Connection between light sensitive nerve cells in eyes and brain that regulate mood

Buzzing the vagus nerve just right to fight inflammatory disease and Vit D for chronic headache

Light and anxiety

Underappreciated External Triggers: Fluorescent Lights and Things …

Oct 3, 2008 – This is the Part V of V Share Posts pertaining to categories of “triggers” that can “get the ball rolling” or accelerate your anxiety. If you’re reading this post first, you may want to go back and read Understanding the Vicious Cycle of Panic,” first to appreciate the idea that while anxiety may appear to come “out …

Light Sensitivity and Anxiety – TheraSpecs

Aug 31, 2017 – In addition, light sensitivity and anxiety is tied to specific conditions. … In fact, migraineurs with light sensitivity between attacks (known as ‘interictal’ photophobia) are more likely to develop feelings of depression, anxiety and stress.

Types of Visual Problems and Anxiety – Calm Clinic

If you find it difficult to see clearly, notice flashes or visual snow, or feel like lights become too bright when you are anxious, it doesn’t necessarily mean there is something wrong with your eyes: these can be part of the body’s natural anxiety response (as inconvenient as they may be). In situations where fear is called for, they …

How Anxiety May Interfere With Your Eyes – Calm Clinic

There are many different ways that anxiety can affect your eyes. The most common ways are: Eye pain and discomfort. Mildly blurred vision. Watery eyes. Light sensitivity. Eye floaters (spots that float across your eye). These are all most common during periods of intense anxiety, and the most common time to experience …

Fluorescent Lights and Anxiety – Stop Anxiety Panic Attack

May 21, 2009 – Have you ever experienced feeling an overwhelming wave of anxiety rapidly wash over you once you have stepped inside a pharmacy, at work or a convenience store? If yes, this is probably because pharmacies and convenience stores are lit with harsh, fluorescent lighting.

Light Therapy for Anxiety and Depression In Your Pocket: Human …

Sep 26, 2017 – With the majority of therapy types costing a pretty penny, it can be easy to get discouraged. However, light therapy for anxiety and depression is one of my favourite forms of treatment and it won’t completely break your bank. Here’s what you need to know.

Anxiety and Sensitive to light: Common Related Medical Conditions

WebMD Symptom Checker helps you find the most common medical conditions indicated by the symptoms Anxiety and Sensitive to light and including Generalized anxiety disorder, Migraine headache (adult) and Panic attack.

Why CFL’s Aren’t Such a Bright Idea | Psychology Today

Sep 15, 2014 – In light of rising environmentally-sensitive brain disorders such as autism and ADHD in children, are energy-saving CFL’s costing us dearly? … a higher visual “load” when processing fluorescentlight, which depletes mental resources and makes the individual more likely to be agitated, disruptive,anxious, …

Mitochondrial disease , anti-oxidants, nutrition test and Dementia

Mitochondrial disease , anti-oxidants, nutrition test and Dementia

From Wikipedia, the free encyclopedia

Mitochondrial disease

Mitochondrial diseases are a group of disorders caused by dysfunctional mitochondria, the organelles that generate energy for the cell. Mitochondria are found in every cell of the human body except red blood cells, and convert the energy of food molecules into the ATP that powers most cell functions.

Mitochondrial diseases are sometimes (about 15% of the time)[1] caused by mutations in the mitochondrial DNA that affect mitochondrial function. Other mitochondrial diseases are caused by mutations in genes of the nuclear DNA, whose gene products are imported into the mitochondria (mitochondrial proteins) as well as acquired mitochondrial conditions. Mitochondrial diseases take on unique characteristics both because of the way the diseases are often inherited and because mitochondria are so critical to cell function. The subclass of these diseases that have neuromuscular disease symptoms are often called a mitochondrial myopathy.

