MitoQ is special among antioxidants because it can concentrate in the mitochondria, the source of most free radicals. MitoQ shows promise in helping the heart, the liver, and the brain. Hopefully the antiaging benefits seen in mice can also be found in humans.

Introduction

MitoQ is a CoQ10 lookalike, and an antioxidant that is attracted to the source of most free-radicals: the mitochondria. Unlike most other antioxidants, it can concentrate hundreds of times in the mitochondria [R, R, RR].

The health of our mitochondria is vital. They provide energy to our hardest-working cells, including those in the heart, liver, and brain. And when they are stressed by inflammation or free radicals, they can kill the cell they live in (apoptosis) [RR].

Mitochondrial damage is a problem in many conditions, from heart and liver disease to Alzheimer’s. It is also seen in aging, osteoporosis, and hair loss [RR].

When free radicals are removed in the mitochondria (by catalase) mouse lifespan is increased by 10% [R]. It is hoped that MitoQ can achieve similar results for people.

CoQ10 is a mitochondrial antioxidant, but the body does not easily absorb it. When taken as a supplement, a lot of it does not reach the mitochondria. MitoQ solves these problems, though it is not quite as powerful an antioxidant as CoQ10 [RR]. It also does not replace CoQ10’s essential role in making energy [R].

MitoQ’s antioxidant function is continually and rapidly renewed by the mitochondria themselves [R].

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A Review of MitoQ’s Health Benefits

1) MitoQ Prevents Free Radical Damage and Cell Death

MitoQ raises glutathione and prevents DNA damage from free radicals, in human cells [RR, R].

It also protects fats from free radicals, in rat cells [R].

In human cells, MitoQ is 800 times stronger than ibedenone (another CoQ10 analogue) at preventing cell death from free radicals [R].

MitoQ prevents cell death (apoptosis) from free radicals, in human cells [R].

2) MitoQ Protects the Liver

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MitoQ reduces inflammation in Hepatitis C patients (phase II clinical trial) [R].

In rats, MitoQ protects the liver from damage due to alcohol (by lowering free radicals and HIF1α) [R].

MitoQ prevents liver fibrosis from free radicals in mice [R].

3) MitoQ Prevents UV Damage

According to a literature review, MitoQ prevents mitochondrial DNA damage from UV better than resveratrol, curcumin, or NAC [R].

4) MitoQ Protects the Heart

In rats, MitoQ prevents heart failure from cocaine or chemotherapy use, by decreasing free radicals [RR].

MitoQ prevents heart failure by preserving energy production and lowering inflammation (TNF-alpha) [RR].

During shock, MitoQ protects heart muscle in rats and mice [R].

5) MitoQ Improves Blood Flow

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MitoQ lowers high blood pressure in rats [R].

The blood vessels harden as we age. MitoQ improves blood flow by increasing elasticity of blood vessels. It also protects blood vessels from free radical damage in mice (by raising MnSOD) [R].

6) MitoQ Decreases Inflammation

In mice, MitoQ prevents inflammation caused by low oxygen by decreasing free radicals (and HIF-1α) [RR].

In mice, MitoQ lowers inflammation from inflammatory bowel disease [R].

It may stop chronic inflammation from killing human cells [R].

In rats, MitoQ helps with infections, by decreasing inflammation and helping cells make enough energy to survive the stress of the infection [R].

MitoQ decreases inflammation from infections, in human cells [R].

7) MitoQ Helps Treat Alzheimer’s Disease

In mice models of Alzheimer’s, MitoQ prevents cognitive decline, nerve loss, injury from free radicals, and build-up of amyloid beta [R].

It can also improve spatial memory in mice models of Alzheimer’s [R].

In worms with Alzheimer’s genes, MitoQ extended lifespan 14%, by protecting the mitochondria [R]. However, it did not do so in normal worms.

8) MitoQ Helps Treat MS (Multiple Sclerosis)

MitoQ slows disease progression, reduces inflammation, and saves spinal cord neurons in a multiple sclerosis mouse model (EAE) [R].

9) MitoQ Decreases Weight Gain and Metabolic Syndrome

In rats and mice on high-fat diets, MitoQ decreases weight gainlowers blood insulin, and lowers blood sugar [R, R, R].

Cardiolipin is a fat that is crucial for the health of our mitochondria. Free radicals can destroy cardiolipin in aging, diabetes, heart failure, thyroid disease, and non-alcoholic fatty liver disease (NAFLD) [RRR].

