There is a vitality, a life force, an energy, a quickening, that is translated through you into action, and because there is only one of you in all time, this expression is unique. And if you block it, it will never exist through any other medium and will be lost.

–Martha Graham, choreographer and dancer

The Anti–Aging Effects of Creatine – An Overview­

• The burning of food in the presence of oxygen takes place in cellular structures called mitochondria. This process is called cellular (or mitochondrial) respiration. Keeping our mitochondria healthy ensures that energy will be produced efficiently within our cells.

• Some of the most promising anti–aging strategies involve nutritional and lifestyle choices which protect the mitochondria from stress, toxins, poor food choices, and a lack of nutrients.

• The essence of life is energy. Contrary to what was once believed, increasing metabolic rate and actually stimulating mitochondrial energy production has health–enhancing and anti–aging effects.

• When the mitochondria are damaged (or when they don’t have the nutrients they need to function properly), the cells can shift energy production towards glycolysis – a relatively inefficient, and ultimately harmful, means of producing energy.

• When the mitochondria aren’t functioning properly, the products of glycolysis (including lactic acid, pyruvate, and inorganic phosphate) accumulate – further suppressing respiration, and often killing cells.

• Age–related disorders like heart disease, cancer, diabetes, and Alzheimer’s disease all show evidence of mitochondrial dysfunction – and a shift towards glycolysis as a means of “emergency” energy production.

• The nutritional supplement, creatine, has been shown to extend lifespan in animal studies; to reduce the production of the age–pigment, lipofuscin; and to improve age–related neurological/mental decline.

• Creatine supplementation may ultimately improve the efficiency of cellular energy production in several ways. Creatine’s anti–aging effects may stem from its ability to reduce the cell’s reliance on glycolysis as a means of energy production. The presence of creatine stimulates the creatine shuttle. The creatine shuttle not only allows for rapid recycling of ATP during intense activity, but, at rest, the production of phosphocreatine (PCr) converts ATP into ADP, and ADP is known to stimulate energy production by the mitochondria.

• Research has indicated that creatine does, in fact, help to stimulate mitochondrial respiration – allowing for the efficient and healthy flow of energy throughout the body. Creatine has been shown to reduce levels of potentially harmful substances associated with glycolysis, including lactate, inorganic phosphate, glucose, and glycation products.

hough the nutritional supplement creatine initially gained popularity as muscle builder and athletic enhancer, it seems that this simple energy nutrient may impart a stunning array of health benefits for athletes and non–athletes alike. In fact, as the scientific research on creatine continues to mount, it’s becoming clear that creatine may be one of the most effective anti–aging substances we have at our disposal. Studies have recently shown creatine to extend lifespan in laboratory animals, and scores of studies have found creatine to exert protective effects throughout the body, in the brain, muscles, heart, skin, bones, connective tissue, and neurological system.

Yet, despite an enormous amount of compelling creatine research, the potential long–term health benefits of this simple, low–cost nutritional supplement are almost completely unknown to all but the most savvy supplement consumers. In this, and upcoming editions of the Integrated Supplements Newsletter, we’ll continue with our Creatine Q & A by taking an in–depth look at the anti–aging effects of creatine.

Q. First off, what does the term “anti–aging” mean exactly?

A. When we use the term anti–aging, we’re simply referring to nutritional and lifestyle interventions which can help to maintain the proper function of our cells, and tissues.

Of course, the idea of “anti–aging” can easily conjure up images of the futile search for the mythical fountain of youth, but the truth is that the scientific study of aging, or gerontology, is a field which has made great strides in recent years. One of the hallmark achievements of this science has been to examine many of the cellular and molecular changes that may be precursors to aging, disease, and bodily degeneration. Long before diagnosable conditions develop, these cellular changes act as warning signals, which, ideally, can be addressed before the damage becomes too great to reverse.

Gerontologists have developed several (often inter–related) theories as to the causes of aging; and, as some of these modern theories gain support via continuing research, it seems that the nutritionally–conscious among us may have great reason for optimism when it comes to forestalling the ravages of old–age.

Q. What sort of cellular changes cause aging?

A. As scientists continue to study the issue, it’s becoming clear that progressive damage to mitochondria is likely to be a primary cause of the many bodily changes we associate with aging.

