As a growing percentage of the population of the United States reaches an elderly age, sarcopenia has become an increasingly larger problem. In fact, sarcopenia used to be something most people knew very little about. Unfortunately, now that it has become so common, the condition has moved into the mainstream.
If you aren’t yet familiar with the condition, the best way to think of sarcopenia is as osteoporosis of the muscle. Sarcopenia is a syndrome characterized by progressive and generalized loss of skeletal muscle mass and strength. As such, it is strongly correlated with physical disability, poor quality of life and death.
Risk factors for sarcopenia include age, gender and overall level of physical activity. Sarcopenia is considered 'primary' (or age-related) when no other cause is evident but aging itself, while sarcopenia is often considered 'secondary' when one or more other causes are evident.
Four of the six major contributing factors to sarcopenia are related to problems with mitochondria, while the other two are indirectly related.
Let me explain each of these terms:
Many scientists believe that sarcopenia results in part from defective autophagy in the muscles. Muscle, as you may know, is made up of tissues with heavy concentrations of mitochondria. This means that one of the best methods to stimulate healthy mitochondrial autophagy is through intermittent fasting, as well as a calorie-restricted diet.
This is because mitochondrial autophagy is critical for the maintenance of mitochondrial function and muscle mass. Keep in mind there is a sweet spot between fasting too much and fasting just enough to reap the benefits. Too much autophagy may be detrimental to muscle development.
Another method of stimulating autophagy is the use of Rapamycin. Rapamycin will diminish the activity of the mTOR pathway, which boosts autophagy.
Mitochondrial Oxidative Stress
The mitochondria, by utilizing oxygen, will produce reactive oxygen species (ROS), which are essentially free radicals. ROS production is associated with mitochondrial DNA mutations induced by oxidative stress and these mutations result in a defective electron transport chain.
The electron transport chain is vital for ATP production. When ATP production drops off, the mitochondria are at risk due to the chronic oxidative stress. This leads to protein loss and muscle atrophy. Ultimately, mitochondrial oxidative stress will diminish the number of functioning mitochondria.
Mitochondria are highly dynamic organelles undergoing coordinated cycles of fission and fusion. This process is referred to as 'mitochondrial dynamics' and its purpose is to help mitochondria maintain their shape, distribution and size.
Their transient and rapid morphological adaptations are crucial for many cellular processes such as cell cycle, immunity, apoptosis and mitochondrial quality control. Imbalances of mitochondrial dynamics negatively affect mitochondrial homeostasis and function, and it has been recently reported that in skeletal muscle these imbalances induce cell senescence and muscle atrophy.
Mitochondria play key roles in activating apoptosis in mammalian cells. Apoptosis is a highly programmed form of cell death. Mitochondrial apoptosis results in the release of proteins from the space between the mitochondrial inner and outer membrane that, once in the cytoplasm, activates certain enzymes that dismantle cells and signal efficient phagocytosis of cell corpses.
Myostatin is a growth factor which plays a negative role in regulating skeletal muscle mass and growth. If myostatin can be blocked there should be an increase in muscle mass. There is a great deal of research on myostatin blockers and there are even shortcuts to increasing myostatin blockers in the body.
An inflammatory cytokine is a signaling molecule that is secreted from immune cells and certain other cell types that promotes inflammation. Inflammatory cytokines are involved in the upregulation of inflammatory reactions. There are three master inflammatory cytokines that are called IL-1, IL-6, and TNF. While their actual names aren’t important, what is important is the damage they can do.
Many disease conditions are the result of an imbalance of the various cytokines with the inflammatory ones predominating. One of the goals is to increase the presence of anti-inflammatory cytokines. The three major anti-inflammatory cytokines are IL-1 A, IL-10, and IGF-1.
In addition to these six factors of sarcopenia, another thing to keep in mind is that muscle health is directly tied to brain health.
Muscles secrete a number of different growth factors, which can have significant effects on the brain preventing cognitive decline. One of these factors is called Brain Derived Neurotropic Factor (BNDF). Increasing BNDF is one of the more important methods of preventing neurodegenerative diseases of the brain. The old adage “a sound body leads to a sound mind” is true.
Knowing all of the above, one question comes to mind:
How can we turn back the clock and help a patient improve their sarcopenia condition?
One thing is for sure; any patient experiencing sarcopenia must begin an exercise program ASAP. Without the patient exercising, all treatments are doomed to failure. Also, exercise should consist mainly of resistance exercises (strength training), but cardio is also very important in maintaining one’s overall health.
Above and beyond a renewed, vigorous exercise program, here are 8 methods we use at PUR-FORM to help prevent and reverse sarcopenia:
EBO2 is a technique that utilizes ozone gas, blood filtration and blood photobiomodulation. This system will produce compounds that stimulate the NrF2 pathway, which diminishes inflammation in the body and acts as a catalyst for the production of NAD. Increased NAD results in the production of more ATP.
Ultimately, this process will improve the health, numbers, and efficiency of the mitochondria. In addition, the benefits of EBO2 not only extend to sarcopenia but to general well being. Reducing inflammation is one of the major methods to reduce inflammaging (inflammation + aging) in the body on many levels.
