A naturally occurring organic acid known ascreatine has long been used by athletes to boost their performance and build muscle strength without steroids. But emerging research is showing that creatine also has important anti-aging effects in vital tissues throughout the body.
As we age, the unique benefits of creatine become more pronounced. From protection against cognitive decline and congestive heart failure to reducing insulin levels and shielding against muscle loss, creatine enhances mitochondrial function that helps reduce the ravages of aging.
Recently, creatine has been found to significantly lower the accumulation of a recognized marker of aging called lipofuscin in the brains of aging mice. As a result, creatine-fed mice lived an average of 9% longer than control animals— that’s equivalent to more than seven years for an average human!
The supplemented animals also performed significantly better on neurobehavioral testing. In fact, creatine is now being hailed by experts as “a starting-point for a novel means of delaying neurodegenerative disease, and/or for strengthening memory function and intellectual capabilities.”
Because of creatine’s vital impact on your body’s energy levels, it should be considered for anyone interested in slowing aging, improving energy levels, and fighting off age-related diseases.
In order to understand how creatine can have such a powerful impact on a wide range of functions within the body, you have to understand the key role that creatine plays in cellular energy supplies.
Mitochondria are found in every cell and are responsible for converting food into the energy the body needs in order to function. Aging leads to the accumulation of dysfunctional mitochondria.
The loss of mitochondrial function can cause the buildup of aging pigments known as lipofuscin. Lipofuscin builds up when a cellular “garbage-disposal system” (i.e., autophagy) breaks down. Eventually, with the decrease in autophagy and related increase in lipofuscin, there is increased oxidative stress, decreased energy production, and ultimately, cell death.
In studies, creatine has been found to help boost cellular energy and to significantly lower accumulation of lipofuscin in the brains of aging mice. Creatine also helps maintain adequate levels of high-energy phosphate-containing molecules in tissues with especially high energy consumption, such as the heart, brain, and muscle. High levels of creatine support the body’s production of ATP, the universal energy-transfer molecule, when ATP itself is used up by these power-hungry tissues.
Ultimately, supplementing with creatine helps restore the energy loss that is at the root of many age-related diseases. As you’ll see in the next sections, creatine supplementation has a positive impact on everything from cognitive decline to cardiovascular health.
Many brain disorders involve a disruption of the brain’s energy supply systems. That applies not only to chronic, age-related diseases such as Parkinson’s, Alzheimer’s, and Huntington’s, but also to acute conditions such as strokes and traumatic brain and spinal cord injuries. Creatine’s role as an energy-enhancer suggests it may be helpful in all of these conditions.
In addition, this energy loss leads to the accumulation of the damaging lipofuscin pigments that are present in all of these neurodegenerative diseases. Creatine’s ability to lower the accumulation of this aging pigment offers promise in the treatment of these cognitive diseases.
Here’s a rundown on what we know about creatine supplementation in brain diseases associated with aging:
Alzheimer’s disease primarily affects memory and cognition, with debilitating loss of the ability to recognize loved ones, to navigate even around the home, and to sustain meaningful conversations.
Creatine supplementation shows promise in addressing the underlying causes of this disease—especially when given in the early stages. This is due in large part to creatine’s role as an energy enhancer. That’s because energy loss from dysfunctional mitochondria plays a major role in this disease—and causes damaging lipofuscin pigments to accumulate as a result.
Creatine also protects brain cells against the root cause of this energy loss, namely the excitotoxicitythat is a hallmark of neurodegenerative diseases in general, and against the toxic Abeta proteins that are unique to Alzheimer’s. Creatine protects against this toxicity, which impairs mitochondrial energy production.
Parkinson’s disease is a disorder of movement control in the brain; it produces tremors, slowed movements, and a characteristic “mask-like” face. Advanced Parkinson’s disease can also include dementia, with symptoms similar to Alzheimer’s.
Creatine can have a positive effect on a number of the factors involved in this disease. For starters, brain tissue from both humans and animals with Parkinson’s disease show abnormally high levels of telltale lipofuscin pigment. This indicates that problems with cellular energy management and waste control are underlying factors in the disease. As we’ve discussed, creatine has been found to lower the accumulation of lipofuscin.
Creatine also enhances the survival and protection of neurons that produce dopamine, the missing transmitter in the disease. Studies have shown that creatine improves patient mood, allows smaller doses of medication to be used, and also reduces the side effects of those meds. This is especially noteworthy for Parkinson’s patients, since the most commonly prescribed medication for Parkinson’s ( L-DOPA, a precursor to dopamine) causes disturbing side effects including out-of-control movements.
Huntington’s disease is a genetic neurodegenerative disorder that involves damage to motor control centers in the brain, and symptoms include wild, out-of-control movements.
As with the other disorders, the brain cells of Huntington’s patients display excessive amounts of the aging pigment lipofuscin—indicating underlying problems with cellular energy. This suggests creatine may be an important component in the battle against this disease.
Remarkably, creatine supplementation has been shown to offer considerable neuroprotection even after the onset of symptoms in animal studies. Supplemented animals also survived significantly longer than controls when creatine was provided in the early and middle stages of the disease. These effects were directly attributed to creatine’s ability to increase brain levels of energy in the form of stored ATP.
Mice with experimental Huntington’s disease that were supplemented with creatine showed slower loss of brain tissue and delayed accumulations of the destructive protein gene huntingtin. Supplemented animals also had improvements in body weight and motor performance, and slower onset of diabetes.
Amyotrophic Lateral Sclerosis (ALS) is a devastating neurodegenerative disease that can strike without warning at almost any age. Sometimes referred to as Lou Gehrig’s disease, it is closely associated with mitochondrial dysfunction in the brain cells that control voluntary movement, resulting in weakening and eventually atrophy of skeletal muscles. Respiratory failure is the major cause of death in ALS patients.
Although it is considered an untreatable condition, creatine could offer symptomatic treatment for those suffering from ALS. In human patients, creatine supplementation at 20 grams/day for seven days, followed by 3 grams /day for up to six months, increased voluntary muscle contractions at the knee in 70% of patients, and at the elbow in 53% of patients. These improvements wore off after six months; however, the researchers concluded that creatine can at least temporarily boost muscle power in ALS patients.
This beneficial effect may be due to creatine’s impact on the neurotransmitter glutamate. The overstimulation of glutamate leads to excitotoxicity, which is a phenomenon implicated in ALS. Animal research showed that creatine helps reduce increases in brain levels of glutamate. Supplemented animals also survived longer and performed better on motor tests.
Strokes most often occur as a result of insufficient blood supply to areas of the brain. Decreased blood flow to the brain is associated with excessive amounts of lipofuscin (the aging pigment). This suggests stroke damage at the cellular level is not unlike that of degenerative diseases of the brain—and indicates that creatine’s ability to lower the accumulation of this aging pigment may make it beneficial for stroke victims as well.
Mouse studies of creatine supplementation show marked reduction in the size of damaged areas after blood flow to the brain is interrupted by a stroke. In addition, creatine supplementation also replenished ATP in the brain that had been depleted as a result of stroke. Human studies of creatine in stroke victims are not yet available. However, given creatine’s strong safety record, researchers recommend that people at high risk for strokes consider supplementing with creatine.