Signs and symptoms

Symptoms include poor growth, loss of muscle coordination, muscle weakness, visual problems, hearing problems, learning disabilities, heart disease, liver disease, kidney disease, gastrointestinal disorders, respiratory disorders, neurological problems, autonomic dysfunction and dementia. Acquired conditions in which mitochondrial dysfunction has been involved are: diabetes, Huntington’s disease, cancer, Alzheimer’s disease, Parkinson’s disease, bipolar disorder,[2][3][4] schizophrenia, aging and senescence, anxiety disorders, cardiovascular disease, sarcopenia, chronic fatigue syndrome.[5]
The body, and each mutation, is modulated by other genome variants; the mutation that in one individual may cause liver disease might in another person cause a brain disorder. The severity of the specific defect may also be great or small. Some minor defects cause only “exercise intolerance”, with no serious illness or disability. Defects often affect the operation of the mitochondria and multiple tissues more severely, leading to multi-system diseases.[citation needed]
As a rule, mitochondrial diseases are worse when the defective mitochondria are present in the muscles, cerebrum, or nerves,[6] because these cells use more energy than most other cells in the body.
Although mitochondrial diseases vary greatly in presentation from person to person, several major clinical categories of these conditions have been defined, based on the most common phenotypic features, symptoms, and signs associated with the particular mutations that tend to cause them.
An outstanding question and area of research is whether ATP depletion or reactive oxygen species are in fact responsible for the observed phenotypic consequences.
Cerebellar atrophy or hypoplasia has sometimes been reported to be associated.


Mitochondrial disorders may be caused by mutations (acquired or inherited), in mitochondrial DNA (mtDNA), or in nuclear genes that code for mitochondrial components. They may also be the result of acquired mitochondrial dysfunction due to adverse effects of drugs, infections, or other environmental causes (see MeSH).
Nuclear DNA has two copies per cell (except for sperm and egg cells), one copy being inherited from the father and the other from the mother. Mitochondrial DNA, however, is strictly inherited from the mother and each mitochondrial organelle typically contains between 2 and 10 mtDNA copies. During cell division the mitochondria segregate randomly between the two new cells. Those mitochondria make more copies, normally reaching 500 mitochondria per cell. As mtDNA is copied when mitochondria proliferate, they can accumulate random mutations, a phenomenon called heteroplasmy. If only a few of the mtDNA copies inherited from the mother are defective, mitochondrial division may cause most of the defective copies to end up in just one of the new mitochondria (for more detailed inheritance patterns, see human mitochondrial genetics). Mitochondrial disease may become clinically apparent once the number of affected mitochondria reaches a certain level; this phenomenon is called “threshold expression”.
Mitochondrial DNA mutations occur frequently, due to the lack of the error checking capability that nuclear DNA has (see Mutation rate). This means that mitochondrial DNA disorders may occur spontaneously and relatively often. Defects in enzymes that control mitochondrial DNA replication (all of which are encoded for by genes in the nuclear DNA) may also cause mitochondrial DNA mutations.
Most mitochondrial function and biogenesis is controlled by nuclear DNA. Human mitochondrial DNA encodes 13 proteins of the respiratory chain, while most of the estimated 1,500 proteins and components targeted to mitochondria are nuclear-encoded. Defects in nuclear-encoded mitochondrial genes are associated with hundreds of clinical disease phenotypes including anemia, dementia, hypertension, lymphoma, retinopathy, seizures, and neurodevelopmental disorders.[8]

A study by Yale University researchers (published in the February 12, 2004 issue of the New England Journal of Medicine) explored the role of mitochondria in insulin resistance among the offspring of patients with type 2 diabetes.[9] Other studies have shown that the mechanism may involve the interruption of the mitochondrial signaling process in body cells (intramyocellular lipids). A study conducted at the Pennington Biomedical Research Center in Baton Rouge, Louisiana[10] showed that this, in turn, partially disables the genes that produce mitochondria.

Examples of mitochondrial diseases include:

  • Mitochondrial myopathy
  • Diabetes mellitus and deafness (DAD)
    this combination at an early age can be due to mitochondrial disease
    Diabetes mellitus and deafness can be found together for other reasons
  • Leber’s hereditary optic neuropathy (LHON)
    visual loss beginning in young adulthood
    eye disorder characterized by progressive loss of central vision due to degeneration of the optic nerves and retina
    affects 1 in 50,000 people in Finland
  • Leigh syndrome, subacute sclerosing encephalopathy
    after normal development the disease usually begins late in the first year of life, although onset may occur in adulthood
    a rapid decline in function occurs and is marked by seizures, altered states of consciousness, dementia, ventilatory failure
  • Neuropathy, ataxia, retinitis pigmentosa, and ptosis (NARP)
    progressive symptoms as described in the acronym
  • Myoneurogenic gastrointestinal encephalopathy (MNGIE)
    gastrointestinal pseudo-obstruction
    Myoclonic Epilepsy with Ragged Red Fibers (MERRF)
    progressive myoclonic epilepsy
    “Ragged Red Fibers” are clumps of diseased mitochondria that accumulate in the subsarcolemmal region of the muscle fiber and appear when muscle is stained with modified Gömöri trichrome stain
  • short stature
  • hearing loss
  • lactic acidosis
  • exercise intolerance
  • Mitochondrial myopathy, encephalomyopathy, lactic acidosis, stroke-like symptoms (MELAS)
  • mtDNA depletion
  • mitochondrial neurogastrointestinal encephalomyopathy (MNGIE)
    Conditions such as Friedreich’s ataxia can affect the mitochondria but are not associated with mitochondrial proteins.