Mitochondria are the energy–generating structures within our cells. As we’ve discussed in previous newsletters, the conversion of foods to energy produces metabolic byproducts called free radicals (also often referred to as reactive oxygen species, or ROS). The more inefficiently our cells produce energy, the more free radicals are produced, causing damage to delicate cellular structures including, and especially, the mitochondria.

To make a long biochemical story short, the mitochondria in our cells are unique among cellular structures in that they contain their own DNA (as you may remember from high school biology class, the vast majority of what we consider “our” DNA is found in the nucleus of the cell).

Though relatively simple relative to the 100,000 genes which comprise nuclear DNA, the mere 37 genes which constitute mitochondrial DNA (mtDNA) are still remarkably important. They contain the blueprints which encode for the structures of the energy “assembly line” known as the respiratory chain. Without mitochondria and their DNA, energy production, and life itself, simply could not exist.

And because mitochondrial DNA resides on the “front lines” of energy production within the mitochondria, mtDNA is quite susceptible to damage via the reactive oxygen species (ROS). This means that, unlike the DNA which is protected within the cellular nucleus, mitochondrial DNA is relatively easily damaged, and is often thought to be nearly impossible to repair. The result of this mtDNA damage is often mitochondria which produce relatively little in the way of usable energy and much in the way of harmful free radicals – think of energy production by damaged mitochondria as being akin to electricity running through a frayed electrical cord – shooting off sparks, but not providing usable energy to the appliance.

When defective mitochondria reproduce, these mutations are passed on, and energy is produced ever more inefficiently. The end result, in aging, is a cellular energy crisis where defective mitochondria are unable to provide for the energy requirements of the cell. Cells which produce energy inefficiently, add up to organs and tissues which function abnormally; and organs and tissues which function abnormally eventually manifest as age–related symptoms and disorders throughout the body. On a macroscopic level, all of the diseases of aging (cancer, diabetes, heart disease, Alzheimer’s disease), and even non–disease manifestations of aging like wrinkled, weather–beaten skin, and general mental decline are associated with significant mitochondrial damage.

The take home lesson is that there is a direct correlation between how efficiently our cells produce energy today (i.e., how healthy our mitochondria are), and our future health. Taking steps in one’s (relative) youth to prevent mitochondrial damage, is an anti–aging strategy which is likely to be very rewarding as we get older.

Q. So if damage to mitochondrial DNA is responsible for aging, does this mean that “it’s all in our genes?” Is our rate of aging dictated by genetics?

A. It’s an interesting question. Genetics certainly does play a role in aging, and, yes, there are some inheritable genetic disorders which affect mitochondrial DNA. But the vast majority of us have mitochondria which function perfectly well at birth and which would continue to do so for many decades if they were taken care of properly. In other words, it’s what we do to our bodies over a lifetime which is the greatest determinant of aging – not any innate genetic defect or “biological clock”.

This is why it’s so exciting to see that there are nutritional strategies which may be able to prevent the mitochondrial damage which often takes place over the natural course of aging.

For example, a recent study published in Neurobiology of Aging examined the effects of lifelong creatine supplementation in mice. The mice fed creatine exhibited:

• A 9% increase in average healthy lifespan.

Study Link – Creatine improves health and survival of mice.

Such simultaneous and multi–faceted improvements in several markers of aging give us clear evidence that creatine supplementation may be able to slow the aging process on a very fundamental cellular level. It’s very likely that creatine supplementation serves to improve the efficiency of mitochondrial energy production.

As evidence, other studies have shown that creatine is, indeed, able to prevent damage to mitochondrial DNA. But according to the following study, creatine doesn’t appear to exert its protective effects simply by “mopping up” free radicals like other antioxidants. It appears likely that creatine is able to improve mitochondrial function, reducing not only free radical production, but also, the formation of other harmful substances produced as a result of inefficient energy production. Such effects give this simple nutritional substance a stunning array of potential health benefits:

Study Link – Creatine supplementation normalizes mutagenesis of mitochondrial DNA as well as functional consequences.

Quote from the above study:

These data indicate that increase of the energy precursor creatine protects from functionally relevant, aging–associated mutations of mitochondrial DNA… The data demonstrate that creatine does not absorb in the UV range and does not act as an antioxidant. Therefore, we hypothesize that protection from UVA–mediated induction of the common deletion is not exerted through direct quenching but through an indirect effect in which creatine, by normalizing the cell’s energy status, reduces the requirement to upregulate a deleterious respiratory chain that again would generate more ROS.

