Category: supplement


article taken from Lef.org

Aged people are in the midst of an escalating Alzheimer’s epidemic.1,2 It is now the sixth leading cause of death in the United States.3

The horrific progression of Alzheimer’s disease from dementia to personal extinction afflicts between 24-30 million people worldwide.4,5 Americans account for approximately one-fifth of those cases, which are expected to triple by 2050.3,6

While there is no cure for Alzheimer’s, there is new hope thanks to the work of a team of researchers at Massachusetts Institute of Technology (MIT.)7

These scientists have identified several correctable factors involved in Alzheimer’s onset—and a novel nutritional intervention that may effectively target them.

In this article, you will learn of the vital role that magnesium plays in protecting the aging brain’s structure and function and why conventional supplements don’t deliver enough magnesium into the brain.

Researchers have found that a new highly absorbable formof magnesium called magnesium-L-threonate concentrates more efficiently in the brain, rebuilds ruptured synapses, and restores the degraded neuronal connections observed in Alzheimer’s disease and other forms of memory loss.

In experimental models, magnesium-L-threonate induced improvements of 18% for short-term memory and 100% for long-term memory.8

Magnesium Deficiency: An Overlooked Cause of Neurologic Decay

Half of all aging individuals in the developed world are magnesium deficient, a nutritional deficit that worsens over time.

Confirmatory data show that Americans are no exception.9,10 For instance, American women consume just 68% of the recommended daily intake of magnesium.11

Magnesium has long been known as a key nutrient for optimal brain function. More recently, scientists have found it specifically promotes learning and memory as a result of its beneficial effect on synaptic plasticity and density.7,8,12

Magnesium works with calcium to modulate “ion channels” that open in response to nerve impulses, which in turn trigger neurotransmitter release. The most important of those channels is controlled by a complex called the NMDA receptor.13,14 NMDA receptors play an important role in promoting neural plasticity and synaptic density, the structural underpinnings of memory.15-17

Magnesium deficiency can cause symptoms ranging from apathy and psychosis to memory impairment.13,18 Insufficient magnesium slows brain recovery following injury from trauma19 and in laboratory studies accelerates cellular aging.20

Ominously, magnesium deficiency may produce no overt symptoms in its initial stages.21

Part of the problem is that it is difficult for the body to maintain sufficiently high concentrations of magnesium in the brain.8

For this reason, researchers have long sought ways that higher magnesium brain concentrations might be achieved and sustained.

A Breakthrough Form of Magnesium

Scientists have been challenged to find a way to raise magnesium levels in the brain.8 Even intravenous infusions cause only a modest elevation of magnesium levels in the central nervous system.22

An innovative team of researchers from the Massachusetts Institute of Technology (MIT) recently found a way to surmount this obstacle. They formulated a new magnesium compound called magnesium-L-threonate or MgT that in lab tests allows for oral administration while maximizing magnesium “loading” into the brain.7,8

Based on prior research, they meticulously documented that increased levels of magnesium in the brain promote synaptic density and plasticity in the hippocampus.14 Up until now, however, no widely available forms of magnesium met the criteria needed for rapid absorption and efficient transfer into the central nervous system.8

By contrast, MgT yielded compelling results.

MgT oral supplements increased magnesium levels in spinal fluid, an index of measurement in brain magnesium by about 15%, while none of the other magnesium compounds tested produced significant elevations.8 While a 15% increase may not sound like a lot, it induced a profound effect on neurological function.

To evaluate the effects of MgT on memory, the researchers tested it against currently available magnesium compounds. They used a simple assessment of learning and memory called the Novel Object Recognition Test or NORT. A high NORT score means that the animal is good at recognizing and identifying new objects, a skill that is critical in aging humans as well.8 NORT is a good test of function in the hippocampus, which is rich in the NMDA receptors so closely controlled by magnesium.23

The researchers put aged animals through the NORT test, supplementing them with MgT or one of the commercially available magnesium compounds. Only MgT significantly enhanced both short- and long-term memory, boosting scores by 15% for short-term memory and 54% for long-term memory compared to magnesium citrate.8

Better Function of Memory-Forming Synaptic Connections

Given the effect of MgT in increasing synaptic density and plasticity in experimental animals (rats), the research team asked the obvious next question, “Do those changes lead to an increase in the number of neurotransmitter release sites, and, subsequently, to enhanced signal transmission?”8 That, after all, is the hallmark of learning and memory.

Using high-tech microscopic measuring devices, the team demonstrated that the magnesium elevation in brain tissue observed in MgT supplementation increases the number of functioning neurotransmitter release sites.8 This effect could be likened to increasing the number of soldiers on the battlefield: when the call to action comes, a much larger force is prepared to perform.

The final question to be addressed in this series of studies was whether the increased density of synaptic connections directly correlated with the observed improvements in memory created by MgT supplementation.

The researchers systematically plotted out the time-course of the increase in synaptic density following MgT supplementation, and found that it directly paralleled the improvements in memory.8 They also found that when MgT supplementation was stopped, the density of synaptic connections dropped back to baseline, further confirming the correlation. They found that MgT supplementation boosted all of the animals’ performance, not just average performance.

Improvement in Spatial Short-Term Memory

Spatial working memory is an essential memory function, helping you remember where things are and where you are in relation to the world over the short term. It is working memory that enables you to find your car keys as you head out the door or return to the correct page in the magazine you were reading a few minutes ago.

The MIT researchers tested spatial working memory in experimental animals. Without treatment, both young and old animals forgot the correct choice about 30% of the time. After 24 days of MgT supplementation, however, both young and old animals had improved this measurement of memory performance by more than 17%.8

Even more impressive, by 30 days of supplementation, the older animals’ performance became equal to that of their younger counterparts. Since the older animals were more forgetful at baseline than the younger animals that meant that the older animals had a larger percentage memory improvement (nearly 19%) than the younger animals’ more modest 13%.8

When MgT supplementation was suspended, the memory-enhancing effects persisted in younger animals, but in older animals spatial working memory performance declined dramatically, returning to baseline within 12 days.8 When MgT supplementation to the older animals was resumed, however, their memory performance was restored in 12 days.

In other words, magnesium-L-threonate improved memory in both old and young animals, but had a substantially greater effect on aged individuals—the very ones most in need of memory enhancements.

Novel Magnesium Compound Halts Neurologic Decay
Novel Magnesium Compound Halts Neurologic Decay
  • Levels of Alzheimer’s disease and associated memory loss among aging Americans are reaching epidemic levels.
  • The neurodegenerative processes involved in memory loss results from deterioration of connectivity between brain cells but are not a “natural function” of aging.
  • Low magnesium status can accelerate brain cell aging and memory loss.
  • Standard magnesium offers limited protection to brain cells.
  • Magnesium-L-threonate is a new form of magnesium that dramatically boosts levels of magnesium in the brain.
  • Boosting brain magnesium with magnesium-L-threonate enhances synaptic density and plasticity, the structural basis of learning and memory.
  • In numerous experimental models, supplementation with magnesium-L- threonate has been shown to enhance memory and cognitive performance in multiple tests.

Enhanced Spatial Long-Term Memory

Long-term spatial memory is crucial for older individuals. It’s how you remember where you live or how to get to the grocery store. Loss of spatial long-term memory is one of the main reasons that older people with dementia get lost running even simple errands.