2. HYPERBARIC OXYGEN THERAPY (HBOT):
Hyperbaric oxygen therapy raises oxygen levels and will increase mitochondrial efficiency and ATP production. In addition, certain hyperbaric oxygen treatments can lead to telomere lengthening, which is responsible for reverse cell aging. Lastly, HBOT is able to stimulate the release of more stem cells into circulation, improving respiration and increasing mitochondrial mass.
3. INTERMITTENT HYPOXIA TRAINING:
Our clinic is one of the very few clinics able to utilize intermittent hypoxia therapy (IHT) via a very specialized machine. One huge benefit of IHT is that it can help in the production of a myostatin blocker.
Myostatin blockers are one of the Holy Grails of body builders. All studies have shown that animals either lacking myostatin or treated with substances that block the activity of myostatin have significantly more muscle mass.
Intermittent hypoxia therapy will directly stimulate many beneficial pathways in the body to reduce inflammation and aging. We have both a machine and the ability to perform blood flow restriction training (BFR) as well.
BFR uses specialized tourniquets during exercise. These tourniquets deprive the muscles of blood flow and subsequently oxygen. Many times, we will combine IHT with HBOT to get the best of both worlds. Like HBOT, IHT can also increase stem cell output from the bone marrow.
At PUR-FORM we have both a red light therapy bed and an infrared sauna. Each of these devices can have a profound effect on reducing inflammation, increasing muscle health and improving immunity.
Dr. Michael Hamblin, Ph.D. a Principal Investigator at Wellman Center for Photomedicine, Massachusetts General Hospital, and an Associate Professor at Harvard Medical School, recently wrote:
“In the near future, sport agencies must deal with ‘laser doping’ by at least openly discussing it because the aforementioned beneficial effects and the pre-conditioning achieved by laser and LED irradiation will highly improve athletic performance.”
Again, the reason for this is because photobiomodulation seems to have a direct effect on mitochondria in muscles. As you now know, increased mitochondrial health will lead to increased muscle health, which can help reverse sarcopenia.
5. IV THERAPY AND OTHER ADJUNCT TREATMENTS:
Since a decline in muscle mass can many times be attributed to a decline in mitochondrial efficiency, giving intravenous NAD can help to correct these problems.
NAD+ is a cofactor, or a “helper molecule,” for a large class of enzymes called sirtuins. These enzymes require a non-protein chemical cofactor like NAD+ to function. The effects of sirtuins go well beyond metabolism. They play key roles in inflammation, transcription of genes, programmed cell death, and of course, aging.
Different sirtuins are located in different aspects of the cell. They have varying targets including DNA modulation, energy homeostasis, and cell cycle control, just to name a few.
It is well known that mitochondrial oxidative capacity and NAD synthesis are reduced in sarcopenia. NAD is also used by various enzymes that repair DNA damage found in muscle tissue.
Other IV modalities include a number of formulas including vitamin C, curcumin, resveratrol and more. These compounds, along with others, stimulate the immune system and collagen production.
We also have at our disposal various combinations of peptides, which can positively affect the telomeres or the mitochondria or both. We have one set of peptides that we call our mitochondrial rescue formula. Another peptide that comes to mind is follistatin, which can block myostatin.
6. CYTOKINE THERAPY:
Many of our other modalities will produce a variety of cytokines that will nullify the effects of the inflammatory cytokines. We also have a propriety method of delivering anti-inflammatory cytokines via the use of cytokines delivered via an iontophoresis patch.
7. STEM CELLS:
We are one of the few facilities with the technical knowledge to stimulate and process a patient’s own VSELs. In fact, we have a propriety method to stimulate the body to produce more of them and we have an additional method to activate them.
To that end, we offer a package called “The Triad”.
The Triad consists of a VSELS treatment, an NAD IV and an EBO2 treatment. We are also looking into the aspect of using culture-expanded stem cells from the patient’s adipose tissue.
These modalities will increase stem cell output from the bone marrow.
There are several important supplements that may help fend off sarcopenia.
In addition to NAD+, which we’ve mentioned, a Nitric Oxide (NO) stimulator may help as well. Nitric Oxide is one of the most important signaling molecules in the body. As one ages the amount of NO in the muscle decreases, leading to sarcopenia. We can help reverse this by providing extra NO. Two products from HumanN that supply NO are SuperBeets and Neo-40.
Several nutrients, including creatine, vitamin D, and whey protein, have also shown great promise in combating sarcopenia.
Other nutrients, such as omega-3 fatty acids, carnitine compounds, and the amino acid glutamine have biological effects that may be beneficial in promoting healthy muscle mass.
There are also several foods that seem to fight sarcopenia via a myostatin blockade, including green tea, cocoa, cauliflower, broccoli, magnolia, apple peel, sea cucumber extract, and holy basil. One other supplement high on our list is spermidine.
Spermidine is a potent stimulator of autophagy and is able to stimulate a number of anti-aging pathways and reduce inflammation.
THE BOTTOM LINE:
Sarcopenia is an increasingly serious problem for our aging population. While the number one way to combat it is to begin a serious resistance training program to build muscle, the treatments I just listed will have a profound effect on not only halting advanced sarcopenia, but on boosting mitochondrial production and preventing future muscle deterioration.
– Dr. P