The above study showed that creatine prevented the mitochondrial DNA damage to fibroblast cells caused by exposure to ultraviolet light (in particular, ultraviolet A or UVA). The researchers specifically exposed these cells to levels of UV rays which would mimic the exposure our skin cells would be likely to receive during “a regular summer holiday.” Ultraviolet light is well–known to cause skin aging (photoaging) and wrinkles, so, given the results of this study, it may only be a matter of time before we see creatine supplements being marketed to support healthy, youthful skin. And it’s important to realize that creatine is likely to exert similar protective effects upon mitochondrial DNA in cells throughout the body – which would account for creatine’s far–reaching anti–aging effects.

Q. If mitochondria produce free radicals as natural byproducts of energy production, should we be trying to produce or expend less energy if we want to prevent aging?

A. In the early days of anti–aging research, many scientists believed that this was the case, but the idea has been largely abandoned in light of subsequent research.

In what’s simplistically called the “wear–and–tear” hypothesis of aging, it was assumed that the more energy our body expended, the quicker our body would “wear out” – in much the same way that a car with high mileage is more apt to suffer engine trouble than a car with low mileage.

Following on the heels of this wear–and–tear hypothesis, has been the similar, yet more refined, rate–of–living theory, which sought to explain lifespan in terms of metabolic rate. According to this theory, the lower an organism’s metabolic rate (i.e., the less energy it produces), the longer its lifespan will be. Early research even seemed to support these hypotheses, somewhat.

For instance, it’s been well–documented that one of the most successful ways to increase lifespan in laboratory animals is to restrict the amount of calories they consume. Advocates of the “wear–and–tear” and rate–of–living theories understandably interpreted the calorie restriction (CR) findings to mean that if animals were forced to metabolize less food (i.e., the energy–producing mitochondria did less work), then the animal would naturally live longer.

But subsequent anti–aging research has shown repeatedly that actually stimulating mitochondrial energy production (mitochondrial respiration) is associated with increased longevity. Many species with notably high metabolic rates consume more food (for their weight) and live longer than species with lower metabolisms. This phenomenon is also evident within species – smaller dogs are well known to consume greater amounts of food relative to their bodyweight than large dogs, and yet small dogs have a much longer lifespan than large ones:

Study Link – Age–related changes in the metabolism and body composition of three dog breeds and their relationship to life expectancy.

Quote from the above study:

. . .energy expenditure was almost 60% greater for the smallest compared with the largest breed. On average, however, the life expectancy for the smallest breed was a further 6 years (i.e. 14 years in total), whereas for the largest breed it was only another 6 months (i.e. 8.5 years in total). . . High energy expenditure in dogs appears positively linked to increased life expectancy, contrary to the finding across mammal species and within exotherms, yet resembling observations in other intraspecific studies.

So, it’s becoming clear that whatever the mechanism by which caloric restriction extends lifespan, it is not simply because it reduces metabolic rate, or energy production.

In fact, it’s important to recognize explicitly that energy is the essence of life. We can sometimes draw analogies between the human body and non–living things to illustrate how energy production takes place in living systems. But it’s important to remember that these are just analogies – we are not machines which inevitably wear out over time. Unlike an automobile, or a power plant, or a factory, running our cells at “full capacity” actually enhances the processes of growth, repair, recovery, and life itself.

To understand why this is, and to understand exactly how an energy–associated molecule like creatine may play into the picture, it’s important to have a basic understanding of the assembly line our cells use to produce energy. As we’ll see, free radical damage from energy production is actually reduced significantly when energy production is flowing smoothly, and increased significantly when certain factors (poor food choices, a lack of activity, nutrient deficiencies, or cellular toxins) impair the energy–production process.

In vastly simplified terms, energy production within our cells begins outside of the mitochondria with glycolysis (the breakdown of glucose). As a result of glycolysis, the sugar, glucose, is converted into pyruvate, and in the process, NAD (nicotinamide adenine dinucleotide) and small amounts of the energy molecule, ATP, are formed.

Glycolysis can provide a small amount of ATP for the cell very quickly, but usually only for a short period of time. As the oxygen in the cell is used up during heavy exertion, the pyruvate produced is quickly converted to lactic acid – making glycolysis a relatively inefficient means of energy production.

This is why weight–training, which engages the glycolytic system, is said to be anaerobic (in the absence of oxygen) activity. As we all know, lactic acid builds up relatively quickly when we lift heavy weights, which is commonly thought to be why muscles fatigue rapidly during this type of training.