To test spatial long-term memory in MgT-supplemented animals, the researchers used a maze that required the animal to swim and find a submerged platform on which to rest. Again, both old and young animals supplemented with magnesium-L-threonate learned significantly faster than untreated animals during the training sessions.8

Enhanced Spatial Long-Term Memory

One hour after the training period, the researchers removed the submerged platform, causing the animals to have to search for its last location. Both young and old supplemented and unsupplemented animals remembered where the platform had been over the short term and were searching for it in the correct quadrant of the maze.

But after 24 hours, a remarkable difference was observed. Untreated animals, both young and old, completely forgot where the platform had been hidden, randomly searching in all quadrants of the maze. Supplemented animals, on the other hand, continued to search in the correct part of the maze more than twice as long as they looked in incorrect areas.8 That translated into improvements in spatial long-term memoryof 122% in younger supplemented animals, and nearly 100% in older supplemented animals.

In short, MgT supplementation doubled the accuracy of long-term spatial memory in older animals, and more than doubled it in younger animals.

Better Recall

One critical memory function is the ability to bring up an important memory based on only partial information, a function called pattern completion.8 You use pattern completion memory to find your way around a familiar neighborhood after dark or following a heavy snowstorm. In both cases, some familiar cues are gone, but a healthy brain will fill in the missing details by completing a recognizable pattern.

As decsribed on the previous page, when researchers removed some of the external visual cues from the water maze, younger animals had no particular difficulty finding their way to the hidden platform during the first 24-hour period. Older animals, on the other hand, demonstrated substantial impairment when familiar cues were missing, spending more than twice as much time searching for the missing platform. When given MgT for 30 days, however, older animals performed as well as the younger ones, quickly finding the platform even when many of the external cues were unavailable.8

In human terms, this kind of improvement could mean the difference between a routine trip to the grocery store at dusk versus getting lost in the dark.

Having successfully demonstrated that magnesium-L-threonate (MgT) improves multiple forms of learning and memory in living animals, the research team sought to explore the cellular and molecular basis of that improvement. They wanted to understand in a detailed fashion just what changes the MgT was producing in the brains of older animals that helped them form stronger, more stable memories.

What they determined was compelling.

Better Recall

Increased Brain Cell Signaling

The first step was to determine the effects of MgT supplementation on signaling between brain cells mediated by what are known as NMDA receptors. These receptors operate through varying concentrations of calcium and magnesium in brain tissue, making them a logical point of observation.

The first finding was that MgT treatment in animals resulted in stronger signaling at essential brain cell synapses.8 This increase in signaling was accomplished by a 60% increase in production of new NMDA receptors and by increases of up to 92% in related proteins that play essential supporting roles in brain signal transmission.8

Higher Memory- Forming Synaptic Plasticity and Density

Synaptic plasticity, or the ability to rapidly change the number and strength of brain cell synapses, is critical to the brain’s ability to form, retain, and retrieve memories. The research team compared synaptic plasticity in the brains of MgT-supplemented animals versus controls.8

They found that production of a very special subunit of the NMDA receptor, one closely associated with synaptic plasticity, was selectively enhanced by MgT supplementation.8 This molecular change is known to cause potent long-term increases in synaptic strength, and hence a greater capacity for information storage and memory.8,24-26

The result of these increases in NMDA receptor numbers was a 52% enhancement in long-term potentiation,8 which is the cellular equivalent of memory formation in the brain tissues of MgT-supplemented animals.27,28

Memory depends not only on synaptic plasticity, but also on the healthy physical structure of synapses between brain cells. Unfortunately, synaptic connections in the memory-rich hippocampus region of the brain decline with aging, which directly correlates with memory loss.8,29,30,31

One of the most vital structures to be found at brain cell synapses is the synaptic bouton, from the French word for button. When an electrical impulse reaches a pre-synaptic bouton, and ample calcium and magnesium are present, neurotransmitters are released to transmit the impulse to the next neuron in line. The greater the number and density of synaptic boutons, the stronger the electrochemical signal that the synapse can produce, and the more sustained the memory that is created.32

When the researchers examined the brains of control and MgT-supplemented animals under a high-power microscope, they readily detected much greater densities of synaptic bouton proteins in tissues from the supplemented animals. Those proteins are essential for neurotransmitter release in the several regions of the hippocampus vital for memory formation and retrieval.8 Remarkably, the density of the synaptic boutons was closely correlated with the memory performance of each individual animal on the novel object recognition test.

Mechanisms of Brain Aging and Memory Loss
Every memory you have, even those you’ve lost, produces physical changes in your brain. Memories form and are stored in multiple brain regions, but the most active and essential area is the hippocampus, a small, sea horse-shaped structure deep in the center of your brain.

Hippocampal memory enables you to recognize and distinguish between old friends and new acquaintances, or to find your way around a well-known floor plan. It is also used to comprehend and navigate new experiences based on old ones.

This puts the hippocampus squarely at the center of your ability to assimilate new information and integrate it with what you already know. As you learn and experience new events, cells in your memory centers tighten and enhance their neuronal connections, known as synapses.35

The ability of brain cells to quickly form new synapses and remove old ones is referred to as neurologic plasticity. Large numbers of synapses, and a high density of specialized synaptic structures called boutons, promote rapid retrieval and processing of the information stored by connected cells.36 In essence, neuronal plasticity is the physical equivalent of learning, while synaptic density is roughly the equivalent of memory.

Young brains exhibit high levels of neurologic plasticity that produce large numbers of interconnected synapses. That’s why young people learn quickly and have strong memories.

With aging, however, the numbers of synapses, and the ability to rapidly form new ones, steadily declines.37 And that’s just in “normal” aging.29 People with Alzheimer’s disease, or its precursor, mild cognitive impairment (MCI) experience more rapid loss of both plasticity and synaptic number.30,38-40 And that’s when memories begin to fade, or worse, to be lost entirely.

Since time immemorial, people have suspected that specific nutrients can positively affect cognitive functions such as learning and memory.41 It’s now known that many nutrients can actually modify aging brain function, in part by increasing formation of brain synapses.42

Magnesium has been established as having a positive impact on both neural plasticity and synaptic density.7,8,12

Near-Term Research

The MIT team is rapidly putting in place two human studies of MgT on memory function, with results expected in the near future. Meanwhile, they have recently discovered several new roles for MgT in managing memory, in this case unwanted memories of the kind associated with post-traumatic stress disorder (PTSD).

Fear memories are expressed in response to objects or events previously linked with a potential danger. Over time, fearful reactions can dissipate when the triggering event is experienced in a safe environment.

Animal studies reveal that MgT enhances this process, so that events which previously caused an emotional response no longer trigger fear.33,34 MgT helps the pre-frontal region of the brain block the return of old fear memories.33,34

Research reveals that MgT works by enhancing neural plasticity in the hippocampus and prefrontal cortex.34 These findings led the researchers to recommend that elevating brain magnesium with MgT be used to dampen traumatic memories and treat PTSD, anxiety, and depression.33,34

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BACKGROUND:

beta-Alanine (betaA) has been shown to improve performance during cycling. This study was the first to examine the effects of betaA supplementation on the onset of blood lactate accumulation (OBLA) during incremental treadmill running.

METHODS:

Seventeen recreationally-active men (mean +/- SE 24.9 +/- 4.7 yrs, 180.6 +/- 8.9 cm, 79.25 +/- 9.0 kg) participated in this randomized, double-blind, placebo-controlled pre/post test 2-treatment experimental design. Subjects participated in two incremental treadmill tests before and after 28 days of supplementation with either betaA (6.0 g.d-1)(betaA, n = 8) or an equivalent dose of Maltodextrin as the Placebo (PL, n = 9). Heart rate, percent heart rate maximum (%HRmax), %VO2max@OBLA (4.0 mmol.L-1 blood lactate concentration) and VO2max (L.min-1) were determined for each treadmill test. Friedman test was used to determine within group differences; and Mann-Whitney was used to determine between group differences for pre and post values (p < 0.05).

