mitochondrial mutations induced by statins began to be reported as the cause of increasing numbers of serious disabilities affecting neurons of the brain as well as causing muscle damage. Inhibition of CoQ10 was allowing free radical excess to mutate our mitochondria. The World Health Association reported excess ALS in statin users world-wide. A new word was coined, cerebromyopathies, and currently, reports of ALS associated with statin induced mitochondrial mutations are in the research news.

At the present time there is no way to prove statin etiology, just the large numbers that occur shortly after statins are started. Being based on mitochondrial mutations it does not go away when statins are stopped.

Cases are accumulating, more rapidly now that much higher dosing is used. We have no markers, no tumor mass, no blood level of a substance, no measurement that shouts “statins.” My rheumatologist suggested ALS as the best fit diagnosis. She had already had my nerve and muscle conduction studies done, which were reported as within normal limits.

My neurologist generally agreed that ALS fit with my muscle atrophy and weakness and volunteered that he wondered about the mitochondria. He said he had been seeing much statin damage of this type and suspected mitochondrial mutations might have occurred. As a matter of fact he was thinking of specializing in just this area.

The more I thought about it the more I agreed with him. This had come up before many times in my reading. In fact many researchers think that mutations in our mitochondria are a primary factor in chronic disease and old age. Is it possible that statins were subtly damaging our mitochondria, producing premature aging and debility? The more I think about this the more worried I become. Right now that is the best explanation for the clinical picture that has emerged over the past decade.

At the present time my own case of Lipitor associated ALS has progressed to the point where I have finally had to give up my long daily walks. Because of my lifetime focus on muscle conditioning and regular exercise, I delayed this action much too long. Instead of conditioning my weakened muscles I was straining them far beyond their capacity.

The best way I can describe my reasoning is picture a muscle as made up of thousands of muscle fibrils. By now I had lost so many myofibrils that the remaining 30-40% of normal myofibrils were insufficient to move about a man of my stature. Just to get out of a chair and walk across the room was a major effort. Extra exercise is counterproductive, straining muscles already working as hard as they could.

I have begun the use of a cane for short trips. Recently, on my return trip from collecting the daily mail, a gray-haired neighbor lady came to her doorway as I walked past her driveway, concern written on her face, and she asked me if she could drive me home. My performance walking with a cane was that bad. My mood was black for the rest of the day; bless her heart! If I really concentrate I can walk a straight line.

I see my case as being primarily of the spinal muscle type and can imagine “ragged red myofibrils” in the muscle biopsy I have yet to have. I am not about to waste insurance dollars for expensive tests when there is so little proven help. I know what the diagnosis is. I have some 250 other statin victims in my repository just like me. If it looks like a horse, sounds like a horse and smells like a horse, it’s a horse! And I believe Lipitor caused it but I can’t prove it other than by the sheer numbers of victims walking this path.

November 2008 Update

I finally have had to stop my daily walks, a life long habit. Muscles in my legs and low back cannot be rehabilitated. I have just so many remaining functional muscle fibers and finally I have reached the point that just standing for a few minutes is all I can do.

I can follow my wife around with a grocery cart pretty good but without it I break into a cold sweat and look for a chair. My talks on statins are no longer on my feet before a chart or blackboard. I sit down just lke everyone else and it works well. Before the diagnosis was made I used to wonder why I was drenched in sweat at the end of my talks. Never occurred to me it might be ALS and that I was close to exhaustion.

I have never been exhausted before. My neurologist and I are both convinced the mechanism of action must be mitochondrial mutations. After all that’s what statins do, they wipe out CoQ10 and glutathione, our primary anti-oxidant defense against free radical damage and mitochondrial mutation.

In addition to peripheral neuropathy, statin use in my case had somehow triggered a primary lateral sclerosis type of response (currently under neurological and genetic investigation) suggesting two completely different forms of statin neurological damage (nerve fiber versus neuronal.)

As to my progressive muscle weakness I had to give up walking without assistance completely as being counter-productive. On the positive side I found a three wheel walker device which transfers weight bearing to my arms and shoulders so now I am walking again with much greater stability and co-ordination.

March 2009 Update
Three months have passed during which time I knew I had become a symbol of persistence to many others in this retirement community as I passed their homes each morning dutifully pushing my walker. Then to their surprise one morning I briskly walked my path using only a lightweight walking stick. My surprise was just as great as theirs for I had no idea my response to my new supplement plan would be so impressive. One month earlier I had started my new regimen of taking all of the supplements I had deemed essential to mitochondrial maintenance.