Under less physically demanding conditions, when oxygen is present, the pyruvate formed from glycolysis is (ideally) able to enter what’s called the Krebs cycle (or citric acid cycle) within the mitochondria. The Krebs cycle generates (among other things) a bit more ATP, carbon dioxide, and a reduced (having a hydrogen ion added) form of NAD called NADH.

This NADH is then transferred to the major ATP–generating part of the energy assembly line, the electron transport chain, located in the mitochondria. The process by which ATP is produced by the electron transport chain is known as oxidative phosphorylation (OXPHOS, for short). Under ideal conditions, the majority of the cells’ ATP will be produced by OXPHOS.

Now, of course, it’s common knowledge that when we tax our muscles with a really intense workout, the result is a build–up of lactic acid. The reason for this is because the body is breaking down glucose (glycolysis) into pyruvate faster than the Kreb’s cycle in the mitocondria can use it. The pyruvate then “spills over” into lactic acid production rather than being more completely metabolized in the mitochondria (via the Krebs cycle and OXPHOS).

But it’s very important to realize that lactic acid production doesn’t just occur during exercise. Any stress which inhibits the flow of energy through the mitochondria, or which causes mitochondrial damage, can result in an increase in lactic acid production. Such stresses could be emotional/psychological in nature, or could include estrogen excess, a poor diet, a lack of key nutrients, environmental and dietary toxins, or simply, the aging process itself.

In the presence of these stressors, inefficient production of energy by the mitochondria (and, possibly, even lactic acid itself) serves to damage the mitochondria. Once the mitochondria become damaged, the result is a vicious downward spiral of increased free radical and lactic acid production, cell dysfunction, and cell death. Such progressive mitochondrial dysfunction is now well known to play a central role in the aging process, and in age–related degenerative diseases such as Alzheimer’s disease, diabetes, cancer, and heart disease.

So, in essence, our primary goal if we wish to forestall age–related changes in our body is to see to it that the “assembly line” of energy production is functioning as efficiently as possible.

In biochemical terms, we want to see to it that glucose (our body’s main fuel) is converted into pyruvate, which is then taken up by the mitochondria and cycled into the Krebs cycle (with the resultant production of carbon dioxide, ATP and NAD). Then, ultimately, the maximal and most efficient production of ATP will be driven (with the NAD produced from the Krebs cycle) via oxidative phosphorylation (OXPHOS).

In simple terms, healthy mitochondria are absolutely necessary for this flow of energy to function properly.

Q. So, when our mitochondria aren’t functioning properly, the products of glycolysis can’t be metabolized properly, which predisposes us to aging and age–related diseases?

A. Yes, exactly. Glycolysis is a normal part of how our cells convert glucose to energy, but certain stressors can cause the process to go awry. When the mitochondria are functioning properly, the products of glycolysis are metabolized efficiently in the mitochondria (via the Krebs cycle, and OXPHOS). But sometimes, damage to the mitochondria causes the products of glycolysis to “build up” in the cell – even in the presence of sufficient oxygen (which would normally drive energy production by the mitochondria). We can think of the buildup of glycolytic metabolites as a metabolic “logjam” which takes place when the products of glycolysis can’t enter, or be metabolized properly by the mitochondria.

When the mitochondria can’t complete the oxidation of glucose properly, it is then metabolized via alternate routes outside of the mitochondria. In other words, in glycolysis, instead of “burning” efficiently in the presence of oxygen as it should, glucose “ferments” into other substrates. In human physiology, the most obvious “fermentation” product of glycolysis is lactic acid, which is a clear marker of inefficient energy production. There are likely to be many factors involved, but it’s safe to say that lactic acid and related products of glycolysis are universally harmful to the cell.

Q. What are some of the harmful effects of glycolysis and lactic acid?

A. Though most people still associate “lactic acid” only with exercise fatigue, lactic acid is also a general marker of cellular stress and dysfunction. After trauma or surgery, for example, if a patient goes into shock, the degree of lactic acid production correlates very strongly with a fatal outcome.

Study Link – Excess Lactate: An Index of Reversibility of Shock in Human Patients.

Quote from the above study:

The levels of excess lactate correspond to severity of circulatory failure, and an excess of more than 4 millimoles per liter prognosticates a fatal outcome.