RESULTS:

The betaA group experienced a significant rightward shift in HR@OBLA beats.min-1 (p < 0.01) pre/post (161.6 +/- 19.2 to 173.6 +/- 9.9) but remained unchanged in the PL group (166.8 +/- 15.8 to 169.6 +/- 16.1). The %HRmax@OBLA increased (p < 0.05) pre/post in the betaA group (83.0% +/- 9.7 to 88.6% +/- 3.7) versus no change in the PL group (86.3 +/- % 4.8 to 87.9% +/- 7.2). The %VO2max@OBLA increased (p < 0.05) in the betaA group pre/post (69.1 +/- 11.0 to 75.6 +/- 10.7) but remained unchanged in the PL group (73.3 +/- 7.3 to 74.3 +/- 7.3). VO2max (L.min-1) decreased (p < 0.01) in the betaA group pre/post (4.57 +/- 0.8 to 4.31 +/- 0.8) versus no change in the PL group (4.04 +/- 0.7 to 4.18 +/- 0.8). Body mass kg increased (p < 0.05) in the betaA group pre/post (77.9 +/- 9.0 to 78.3 +/- 9.3) while the PL group was unchanged (80.6 +/- 9.1 to 80.4 +/- 9.0).

CONCLUSIONS:

betaA supplementation for 28 days enhanced sub-maximal endurance performance by delaying OBLA. However, betaA supplemented individuals had a reduced aerobic capacity as evidenced by the decrease in VO2max values post supplementation.

FULL article:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2887393/?tool=pubmed

 

L-Dopa: It’s more than an anti-Parkinson drug

By James South, MA

L-dopa, also known as Levodopa and L-3, 4-dihydroxyphenylalanine (1), is best known to the world as a treatment for Parkinson’s disease (PD), a neurological disorder. Indeed, as Hauser and Zesiewicz remark: “L-dopa and peripheral decarboxylase inhibitor (PDI) (Sinemet) therapy remains the gold standard for symptomatic treatment for PD. It provides the greatest anti-Parkinsonian benefit with the fewest side effects” (2). Yet even though it is used to treat a disease, L-dopa is not an artificial human-created drug. It is a natural amino acid derivative that occurs in food, (making up 13% of the velvet bean) (1) and is normally present in the human brain (3). L-dopa is the precursor for the neurotransmitter dopamine (DA) (3), and is produced by the action of the enzyme tyrosine hydroxylase on the amino acid tyrosine (3). DA is the precursor of the brain neurotransmitter noradrenalin (NA), yet administration of L-dopa preferentially increases brain DA, while giving tyrosine increases NA more than it increases DA (3).

L-Dopa: Growth hormone releaser

If L-dopa were useful only as a PD treatment, it would be of little interest to most people. Yet L-dopa has uses beyond PD. It has been known for over 30 years that it is an effective stimulant of human growth hormone (HGH) release. In 1970, Boyd and colleagues found that a 500mg oral dose …”caused a significant rise in plasma growth hormone in PD patients, initially starting therapy or on chronic L-dopa therapy for as long as 11 months. The rise in plasma growth hormone persisted for 120 minutes after the administration of the drug.” (4). Boden and his co-workers gave 500mg of the drug orally to four male and five female volunteers. “HGH levels rose sharply at 45 minutes from the basal value of 0.8mg/ml, to a maximum of 10.0mg/ml at 90 minutes (p<0.001) and declined thereafter. This rise occurred in eight of the nine subjects.” (5). Hayek and Crawford reported that six out of seven “constitutionally short children” responded to oral L-dopa (200-500mg), “…with elevations in HGH concentration above 7mg/ml, peak levels occurring between 30 and 120 minutes after drug administration..”. (6).

In 1975, Ajlouni and colleagues reported the effects of 500mg of oral L-dopa on eight normal and 8 non-obese insulin-dependent diabetic subjects. The normal subjects increased their plasma HGH from 1.5mg/ml before L-dopa, to an average 21mg/ml at 90 minutes post L-dopa, with all subjects showing at least a 10 mg/ml increase. The diabetics increased from 2.5mg/ml to 20mg/ml from 60-90 minutes post L-dopa. Giving 100 grams (3 _ ounces) of glucose with, or 30 minutes after the drug totally suppressed the expected HGH increase (7).

Obesity has been shown to blunt HGH release after oral L-dopa. Laurian and his co-workers tested 17 obese, non-diabetic and six normal weight volunteers. All 17 obese subjects failed to respond to L-dopa, while the normal weight subjects had HGH increases of 10-11mg/ml at 90 and 120 minutes after the drug was administered. The 17 obese men and women subsequently lost 12-50kg. After weight loss, 8 people secreted HGH in response to L-dopa, but at levels only 50-60% of the normal weight people. 9 formerly obese people still failed to respond to it (8).

Barbarino and colleagues gave 500mg orally to 12 obese people, with no significant HGH increases. When some of the subjects were given 40mg oral Propranolol, two hours before L-dopa, they then showed HGH response, although at only 50-75% of the level shown by 12 normal weight subjects given L-dopa, whose serum HGH levels reached 7 to 32mg/ml 60-120 minutes after L-dopa (9).

Greenspan et al. compared HGH response to L-dopa in 44 young patients (31-44 years of age) and 42 older patients (64-88 years of age). All were considered “healthy participants”. Plasma HGH increased by 221% in the young patients and 167% in the older patients. The post L-dopa HGH levels were similar in young and old (4.5 and 4.8mg/ml) (10).

The preceding studies illustrate some of the studies showing that 500mg oral L-dopa is an effective stimulator of HGH release. Whether a person is male or female, young or old, diabetic or not, thin or obese (possibly with Propranolol), a PD patient or not, L-dopa is a natural HGH-releasing agent when taken on an empty stomach. For those who can’t afford HGH injections, or just don’t like self-injecting,L-dopa may provide a reasonable alternative.

Dopamine – Neuroregulator of movement

It is common knowledge that bodily movement becomes more difficult with age. Elderly people move at a slower pace, often walking with a shuffling or stooped gait. Hand-eye co-ordination deteriorates and it can become more difficult to get out of a chair. Joints stiffen, muscles weaken and hands tremble. In many ways, the dyskinesia (difficulty performing voluntary movements) of old age resembles a mild form of Parkinson’s disease. Marshall and Berrios believe there is a connection. They point out that “The dopamine-containing neurons of the brain have long been known to be essential for normal movement and sensori-motor integration. The movement disturbances of Parkinson’s disease, for example, are attributable to a loss of dopamine-containing neurons that innervate forebrain structures, particularly the neostriatum. Damage to these neurons of young adult mammals results in sensorimotor disturbances similar to Parkinsonism. The symptoms of this clinical disorder and its analog in animals are frequently controlled by administration of L-dopa, apomorphine or similar compounds. Our findings suggest that advanced age may represent another link between movement disturbances and the deterioration of dopaminergic neurotransmission.

This conclusion is supported by recent clinical investigations that have noted similarities between the movement disturbances of Parkinsonian and those of non-diseased elderly individuals.” (11).