One thing my research had shown me was that of the many supplements that have been tested by various researchers studying mitochondrial health over the past decade, twelve clearly stood out. I know this can be argued indefinitely but from my perspective as a reasonably well-trained and well-informed MD, these twelve seem to be critical.

I had tried robust doses of CoQ10 both with and without selenium for a time, and glyconutrients and lecithin for half a year while participating in a study of their combined effectiveness on peripheral neuropathy with no significant effect on the process that was robbing me of strength and stability and turning my muscles to jelly, but I had never tried all twelve supplements together. Never for a moment did I think I could need all twelve critical supplements simultaneously, but how else to tell my need other than all at the same time?

I also convinced myself that ultimate dosage of each was not critical as long as some was being taken in. I completely understand that this can be grossly underdone and judgment was important. I also made once daily dosing of critical importance to me. In my conservative and traditional world, If there is anything worse than opening 12 supplement bottles daily, it was having to do it twice a day. I next mandated that all supplements requiring dissolving in liquid be done at the same time for convenience sake.

The rationale for use and dosage of each are discussed in the mitochonrial mutations chapter of my forthcoming book the Statin Damage Crisis. Everyone is different and everyone’s needs are different.

At the end of one week I was seeing improvement. By the middle of the fourth week I ventured forth with my walking stick (for stability) and surprised my neighbors and that’s where I am at present. I am highly motivated, perhaps more than most. I keep telling myself this is all placebo effect, knowing full well that this can be very powerful. But even my wife remarks on the new muscular look of my thighs and there seems no disputing my new energy. March 2nd 2009 was my 78th birthday and my vision of an imminent wheelchair existence has been replaced by hope of active life yet.

As a word of caution, yesterday my new freedom led me on a two-mile walk through a nearby abandoned orange grove where I stumbled and almost fell while crossing a drainage ditch. Pulled some muscle fibers in my upper back while I clung for support on my walking stick. Might have been better if I had fallen but please do not take on too much too soon. Your body is never the same as it used to be. Some things we just have to accept.

July 2009 Update

Despite my initial improvement gained from a battery of nutritional supplements permitting me to walk freely again, over the past several months it is clear that the strain of activity is gradually wearing me down. I recently traveled to Vermont but the immense effort required and the strains of travel took its toll and has set me back greatly. After almost a decade of studying the mechanisms of actions of the statins I am close to the end of my capabilities.

Actually, everything that needs be said about the statin drugs is on this website and in my books. There is now very little reason for my further input. I have written extensively about the side effect profile of statins. With the help of Frank Pfrieger we now know how necessary cholesterol is to cognitive function in our brains. The symptoms of amnesia, confusion, disorientation, forgetfulness and dementia are inevitable for many with statin exposure due to the inhibitory effects of statins on brain cholesterol.

That statins, also known as reductase inhibitors, also block the mevalonate pathway causing a wide range of side effects, including permanent neuropathy and myopathy, ALS and other neurodegenerative illnesses, heart failure, gross personality changes, loss of libido and far more is well documented in my material and fully referenced.

Finally my most important contribution has been to direct attention to the ability of statins to cause DNA damage. This action, like inhibition of brain cholesterol and mevalonate pathway inhibition is also inevitable for many – causing mitochondrial mutations creating both premature aging and the chronic diseases of the brain, nerve, muscle and bone common to aging. Statins are robbing many of us of our golden years, using the same physiologic mechanisms as normal aging. Suddenly within a few months victims become aged like me, diminished to the point where wheelchair existence is imminent.

Traditional medicine has nothing to offer. Nutritional supplements seem to be our only hope at present, using the full range known to be vital for mitochondrial function. CoQ10 is vital in prevention of statin damage but once the damage is done, all the CoQ10 in the world cannot by itself repair mitochondrial damage. The possibility of repair, it seems, can currently only come from the broad battery of nutritional supplements I mention in my book, the Statin Damage Crisis.

Now I have told you all I know. I have done my job. Please accept my apologies for being near 80 and “out of gas.” Many doctors and other qualified people have taken up the banner and will guide you. I know of no better goodbye than what the Spanish have given us: Vaya con Dios – “Go with God”.

Duane Graveline MD MPH
Former USAF Flight Surgeon
Former NASA Astronaut
Retired Family Doctor

I have been telling my patients,friends, and family how important CoQ10 is in protecting the mitochondria. The other supplement I take to protect and possibly rebuild the mitochondria is Resveratrol. Most of the neuroscience points to mitochondria dysfunction as the main cause for neurological failure.

Read to the bottom about the knee study. I read this paper several years ago and it was a true eye opener.