Note: In the name of scientific correctness, it’s worth noting that the term “lactate,” as used in the above study, is probably more precise than lactic acid – there is considerable debate as to whether our cells actually produce lactic acid or lactate as a byproduct of glycolysis, but because either one would be a marker of inefficient energy production and mitochondrial dysfunction, this doesn’t really matter for our discussion.

In order to get a feel for the types of harmful effects glycolysis and its metabolic byproducts can impart upon the body, it will probably help to look at cellular respiration in terms of the other type of respiration with which we are all familiar – namely, breathing. Many of the “respiratory defects” which often affect the young (asthma, anxiety, panic disorder) mimic themselves on a cellular level in the degeneration of aging. When we look at these disorders conceptually, we’ll find the common thread of impaired mitochondrial energy production running throughout.

Quite obviously, when our body senses an increased energy demand, it will trigger our rate of breathing to increase. Our breathing during a jog, for example, will naturally be much faster and deeper than when we are reading a book, or watching television.

Under periods of high oxygen demand, our cells will (ideally) be able to utilize the oxygen taken in, and will increase their production of carbon dioxide (remember, the utilization of oxygen, and the production of carbon dioxide occurs in the mitochondria). For this reason, we can conclude that the delicate balance between oxygen taken in, and carbon dioxide produced, is a function of the health of our mitochondria.

And, although it’s commonly seen merely as a “byproduct” of breathing, carbon dioxide actually serves some very important physiological functions. In fact, one of the reasons it’s so important to maintain healthy mitochondria, is to ensure the continuous production of sufficient amounts of carbon dioxide. For example, contrary to common misconception, it’s actually the bodies’ response to carbon dioxide (not oxygen) which controls our rate of breathing.

A low level of carbon dioxide production by the mitochondria is indicative of inefficient oxygen use, and will trigger faster, deeper, breathing patterns to supply more oxygen to the cell. But, in a seemingly ironic twist of fate, the more oxygen we take in, the less of it we can actually use (low levels of carbon dioxide actually make the oxygen–carrying hemoglobin molecule latch on to oxygen tighter, making it less apt to supply oxygen to the cells – this is called the Bohr effect).

So, as a result of increased breathing, oxygen delivery to the mitochondria actually becomes worse, and carbon dioxide production is reduced – at the same time we’re “blowing off” more carbon dioxide in the air we exhale. The result is a drastic drop in carbon dioxide levels, which often manifests in such things as hyperventilation, anxiety, or panic reactions. This cellular chain of events is a clear indication of why these disorders are always self–perpetuating.

Q. Why would a lack of oxygen cause us to breathe deeper, if this can’t even deliver more oxygen to the cells?

A. The reason probably lies in our evolutionary history. The control of respiration is undoubtedly linked somewhat to the “fight or flight” response. It’s fair to assume, that during the early stages of our evolution, (out of necessity) humans were much more active than we are today. As such, in our primordial ancestors, the need for oxygen was probably always linked to some sort of physical activity. This physical activity served to produce sufficient carbon dioxide by dramatically increasing mitochondrial function. In other words, our bodies have evolved to supply us with oxygen for activity – far more oxygen than relatively sedentary people could ever need.

Once hemoglobin (the oxygen–delivery protein) is saturated with oxygen, it requires carbon dioxide to release this oxygen to the tissues. But without the carbon dioxide which is produced in the mitochondria (via the Krebs cycle) as a result of energy production (physical activity), oxygen simply cannot be released from hemoglobin properly. This is the essence of hyperventilation – suffocation in the presence of oxygen.

Along these lines, we can see why moderate (not excessive) exercise is known to be therapeutic in disorders characterized by “hyperventilation.” Asthma, panic attacks, anxiety, and depression have been known to improve in response to the moderate type of physical activity which engages mitochondrial respiration.

In the popular media, we often hear about exercise and “endorphins,” but it’s far more likely that the positive psychological effects of exercise are a response to improved mitochondrial function. Intense exercise, of course, could have the opposite effect, which is why it’s often tricky to administer exercise in the correct “dose.”

It seems likely that the sum total of the mitochondrial stressors we have to deal with today (poor nutrition, nutritional, hormonal, and environmental toxins, a hectic lifestyle, etc.) have made mitochondrial damage, and a “hyperventilated” metabolism common. In other words, the flow of energy through the mitochondria isn’t always rectified by increasing physical activity. Sometimes, the mitochondria themselves are damaged, or there are nutritional deficiencies which are only made worse by physical activity. This is why we should continually try to find and rectify all factors which inhibit mitochondrial function. It’s important to recognize that if we don’t address these other stressors, exercise can sometimes do more harm than good.