Marshall and Berrios noted that aged rats swim very poorly compared to young rats. In a 15 minute swimming test, young rats swim with vigour for most of the test, with their performance declining gradually. Old rats are significantly impaired after 6 minutes, unable to sustain a horizontal position in the water, frequently sinking below the water. Young rats, whose dopamine neurons are damaged, swim just like the old rats. Giving old rats intraperitoneal L-dopa injections 15 minutes before the test restores their ability to swim just like the healthy young rats (11).

Papavbasiliou and co-workers compared old mice who were fed L-dopa-enriched, with regular mice chow since youth. They noted a profound decrease in motor activity with aging in the regular, chow-fed old mice, but no loss of motor activity in the L-dopa-fed old mice. They concluded: “…motor impairment is an age-related phenomenon in mice associated with selective alterations in brain dopaminergic systems, which may be prevented by dietary Levodopa.” (12)

Thus, the animal evidence combined with the effectiveness of L-dopa in PD, and the similarity of the neuromuscular degeneration typical of “normal” aging to PD, all suggest that it may provide a remedy for maintaining more normal “motor activity” throughout middle age into old age. On an anecdotal basis, I have confirmed with various friends and colleagues during the past 20 years that modest L-dopa supplementation (typically 100mg Sinemet ®/day) has increased their sense of neuromuscular co-ordination, strength, vigour and greater “drive to action”.

Dopamine : The “warming” neurotransmitter

In their recent book “Balance Your Brain, Balance Your Life”, neurologist, Dr. Jay Lombard and preventative medicine specialist Dr. Christian Renna have provided evidence that our health, energy and happiness are significantly affected by our personal brain balance of “warming” and “cooling” neurotransmitters (13). Dopamine, noradrenalin (norepinephrine), acetylcholine and glutamate are the major “warming” neurotransmitters (NTs), while serotonin and GABA are the chief “cooling” NTs (13). They note that “warming” NTs are dominant in the daytime, while the “cooling” counterparts predominate at night, and that “….dopamine is our principal warming neurotransmitter…”(13). A broad array of symptoms may indicate possible warming NT/DA deficiency, including weight gain, drop in energy level, apathy, difficulty concentrating, loss of interest in things that were formerly pleasurable, irritability, not wanting to get out of bed, decreased testosterone in men, depression, spaciness or forgetfulness, reduced speed of information processing and capacity for abstract thought, to name just a few (13). Lombard and Renna provide a 150 question self-test to help assess if one might be suffering a warming or cooling NT deficiency, a modest (100mg Sinemet ®) L-dopa supplement taken at breakfast might reasonably be part of a plan to restore neurological balance to the brain, since L-dopa is more specific to increasing brain DA than the L-dopa precursors phenyl-alanine and tyrosine (3).

L-Dopa : The controversy

It was announced in the American media in early 2004 that actor, Michael J Fox, who has suffered early onset PD for over a decade, recently began a “new” (for him) therapy that brought virtually miraculous relief from his ever-worsening PD. The drug was Sinemet ®. The obvious question is, why had his doctors delayed giving him the “gold standard” PD treatment (2) for so many years? The answer involves some extremely complex biochemistry and brain physiology, and is relevant to L-dopa use by those not suffering the disease.
If one looks at the vast literature on L-dopa, one finds two completely different views about L-dopa and DA. One body of scientific literature says L-dopa and DA are highly toxic to DA – using neurons, while another body of evidence pronounces L-dopa to be not only non-toxic, but claims that it will “….increase reduced glutathione (a critical intra-cellular antioxidant), protect dopamine neurons from oxidants, increase cell survival, and promote neuritic extension, or nerve growth.” (2)

What could make L-dopa/DA toxic to dopaminergic neurons? L-dopa/DA both can oxidise to generate toxic free radicals, quinines, hydrogen peroxide and lipid peroxides (14). L-dopa may create excito-toxic metabolites (14). Chronic L-dopa administration may inhibit complex 1 of the mitochondrial electron transport chain, simultaneously reducing mitochondrial ATP energy production and increasing free radical/oxidant levels (15). Indeed, Parris Kidd has argued that PD is the result of “multifactorial oxidative neurodegeneration”, brought about by known and unknown environmental insults (such as heavy metal or pesticide poisoning) and metabolic derangements (such as poor antioxidant status). He also argues that the naturally high levels of DA in the substantia nigra (the brain region that “melts down” in PD) plays a key role in promoting such oxidative neurodegeneration (16). It should be noted, however, that “Evidence supporting a toxic action of levodopa or DA on dopaminergic neurons arises largely from in vitro, or test-tube studies.” (14).

L-Dopa : Not harmful

As mentioned previously, a large body of evidence finds L-dopa harmless or even beneficial to DA neurons. Thus, Mean et al remark: “The effects of L-dopa on dopamine (DA) neurons are quite different in vivo (living organisms) and in vitro. Whereas, relatively low levels of L-dopa are toxic in culture…, the drug has not been seen to damage DA neurons in healthy animals….or humans…” (17). “It has not been possible to demonstrate a toxic effect of chronic levodopa treatment on dopaminergic neurons of healthy rats and mice.” (14) “Treatment for 120 days, (equivalent to roughly 10 human years) with maximally tolerated doses of L-dopa and carbidopa (Sinemet ®)…failed to produce biochemical, histological, or behavioural evidence of damage to the nigrostriatal dopaminergic tract in rats.” (18) A 1986 case report found that a 76 year old man who was treated with Sinemet ® L-dopa over 4 years, equivalent to 8-10kg of plain L-dopa. (19). The authors concluded: “Nevertheless, this case report emphasises that the burden of proof for a cytotoxic effect of levodopa in man remains with its proponents.” (19).

L-Dopa to the rescue

Many studies have actually found L-dopa to have a “neurotrophic”, or health-promoting effect on DA neurons. Thus Murer and colleagues report: “Our results clearly indicate the absence of toxicity of a pharmacologically effective chronic levodopa treatment on remaining dopaminergic neurons of rats with moderate and severe 6-OHDA-induced lesions. In addition, they clearly suggest that chronic levodopa administration induced a partial recovery of remaining dopaminergic neurons in moderately lesioned rats.” (14). Mena et al cultured DA neurons with cortical astrocytes (glial cells), then fed them L-dopa. “This study demonstrates that L-dopa has neurotrophic effects on DA neurons, stimulates elaboration of neuritis, and protects DA neurons from cell death.” (17). Han and colleagues found that giving L-dopa or rat mesencephalon (DA neurons) cultures increased levels of the critical antioxidant glutathione. They note: “When mixed mesencephalic cultures were exposed to strong oxidant stress….a loss of viability was seen. Cultures pre-treated with L-dopa….were protected from loss of viability.” (20). Uitti and co-workers studies survival data for all Olmsted county PD patients seen at the Mayo Clinic from 1964 to 1978. 61% of the 179 patients were levodopa-treated. They found that the treatment significantly lengthened life of PD patients compared to those not receiving the drug. “We believe our study provides compelling evidence in support of decreased mortality associated with the treatment in PD patients….Levodopa therapy improved survival unconditionally, in that it did not require early institution. We found no evidence for increased mortality in patients treated with levodopa, as one might expect hypothetically, on the basis of levodopa-related oxidative stress mechanisms.” (21).