MitoQ increases cardiolipin in the livers of rats on high-fat diets [R].

10) MitoQ Attacks Cancer

MitoQ attacks human breast and lung cancer cells, by paradoxically increasing free radicals in these cells [R].

11) MitoQ May Extend Lifespan

MitoQ increased lifespan and reduced telomere shortening in human fibroblast cells under oxidative stress, but did not help in normal conditions [R].

MitoQ extended lifespan in transgenic worms with Alzheimer’s genes but did not so in normal worms. Nor did it extend life in normal flies. It may prolong life by protecting against disease, but may not fight normal aging [R, R].

Clinical Trials

MitoQ reduced inflammation (AST, ALT) in chronic Hepatitis C patients (40-80 mg/day for 28 days) [R].

MitoQ did not improve Parkinson’s Disease in 128 patients [R]. Patients tolerated a dose of 40-80 mg/day for 12 months. Study authors explained that patients have already lost 80% of their dopamine by the time they are diagnosed and this treatment may come too late [R].

Other

MitoQ may help treat Huntington’s Disease in human cells [R].

It may help treat hemorrhage in rats (by reducing TNF-α and IL-6) [R].

MitoQ may help diabetic kidney disease in mice [R, R]

Technical

  • The concentration of MitoQ in test tube studies is often 10-100 times more than the dose used in humans and animals. Thus some effects are not comparable [R].
  • MitoQ may cause a mild uncoupling and decreases ATP synthesis. This may decrease the production of free radicals [R].

Risks and Side Effects

It did not harm healthy mice when given at high doses for 28 weeks. It caused no DNA damage, free radical damage, or major changes in metabolism. [R].

It decreases water and food intake in obese mice [R].

MitoQ may acidify cells, increase mitochondrial calcium, and cause cells to make less energy [R, R, R].

MitoQ can increase free radicals under certain conditions (pro-oxidant effects) [R, RR].

Joe’s Experience

I took MitoQ for a bit and I liked it, but I found that you needed to take 20-40mg to notice a difference.  I think it’s a good supplement for people experiencing oxidative stress.

User Reviews

Users reported the following beneficial effects:

Most common benefit: increased energy.

Improved energy, focus, clarity, and calm; less fatigue, brain fog, depression, chronic pain; increased dreaming; improved energy in Fibromyalgia, chronic fatigue, and Lyme disease.

Most common disease: multiple sclerosis. 

In multiple sclerosis: better mobility and cognition, more energy, a significant change in symptoms, “an improvement in my ability to complete a sentence”, better coordination and strength, help with brain fog, fatigue, and mental processing problems; alertness; and improved balance.

Less heart palpitations.

Users reported the following lack of effects or side effects:

Not feeling different after months or years of use.

Failure to heal multiple sclerosis or treat the symptoms of multiple sclerosis except for increased energy.

Acne; headaches when MitoQ is combined with Niagen; racing heart and possible kidney harm (raised creatinine) which resolved after discontinuation; EKG changes (QTc);

Dosage

In one clinical trial, patients with Parkinson’s disease tolerated 40-80 mg/day for 12 months [R].

MitoQ.com recommends 10 mg/day [R].

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2 COMMENTS

  • Pp

    I just stopped mitoq after 1 gear taking it due to it ability to destruct neural stem cells. Would recommebd adding a word of caution on that :

    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4509707/

    1. Jack Mclovin

      Thanks PP, fair call, each to their own.

      Here’s a quote from that article:

      “MitoQ treatment dose dependently increased the proportion of SSEA1-negative cells, as a possible sign of impaired stemness of the iPSC. This was not associated with increased cell death.”

      Notice that the researchers say that it’s a “possible” sign of impaired stemness. Yet the cells didn’t actually die. So they are already questioning their own conjecture of impaired stemness due to SSEA1-negativity.

      SSEA1-positive cells are found in around 50% of adenocarcinomas (a type of cancer) and are indicative of Hodgkin’s lymphoma.

      And yet increasing SSEA1-negative cells is bad? SSEA1 positive cells are highly tumorigenic (in vivo) and can turn into SSEA1 negative. [R – https://www.ncbi.nlm.nih.gov/pubmed/19427293%5D

      Also, the variance to N value ratios on the study’s graphs are appalling when matched with their conclusions.

      I’m at least going to keep taking it. If anything this only adds to my case. Thank you.

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