Looking at mitochondrial dysfunction as being akin to hyperventilation can give us some meaningful clues as to how to approach the issue. It’s common practice when hyperventilating for people to breathe into a paper bag. In doing this, a person is able to elevate carbon dioxide levels by inhaling the carbon dioxide they just exhaled. It’s also possible to consciously control breathing in order to allow the cells to “hold on to” more carbon dioxide. But, as we shall see, the same basic respiratory defects underlying hyperventilation, panic, and anxiety, also underlies the cellular changes of aging. Correcting these defects in the long–term requires that we increase carbon dioxide production on a cellular level by enhancing mitochondrial function.

Of course, the relationship between hyperventilation, panic and anxiety, exercise, and the disorders of aging aren’t immediately apparent to the average person. But when we look at them from the perspective of cellular energy production, the parallels become stunningly clear.

Interestingly, it has been found that people with panic disorder (which is often conceptualized as a type of chronic hyperventilation) respond to low carbon dioxide levels with an exaggerated lactic acid–response (i.e. increased glycolysis). And, again, this occurs even when sufficient oxygen is present:

Study Link – The lactic acid response to alkalosis in panic disorder: an integrative review.

Quote from the above study:

Panic patients consistently show exaggerated lactic acid response to alkalosis, whether produced by hyperventilation or by sodium lactate infusion. Understanding why this occurs may provide important clues to the pathogenesis of panic disorder. Although brain hypoxia [lack of oxygen] from excessive hypocapnia [lack of carbon dioxide]–induced cerebral vasoconstriction is often cited as the mechanism of elevated brain lactic acid in panic disorder, studies of brain metabolism show that hypocapnia rarely leads to brain hypoxia.

For the purpose of scientific studies, infusions of lactate are even used to trigger panic attacks in susceptible individuals (the following study found that the infusion of sodium bicarbonate had the same panic–inducing effect as lactate only when it reduced carbon dioxide levels – further evidence of mitochondrial dysfunction playing a major role).

Study Link – A comparison of sodium bicarbonate and sodium lactate infusion in the induction of panic attacks.

Quote from the above study:

Infusion of sodium lactate has been shown by a number of investigators to induce panic in patients with panic disorder, but the pathophysiology underlying this phenomenon is unknown. One theory to explain lactate's anxiety–producing effects involves its ability to induce alkalosis because of metabolic conversion to bicarbonate. To test this hypothesis, we administered both sodium lactate and sodium bicarbonate infusions in counterbalanced order to patients with panic disorder… Although the rate of panic between the two infusion responses was not significantly different, several aspects of response to the two infusions indicated that lactate may be a more potent producer of anxiety than bicarbonate. An unexpected finding was that bicarbonate panickers had a reduction in arterial carbon dioxide pressure during the infusion, while bicarbonate nonpanickers had an increase in arterial carbon dioxide pressure during the infusion. Induction of hyperventilation and subsequent hypocapnia appears to be a common denominator between lactate– and bicarbonate–induced panic.

Even more interesting, especially as it relates to our discussion of creatine, is the finding that panic disorder patients have low levels of creatine and phosphocreatine in the regions of the brain thought to be affected in panic disorder:

Study Link – Reduced Levels of Creatine in the Right Medial Temporal Lobe Region of Panic Disorder Patients Detected with 1H Magnetic Resonance Spectroscopy.

Quote from the above study:

The concentration of creatine and phosphocreatine, metabolites involved in energy–dependent systems in brain, was significantly lower in the right medial temporal lobe region of panic disorder patients compared to healthy subjects.

As we’ll see, creatine has been shown in several studies to reduce lactate/lactic acid production. Of course, most people simply associate this effect with the athletic benefits creatine is well–known for. But creatine’s effect on balancing cellular energy production is likely to hold the key to its anti–aging benefits.

In the continuation of this article, we’ll look at some age–related disorders like cancer and diabetes, which are characterized similarly by a “hyperventilated” metabolism – including mitochondrial dysfunction, excessive glycolysis, and lactate production. We’ll also dig a bit deeper into exactly how creatine supplementation may be able to shift the cellular energy balance away from glycolysis, and its harmful byproducts, and towards healthy mitochondrial respiration.