L-Dopa : Resolving the controversy

As Murer and colleagues note, “Evidence supporting a toxic action of levodopa or DA on dopaminergic neurons arises largely from in vitro studies.” (14). More precisely, L-dopa toxicity evidence arises from one type of in vitro study – those wherein L-dopa is added to cultures containing DA neurons, but which are without glial/astrocyte cells (17, 20, 23-25). Glial/astrocyte cells are non-nerve cells that support, structurally and nutritionally, the nerve cells of the brain, retina and spinal cord (22). It is generally estimated that there are 10 times the number of glial cells than neurons in the brain. They surround nerve cells, providing mechanical support and nutritional/ antioxidant/ detoxicative/ neurotrophic services to neurons (17, 20, 26).

Mena et al. found that “In……embryonically derived glia-free (DA) neurons, …L-dopa is toxic.” (17). Han and colleagues reported that “…pure neuronal cultures (without glia) were exquisitely sensitive to the toxic effects of L-dopa.” (20). Michel and Hefti found both DA (formed from L-dopa in DA neurons) and 6-hydroxy DA (potentially formed through oxidation of DA) were potent neurotoxins to DA neurons (23). They also noted that “…our cultures contain a relatively small percentage of non-neuronal (glial) cells, and neurons are not embedded in a matrix of glial cells as in the living brain….” (23). Pardo and co-workers found that “…DA neurons are affected by L-dopa more severely, earlier, and with a lower concentration than non-DA cells.” (24). They also reported that “…our cultures….are enriched in neurons and almost (completely) lack glia (1-2% of the total population).” (24). Walkinshaw and Waters found “…that L-dopa induced death of catecholaminergic cells in vitro with an active programme of apoptosis.” (25). They also used “pure” neuronal cultures without glial cells.

Glial cells to the rescue

In contrast, many studies have used L-dopa with DA neurons combined with (“co cultured with”) glial/astrocyte cells. They have uniformly found different (and positive!) effects when L-dopa is given to DA neuron/glial combinations, which is the way neurons naturally occur in the living brain (23). Thus, Mena and co-workers found that when L-dopa was added to “dopamine neuron/cortical astrocyte (glia) cultures,” “L-dopa…protected against dopamine neuronal cell death and increased the number and branching of (neurite) processes.” (17). Mean and colleagues reported elsewhere that “L-dopa kills dopamine neurons in culture but is the most effective drug for the treatment of Parkinson’s disease, where it exhibits no clear toxicity. While glial cells surround and protect neurons in vivo, neurons are usually cultured in vitro in the absence of glia. We treated fetal mid brain rat neurons with L-dopa mesencephalic glia conditioned medium ….Mesencephalic glia therefore produced soluble factors which are neurotrophic for dopamine neurons, and which protect these neurons from the toxic effects of L-dopa.” (27). Han et al. found that “…a mild oxidative stress (generated by L-dopa) is tolerated by primary cultures of rat fetal mesencephalon (which contain both DA neurons and glial cells)….Therefore, it appears that (pure) neuronal cultures do not respond (to L-dopa) in the same way as mixed cultures, which are comprised of both neuronal and glial cells.” (20). Desagher and co-workers observed that the “…neurotoxic effect of H2O2 (Hydrogen peroxide) on neurons co-cultured with astrocytes was strongly attenuated compared with that observed on a pure population of neurons…” (26). H2O2 is a neurotoxin generated from L-dopa/DA metabolism, which may be primarily responsible for the L-dopa toxicity observed in pure (without glial cells) neuronal cultures (17, 20).

Thus, the L-dopa controversy is clearly resolved. L-dopa (and its products, DA and 6-Hydroxy DA) toxicity is an artefact. An “artefact” is an artificially produced result, “…any structure of feature produced by the technique used and not occurring naturally.” (28). The studies showing L-dopa toxicity required a specific technique: adding L-dopa (or DA/6-hydroxy DA) to neurons without glial cells. Yet in the living brain, DA neurons are naturally surrounded by glial cells, and the number of glial cells surrounding DA neurons actually increases in Parkinson’s disease, in an effort to protect the remaining neurons (17). The L-dopa toxicity studies are classic artefacts, and thus of little or no “real world” significance.

The reader is also referred back to the various studies of L-dopa in living animals and humans summarised in the section headed “L-dopa : not harmful” earlier in this article. These in vivo studies, where L-dopa interacts with DA neurons in living brains naturally “conditioned by glia”, also found not only no harm, but clear evidence of benefits to DA neurons from L-dopa.

L-Dopa neuroprotection

Although the “pure culture” L-dopa toxicity studies do not have direct application to what does on in the brain, they still have produced some interesting and potentially useful information. Although L-dopa was found toxic to DA neurons without glial protectors in these studies, it was typically found that various nutrients and pharmaceuticals could provide partial or even total protection against “L-dopa toxicity”. Thus, Han and co-workers observed that pure DA neuronal cultures were protected from L-dopa toxicity by ascorbate (Vitamin C) (20). Pardo and colleagues also reported, “In the human neuroblastoma cell line NB69, we have previously shown that co-treatment with AA (ascorbic acid) and Deprenyl, totally protected against L-dopa toxicity”. (24). Walkinshaw and Waters found that catecholaminergic PC12 cell death induced by L-dopa in glial-free culture was reduced 67% by co-treatment with vitamin E, 99% by vitamin C and 99.5% by reduced glutathione (25). Mena et al. found that both reduced glutathione, and NAC (N-Acetylcysteine), which induces intracellular glutathione production and is a direct antioxidant as well, provided major protection against L-dopa toxicity in glial free DA neuron cultures (17). Levites and colleagues discovered that the green tea polyphenol epigallocatechin-3-gallate (EGCG) provided almost total neuroprotection from 6-hydroxyDA toxicity in neuroblastoma cells (29). What these reports indicate is that any potential toxicity that might, in a worst-case scenario, somehow occur from use of L-dopa, can be prevented by appropriate nutrients and pharmaceuticals.

L-Dopa and mitochondrial activity

One problem that has been shown to be triggered by L-dopa in living rat brain is a diminution of complex 1 activity in the cerebral mitochondrial electron transport chain. This mitochondrial activity involves transferring electrons from complex 1 enzymes through complex 5 enzymes sequentially, to generate ATP energy (15). Przedborski and co-workers did find a drop in complex 1 enzyme activity after feeding test rats L-dopa at doses equivalent to human Parkinson patient doses (15). However, they also found that “Reduced glutathione, ascorbate, superoxide dismutase, and catalase prevented the effect of levodopa and dopamine on complex 1”. (15). They also observed that “Various inhibitors of monoamine oxidase also prevented the effect of dopamine”. (15). Of course, deprenyl is a well-known inhibitor of monoamine oxidase metabolism of dopamine (30). Shults and colleagues reported that “The activities of complex 1 and complex 2/3 in platelet mitochondria are reduced in patients with early, untreated Parkinson’s disease. Co-enzyme Q10 is the electron acceptor for complex 1 and complex 2. We found that the level of Co-enzyme Q10 was significantly lower in mitochondria from Parkinsonian patients that in mitochondria from age and set-matched control subjects and that the activities of complex 1 and complex 2/3 were significantly correlated”. (31) In a later clinical study, Shults and colleagues discovered that CoQ10 supplements could successfully “slow the progressive deterioration of function” in Parkinson’s disease compared to placebo, with the greatest benefit coming from the highest dose (1200mg/day) (32). Thus, supplements of Vitamin C, deprenyl and CoQ10 can presumably combat any potential diminution of complex 1 mitochondrial activity that L-dopa might otherwise induce.

