Biological aging, also called “senescence,” is defined as: “a progressive deterioration of physiological function, an intrinsic age-related process of loss of viability and increase in vulnerability.” Indeed, as we age, the risk of developing most serious diseases increases greatly, and many of these serious conditions are now classed as “aging-related diseases.” The effects of senescence are therefore by far the leading cause of death, with approximately 65% of all deaths attributed to aging-related causes. In industrialized countries, this figure increases to as much as 90%.
So why does this happen? Some scientists believe it’s simply our genes; that we are programed to deteriorate. But others in the scientific community believe that it’s mostly due to cell damage that we accumulate over time. The energy our cells need to function and grow is provided by tiny organelles within our cells called “mitochondria.” These cellular power plants combine the oxygen we breathe and the food we eat to produce “ATP,” the molecule which provides over 95% of the cellular energy needed to power all living functions. During the generation of ATP, highly reactive molecules known as “free radicals” are produced as a by-product.
The “Free Radical Theory of Aging” postulates that we (and almost all other organisms) age due to cumulative free radical damage to our cells over time. It states that as our cellular machinery and our DNA become damaged, our cells divide and take copies of the corrupted DNA into the new cells. More free radical damage occurs in the new cells and this damage only increases with ongoing generations of cells. Eventually the cells become nonviable and start to die off.
These free radicals attack the mitochondrial and cell membranes, damage DNA and RNA, interfere with normal cell signalling and can trigger cellular death. Known as “oxidative stress,” this damage is linked to mutations, reduced cellular function and has been identified as a significant contributor or consequence of well over 200 diseases. These include many of the serious and most prevalent conditions of the cardiovascular, neurological, musculoskeletal, digestive and immune systems. Not all free radicals are bad however, and our body does use some of them in cellular signaling and in fighting infections.
Given this, an obvious hypothesis arises. If you can control the production of free radicals in mitochondria and reduce oxidative damage, you might be able slow or even reverse the effects of aging. In fact, when you say it plainly like that it doesn’t even seem that complicated.
So why not just take CoQ10 and be done with it? Supplementing with CoQ10, and its reduced form “ubiquinol” (which has slightly better bioavailability) is already very popular but these are not absorbed well from the digestive tract. While positive health effects are seen, neither CoQ10 nor ubinquinol can effectively penetrate the particularly impermeable mitochondrial membrane. Mitochondria produce their own CoQ10, they do not absorb it from the cell, and so replenishing their reserves of CoQ10 has been something no one has been able to effectively achieve, until now.
Enter, “MitoQ.”
MitoQ (mitoquinol mesylate) is a mitochondria-targeted antioxidant; a revolutionary patented formulation of CoQ10 developed at The University of Otago in New Zealand. MitoQ is CoQ10 bound to a special positively-charged ion which makes it water-soluble and able to easily pass through all biological membranes, including the gut, blood-brain barrier and cell membrane. Once inside the cell, positively-charged MitoQ is attracted to, and actively transported inside, the negatively-charged mitochondria. This enables MitoQ to reach concentrations inside mitochondria many hundreds of times higher than outside them, providing a huge antioxidant boost which assists in restoring mitochondrial function and optimum energy production. Another benefit of this mitochondrial targeting is that MitoQ is much less likely than other broad-spectrum and untargeted antioxidants to interfere with the beneficial free radicals involved in cellular signaling.
Although originally developed as a potential treatment for diseases such as Alzheimer’s and heart disease, an early study by Saretzki & Murphy et al showed that MitoQ could prolong the lifespan of cultured human cells and slowed telomere shortening, a hallmark of the cellular aging process. Further studies of MitoQ have also showed excellent results in improving cellular and organ function and reducing the symptoms and progression of many of the most prevalent cardiovascular, neurological and metabolic diseases, all major contributors to age-associated mortality.
For example, The University of Colorado conducted a study in mice which investigated MitoQ treatment for reducing the negative effects of aging on arteries. Old mice, the equivalent of humans in their 70s or 80s, were given MitoQ in their water. After four weeks, their arteries functioned like the age equivalent of a human between 25 and 35.
“One of the hallmarks of primary aging is endothelial dysfunction,” said Rachel Gioscia-Ryan, a doctoral student in CU-Boulder’s Department of Integrative Physiology and lead author of the study. “MitoQ completely restored endothelial function in the old mice. They looked like young mice.”
Based on the results of this study, the Colorado University team are now conducting a clinical trial in humans to test the effect of MitoQ on various key markers of aging. MitoQ has also been selected for the US Department of Health’s Institute on Aging Intervention Testing Program, an exclusive study investigating the most promising potential lifespan extending agents. The aim of the study is to identify interventions that can create at least a 10-15% gain in life span in mice.
MitoQ is available as a range of premium over-the-counter nutraceuticals and anti-aging skin cosmeceuticals. With several promising human studies now underway and more in the planning stage, MitoQ has the potential to reduce the burden of many health conditions, and is already helping thousands of people live healthier and happier lives. Unfortunately, directly measuring a significant increase in human lifespan is very difficult as we live for such a long time and there are so many confounding factors in a real-world setting. However, MitoQ has already shown significant promise in this area, and has emerged as the flagship molecule in the emerging field of mitochondrial medicine; one that has huge potential in preventing and treating serious disease and keeping us feeling healthier for longer.
Originally published on the "Living Better 50" blog.