L-Dopa plus deprenyl: The controversy

Because L-deprenyl was known to reduce MAO-B activity, and MAO-B creates various toxins from metabolising dopamine, deprenyl was routinely combined with L-dopa in treating Parkinson’s disease (PD) patients during the 1980’s up to 1995. Then in 1995, A.J. Lees et al. on behalf of the UK-PD Research Group published a “bombshell” paper on L-dopa/deprenyl use in PD patients (33). The Research Group followed 520 PD patients for 5-6 years. Several hundred patients initially received 375mg L-dopa plus a peripheral decarboxylase inhibitor (PDI) daily, while several hundred others received 375mg L-dopa plus PDI along with 10 mg L-deprenyl daily. After 5-6 years, the mortality rate in the L-dopa/deprenyl group was 60% higher than in the L-dopa only group. The study authors therefore recommended that deprenyl not be used in PD treatment, with an implication being drawn by many life extension/deprenyl “enthusiasts” that L-dopa and deprenyl should not be combined in any context, not just in PD treatment.

L-Dopa/ deprenyl : The other side

The UK-PD study is the only one ever to find increased mortality with deprenyl use in PD, and the study has been severely criticised on various methodological grounds by various PD experts. In response to the study, the British Medical Journal published 7 letters in 1996 criticising the study on various methodological, statistical and comparative grounds (34). A 1996 Annals of Neurology article by 4 PD experts provided a detailed analysis of the Lees’ UK-PD Group study, raising many questions and criticisms. One key criticism is that the UK-PD study was open label (not blinded), and patients could be withdrawn from their treatment group and changed to other treatments (e.g. Parlodel) during the study. 52% of the L-dopa group and 45% of the L-dopa/deprenyl group changed treatment during the study, yet the allocation of end points (death) was based on patients’ original drug assignment, regardless of which drugs the patient was actually taking at the time of death! (This is called an “intent to treat” analysis). When the death rate was compared by Olanow and colleagues only between those remaining on their original drug assignment, there was no statistically significant difference in mortality between the L-dopa and L-dopa/deprenyl groups (35).

Another criticism raised was that a large number of other studies using deprenyl in PD, many combined with L-dopa, failed to find any difference in mortality between deprenyl groups and control groups (36). Olanow and colleagues also pointed out a glaring difference between the Lees study and other L-dopa with or without L-deprenyl PD studies. The death rate was 200-400% higher in both L-dopa only and L-dopa/deprenyl patients in the Lees study compared to that found in a meta-analysis of 5 previous studies, indicating that something odd was going on in the Lees study, irrespective of deprenyluse or not (35). Clinicians D. MacMahon and R. Bland also pointed out that the deprenyl therapy dose needs to be individually titrated, not just given at one (somewhat high) uniform dose, for maximum benefit and safety. They recounted that a quarter of their patients took less than the 10mg dose, with one elderly gentleman finding a mere 1.25mg deprenyl average daily dose (from taking one half 5mg tablet every other day) as his optimal dose (37). A further “refutation” of the Lees UK-PD study occurred in 2000. Donnan and co-workers published a study showing the results of comparing PD patients treated with L-dopa for seven years, to matched control (“comparators”). They concluded that “subjects with PD had twice the rate of mortality relative to age, and sex-matched comparators. However, those subjects who received selegiline (deprenyl) at any time in combination with co-careldopa or co-beneldopa (i.e. L-dopa plus a peripheral decarboxylase inhibitor) showed no significant difference in mortality compared with comparators”. (38). This study thus indicated that the combination of L-dopa plus deprenyl cut the death rate of PD patients dramatically, equalizing (lowering) it to the death rate of age and sex-matched controls without PD and taking neither drug! That is hardly evidence of the toxicity of combined L-dopa/deprenyl treatment.

Already in 1996, Olanow and colleagues had concluded their paper reviewing the UK-PD study with the statement: “It is our opinion that the evidence in support of discontinuing selegiline (deprenyl) in levodopa treated patients, because of fears of early mortality, is not persuasive. Accordingly, we do not recommend that selegiline be withheld in PD patients based solely on the results of the UK study”. (35). Given the data cited in this section, and the further detail contained in references 34-38, I can only conclude there is no good reason to avoid combining L-dopa with deprenyl. Indeed, there is positive reason to do so, given Pardo and co-workers success in completely reversing L-dopa toxicity in pure (with protective glial cells) neuroblastoma cell cultures with ascorbate plus deprenyl, in case one’s own glial cells should somehow “fall down on the job” in protecting one’s own DA neurons when taking supplementary L-dopa.

[Ed.- A report in the British Medical Journal, August 14, 2004 stated that “deprenyl can slow Parkinson’s disease safely.” They further reported that deprenyl can reduce disability and the need for L-dopa, and that the drugs were not associated with increased mortality. In 17 trials involving 3525 patients wit early Parkinson’s disease, the analysis showed no significant differences in mortality, but did find that patients using deprenyl along with L-dopa had better total scores and activity of daily living. In conclusion Professor Keith Wheatley and his colleagues from the University of Birmingham concluded; “Our review provides no evidence that mortality is increased by selegiline (deprenyl) and suggests that this inexpensive drug could be one of the most clinically effective and cost-effective treatments available for early Parkinson’s disease.” They also believe that the 1995 study that suggested there was increased mortality was a chance finding].

L-Dopa : The form matters

From the data summarised in this paper, it is clear that L-dopa has a safe and useful place in the nutrition/pharmaceutical “life enhancement” strategy. Increasing growth hormone output, preserving healthy, vigorous and well-coordinated movement ability into old age, and gaining anti-depressant/ assertiveness/ increased goal-oriented drive benefits from the chief “warming” neurotransmitter dopamine, whose immediate precursor is L-dopa, are sound reasons for L-dopa use outside a PD content. It should be pointed out, however, that the L-dopa used in the human growth hormone studies was “plain” L-dopa, while the “gold standard” L-dopa (Sinemet ®) used in PD, and which is the most widely used form of L-dopa worldwide, is a combination of L-dopa with a peripheral decarboxylase inhibitor (PDI). The PDI prevents L-dopa from being converted to dopamine outside the brain, thereby reducing side effects (such as nausea) while simultaneously getting more L-dopa to the brain (where the PDI cannot enter). It is generally accepted that 100mg Sinemet ® L-dopa is equal to 400-500mg L-dopa alone (19). Thus 100mg Sinemet ® will approximately provide the typical 500mg L-dopa alone dose used in the human growth hormone studies. However, if the Sinemet ® used is a sustained release variety, it will need to be carefully chewed up (sublingualised) to mimic the fast release L-dopa used in the growth hormone studies. For the movement regulation benefits, as well as for the “warming” neurotransmitter benefits, the sustained-release form is preferable. To maximise the benefit/risk ratio, anyone using L-dopa/ Sinemet ® without medical supervision/monitoring, should probably restrict the dosage to 100mg daily. It is also important to note that dopamine is a stimulating neurotransmitter: Coffee works in part through stimulating dopamine release. Some people will be more sensitive to L-dopa than others. Such effects might look like those from drinking too much coffee, and may include irritability, insomnia, agitation, restlessness, etc. If this occurs, reduce dose to 50mg daily, or take it every other day. If an extreme overreaction occurs, you’re dopamine hypersensitive, and its use should be discontinued.

L-Dopa : The program

In addition to taking the 100mg Sinemet ® dose daily (or less if needed), prudence suggests taking one or more of the previously mentioned L-dopa neuro-protectors: vitamin C (ascorbate), vitamin E (d-alpha plus d-gamma tocopherols), glutathione, N-acetylcysteine, CoQ10, EGCG from green tea extract, and L-deprenyl. Two recent studies have shown that a 1.25mg sublingual (buccal) form of deprenyl (selegiline) provides superior results to 10mg of swallowed “conventional” deprenyl (29, 40). There was less of a problem with the so-called “cheese effect” (intestinal MOA-A inhibition) with the 1.25mg sublingual form. There were significantly reduced levels (80% or more reduction) of the toxic deprenyl metabolites amphetamine and methamphetamine with the sublingual form. Blood levels were more stable and uniform. Patients who compared the 1.25mg buccal form to the 10mg conventional dose generally preferred the 1.25mg conventional dose generally preferred the 1.25mg form. A similar degree of MAO-B inhibition occurred with either form. Those wishing to emulate this dosing method can simply take one drop (1mg) of liquid deprenyl citrate under their tongue, (and don’t wash it down the liquid immediately afterwards).

This would actually equate to an approximate 8mg conventional dosage. Taking one drop every other day would approximate 4mg conventional dose per day. Taking one drop every third day would approximately be equivalent to 2.67mg conventional dose daily. Reasonable doses for ascorbate are 250-1000mg, four times daily. Vitamin E: 100-400 IU, d-alpha tocopherol plus 100-400mg gamma tocopherol. Glutathione:1000-2000mg daily on empty stomach. N-acetylcysteine (NAC): 600-1200mg daily. CoQ10: 100-400mg daily taken with fat-containing meal. EGCG (green tea polyphenol): 100-200mg daily.

In vivo and in vitro stimulatory effects of Cordyceps sinensis on testosterone production in mouse Leydig cells

Source

Department of Cell Biology and Anatomy, College of Medicine, National Cheng Kung University, 1 University Road, 701 Tainan, Taiwan.

Abstract

The in vivo and in vitro effects of Cordyceps sinensis (CS) and its extracted fractions on the secretion of testosterone in mice were studied. CS, F2 (water soluble protein), and F3 (poorly water soluble polysaccharide and protein) significantly stimulated in vitro testosterone production in purified mouse Leydig cells. However, F1 (water soluble polysaccharide) had no effect (p>0.05). F2 and F3 stimulated in vitro testosterone production in dose- and time-dependent relationships with maximal responses at 3 mg/ml for 3 h (p<0.05). An in vivo study illustrated that testosterone levels in plasma were significantly increased by CS, F2, and F3, respectively (p<0.05). Because CS, F2, and F3 stimulated both in vitro and in vivo testosterone secretions in mice, it is possible that CS might contribute to an alternative medicine for the treatment of some reproductive problems caused by insufficient testosterone levels in human males.

PMID:
            12899935 begin_of_the_skype_highlighting            12899935      end_of_the_skype_highlighting      
[PubMed – indexed for MEDLINE]

Abstract

The effects of magnesium supplementation on blood parameters were studied during a period of 4 wk in adult tae-kwon-do athletes at rest and exhaustion. Thirty healthy subjects of ages ranging in age from 18 to 22 yr were included in the study. The subjects were separated into three groups, as follows: Group 1 consisted of subjects who did not train receiving 10 mg/kg/d magnesium. Group 2 included subjects equally supplemented with magnesium and exercising 90–120 min/d for 5 d/wk. Group 3 were subject to the same exercise regime but did not receive magnesium supplements. The leukocyte count (WBC) was significantly higher in groups 1 and 2 than in the subjects who did not receive any supplements (p < 0.05). There were no significant differences in the WBC of the two groups under magnesium supplementation. The erythrocyte, hemoglobin, and trombocyte levels were significantly increased in all groups (p < 0.05), but the hematocrit levels did not show any differences between the groups although they were increased after supplementation and exercise. These results suggest that magnesium supplementation positively influences the performance of training athletes by increasing erythrocyte and hemoglobin levels.

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Do you worry about your cholesterol levels sometimes? And do you know about a close friend or neighbour taking medical drugs such as Statins because her doctor had prescribed these class of drugs to lower her cholesterol?

Well, truth be told, statins to the big pharmaceutical companies, are like the major blockbuster movies that Hollywood create – filled with hype and special effects to wow the audience. And just like these blockbuster movies, there are major flops too. Statins are definitely one of those, that flop big time.

But the difference between a bad movie and a bad drug is that you still live after watching a bad movie. You however, slowly die if you get prescribed a bad drug. Because what the doctor doesn’t know about nutritional medicine may be killing you.

Let me share with you why this is so.

What is Coenzyme Q10 (CoQ10)?

First, you need to know what coenzyme Q10 (CoQ10) is. CoQ10 is needed for the functioning of mitochondria, which is the microscopic power stations found in every cell. They generate ATP, which is the form of energy all forms of life need. Cells with the highest energy demands, contain the highest levels of CoQ10, and CoQ10 is needed for good muscle function. The most important dietary sources of CoQ10 are meats and fish.

The Danger of Synthetic Statins

Now, both CoQ10 and cholesterol are synthesized from the same substance, mevalonate. And statin drugs such as Lipitor, Zocor, etc, inhibit the body’s synthesis of CoQ10 because statin drugs are supposed to inhibit cholesterol. Please note that this is not a “side effect,” of statins, but a direct, inherent function of the drugs. In fact, the use of statins can decrease the body’s synthesis of CoQ10 by as much as 40%!

The depletion of CoQ10 can lead to muscle pain and damage. And-Muscle tissue damaged by a statin drug is certainly contrary to maintaining good health, especially when the damaged muscle tissue is part of the heart muscle-the very organ you are taking the drug to protect!

So, can you imagine that the drug, your doctor prescribed to save you, was actually preventing your body from recovering? Of course, many doctors deny the occurrence of any side effects, and tend to dismiss them. This is mainly due to the fact that pharmaceutical manufacturers producing statin drugs rarely publicize their side effects, and when they do, they are buried in the small print or minimized to a very small percentage of total users.

After all, if you had spent billions of dollars in the researching and developing a drug, you would need to recover the cost, wouldn’t you?

Are There Natural Statins?

Of course there are natural Statins such as Red Yeast Rice, Garlic and Hawthorn and Policasanol. Red Yeast Rice contains a naturally occurring statin called Mevastatin. And as with most herbal products, it contains many other natural substances, some of which act synergistically to reduce negative effects. On the other hand, synthetic statin drugs contain only one isolated synthetic chemical. However the problem with natural statins is that they are seldom produced in accordance to pharmaceutical standards, or strict quality control.

Something even better than Natural Statins: Great Synergy between CoQ10 and Alpha Lipoic Acid

It is important to note that if you take any item containing a statin, even a natural one like that in Red Yeast Rice, you should supplement with at least 120 mg of CoQ10 daily to replace that which the statin depletes. Some quality CoQ10 supplements however need a lesser amount than 120mg because they are paired with Alpha lipoic acid (DHLA). Alpha lipoic acid is involved in mitochondrial energy metabolism and recycling oxidised CoQ10. In other words, the alpha lipoic acid would allow the CoQ10 to be absorbed deeper into the blood plasma, and most of the CoQ10 can be directed to the cells that need it most. Hence, even if you find that you have a bottle of CoQ10 supplements that contains more than 100mg of CoQ10, and no alpha lipoic acid with it, chances are, much of these CoQ10 would not be absorbed well into the cells.

Summary

So while waiting for the CoQ10 issue to be settled in future statin studies, which will probably never see the light of the day, you may wish to maintain your cholesterol level by keeping a better diet and to supplement yourself with quality vitamins and minerals before your cholesterol levels start rising. Take natural statins as the second resort. In most cases ensure that your bottle of CoQ10 has alpha lipoic in it so that your healthy cholesterol goals would be met, and you would never ever need to take synthetic statin drugs.

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25 ml Sodium bicarbonate amp $15 superhumangear@gmail.com

The Effect of Sodium Bicarbonate Ingestion on High-Intensity Intermittent Running and Subsequent Performance

Price MJ, Simons C.

Department of Physiology and Sports Science, Faculty of Health and Life Sciences, Coventry University, Coventry, United Kingdom.

Abstract

Price, MJ and Simons, C. The effect of sodium bicarbonate ingestion on high-intensity intermittent running and subsequent performance. J Strength Cond Res 24(7): 1834-1842, 2010-The purpose of this study was to determine the effects of sodium bicarbonate (NaHCO3) ingestion on intermittent running and subsequent performance. Eight healthy men volunteered to take part in the study. One hour after the ingestion of either NaHCO3 or placebo (sodium chloride; NaCl) participants undertook 20 x 24-second runs on a motorized treadmill at the velocity eliciting maximal oxygen uptake (100% v-&OV0312;o2max). After sprint 20 participants performed a run to volitional exhaustion at 120% v-&OV0312;o2max. Capillary blood samples for blood pH, bicarbonate ([HCO3]), and lactate ([Bla]) concentration were taken pre and postingestion, every fifth sprint and after the performance run. After ingestion of NaHCO3, blood [HCO3] increased from resting values (p 0.05). The results of this study suggest that the ingestion of NaHCO3 before intermittent type exercise was sufficient to induce metabolic alkalosis but did not significantly affect performance. However, because significant individual variations in performance were observed, an individual approach to bicarbonate ingestion is recommended based on the intensity and duration of the required performance.

PMID: 20555273 [PubMed – as supplied by publisher]

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BALTIMORE– Two studies presented at the American College of Sports Medicine’s 57thBaltimore show that chocolate milk may be a worthwhile post-exercise recovery beverage. Annual Meeting in

William Lunn, Ph.D., who collaborated on both research studies conducted in the lab of Nancy Rodriguez, Ph.D., FACSM, found in the first study that ingesting chocolate milk after a run supported skeletal muscle protein synthesis during recovery.

Eight male runners in relatively good training shape completed two runs (each 45 minutes at 65 percent of their maximum levels) during two weeks of eating a balanced diet matched to their individual caloric needs. Following each run, the study participants drank either 16 ounces of fat-free chocolate milk or 16 ounces of a carbohydrate-only beverage, matched for calories with the milk.

Following muscle biopsy samples taken during a three-hour recovery period after each run, Lunn found that runners who drank fat-free chocolate milk during recovery had heightened markers of muscle protein repair compared to the carbohydrate drink.

“It’s always helpful for exercisers to learn of additional options for recovery drinks,” Lunn said. “Chocolate milk can be relatively inexpensive compared to commercially available recovery drinks and is easy to make at home, making it a viable and palatable option for many people.”

The second study showed that chocolate milk also contributes to replenishing glycogen stores in muscles, a source of fuel during prolonged exercise. Muscle glycogen levels in the same eight male runners were tested 30 minutes and 60 minutes following ingestion of either the fat-free chocolate milk or the carbohydrate beverage.

Muscle glycogen content was greater for the chocolate milk drinkers at both measurement times, further supporting the use of this drink in recovery nutrition strategies.

The American College of Sports Medicine is the largest sports medicine and exercise science organization in the world. More than 35,000 international, national and regional members and certified professionals are dedicated to advancing and integrating scientific research to provide educational and practical applications of exercise science and sports medicine.

-30-

Note: These studies were supported by a grant from the National Dairy Council and National Fluid Milk Processor Promotion Board.

The conclusions outlined in this news release are those of the researchers only, and should not be construed as an official statement of the American College of Sports Medicine.

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The effects of caffeine ingestion on performance time, speed and power during a laboratory-based 1 km cycling time-trial.

Wiles JD, Coleman D, Tegerdine M, Swaine IL.

Department of Sport Science, Tourism and Leisure, Canterbury Christ Church University, Canterbury, UK. j.d.wiles@cant.ac.uk
Abstract

There is little published data in relation to the effects of caffeine upon cycling performance, speed and power in trained cyclists, especially during cycling of approximately 60 s duration. To address this, eight trained cyclists performed a 1 km time-trial on an electronically braked cycle ergometer under three conditions: after ingestion of 5 mg x kg-1 caffeine, after ingestion of a placebo, or a control condition. The three time-trials were performed in a randomized order and performance time, mean speed, mean power and peak power were determined. Caffeine ingestion resulted in improved performance time (caffeine vs. placebo vs. control: 71.1 +/- 2.0 vs. 73.4 +/- 2.3 vs. 73.3 +/- 2.7 s; P = 0.02; mean +/- s). This change represented a 3.1% (95% confidence interval: 0.7-5.6) improvement compared with the placebo condition. Mean speed was also higher in the caffeine than placebo and control conditions (caffeine vs. placebo vs. control: 50.7 +/- 1.4 vs. 49.1 +/- 1.5 vs. 49.2 +/- 1.7 km x h-1; P = 0.0005). Mean power increased after caffeine ingestion (caffeine vs. placebo vs. control: 523 +/- 43 vs. 505 +/- 46 vs. 504 +/- 38 W; P = 0.007). Peak power also increased from 864 +/- 107 W (placebo) and 830 +/- 87 W (control) to 940 +/- 83 W after caffeine ingestion (P = 0.027). These results provide support for previous research that found improved performance after caffeine ingestion during short-duration high-intensity exercise. The magnitude of the improvements observed in our study could be due to our use of sport-specific ergometry, a tablet form and trained participants.

PMID: 17035165 [PubMed – indexed for MEDLINE]

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Pérez-Guisado J, Jakeman PM.

Department of Medicine, University of Córdoba, Córdoba, Spain. pv1peguj@uco.es
Abstract

The purpose of the present study was to determine the effects of a single dose of citrulline malate (CM) on the performance of flat barbell bench presses as an anaerobic exercise and in terms of decreasing muscle soreness after exercise. Forty-one men performed 2 consecutive pectoral training session protocols (16 sets). The study was performed as a randomized, double-blind, 2-period crossover design. Eight grams of CM was used in 1 of the 2 training sessions, and a placebo was used in the other. The subjects’ resistance was tested using the repetitions to fatigue test, at 80% of their predetermined 1 repetition maximum (RM), in the 8 sets of flat barbell bench presses during the pectoral training session (S1-4 and S1′-4′). The p-value was 0.05. The number of repetitions showed a significant increase from placebo treatment to CM treatment from the third set evaluated (p <0.0001). This increase was positively correlated with the number of sets, achieving 52.92% more repetitions and the 100% of response in the last set (S4'). A significant decrease of 40% in muscle soreness at 24 hours and 48 hours after the pectoral training session and a higher percentage response than 90% was achieved with CM supplementation. The only side effect reported was a feeling of stomach discomfort in 14.63% of the subjects. We conclude that the use of CM might be useful to increase athletic performance in high-intensity anaerobic exercises with short rest times and to relieve postexercise muscle soreness. Thus, athletes undergoing intensive preparation involving a high level of training or in competitive events might profit from CM.

PMID: 20386132 [PubMed – in process]