The effective overall energy unit for the available body energy is referred to as the daily glycogen generation capacity,[11][12][13] and is used to compare the mitochondrial output of healthy individuals to that of afflicted or chronically glycogen-depleted individuals. This value is slow to change in a given individual, as it takes between 18 and 24 months to complete a full cycle.

The glycogen generation capacity is entirely dependent on, and determined by, the operating levels of the mitochondria in all of the cells of the human body;[14] however, the relation between the energy generated by the mitochondria and the glycogen capacity is very loose and is mediated by many biochemical pathways.[11] The energy output of full healthy mitochondrial function can be predicted exactly by a complicated theoretical argument, but this argument is not straightforward, as most energy is consumed by the brain and is not easily measurable.


Mitochondrial diseases are usually detected by analysing muscle samples, where the presence of these organelles is higher.

Connie’s comments:  NIH created nutrition tester which test for anti-oxidant levels can be used as my initial experiences with various test results where Dr Oz got 85k high score and I have 41k lower from 2 years ago of 55k.

Email to be a nutrition test site with this Raman Spectroscopy tester to suggest nutrition protocols ( AGELOC family which resets gene expression to younger you)  at:


Although research is ongoing, treatment options are currently limited; vitamins are frequently prescribed, though the evidence for their effectiveness is limited.[15] Pyruvate has been proposed in 2007 as a treatment option.[16] N-acetyl cysteine reverses many models of mitochondrial dysfunction.[17]. In the case of mood disorders, specifically bipolar disorder, it is hypothesized that N-acetyl-cysteine (NAC), acetyl-L-carnitine (ALCAR), S-adenosylmethionine (SAMe), coenzyme Q10 (CoQ10), alpha-lipoic acid (ALA), creatine monohydrate (CM), and melatonin could be potential treatment options.

Anti-oxidants and colored fruits and veggies are your first defense.

ageloc r2 black hair 2


CQ10 for seniors and the aging brain

Coenzyme Q10 is a molecule found in mitochondria. It has a critical role in producing energy for the body. When you are taking statins meds for hypercholesterol, CQ10 is recommended. Some cosmetics for firming and toning the skin include CQ10. I take CQ10 after an intense workout. Those with chronic fatigue needs CQ10 supplementation.


By Dr Sinatra

What Are the Benefits of CoQ10?

  • Improved Energy: One of the Top Benefits of CoQ10: One of the biggest benefits of CoQ10 is that it sparks energy production in every cell of your body, including your heart which is the largest energy consumer in your body. Supplementing with CoQ10 is not only important for maintaining energy for your heart, but every cell in your body. In fact, people often tell me that they have more energy after adding a good CoQ10 supplement to their routine.
  • CoQ10 Facts: What You Should Know: Unfortunately, many doctors are still in the dark when it comes to the importance of CoQ10. Here are the important facts you need to know about this vital nutrient.
  • An Amazing Story About the Benefits of CoQ10: I’ve long-known that CoQ10 is an extremely powerful nutrient that can make a huge difference in your heart health and overall quality of life. That point was driven home to me when I did a lecture in Florida, and was greeted by some of the very same patients I had put on CoQ10 years earlier who were still enjoying good health and vitality. So, I wanted to share that story with you.

What Is the Right CoQ10 Dosage?

  • How Much CoQ10 Should You Take? One of the top questions I get is what is the right CoQ10 dosage to take. My suggested dosages depend on several factors, including your age, whether you take cholesterol lowering statin drugs, and even how often you exercise. Here’s how to determine the right dosage for you.
  • Medications that Deplete CoQ10 & The CoQ10 Dosage You Need: Many people know that cholesterol lowering statin drugs deplete CoQ10, but did you know that statins aren’t the only drug that affects CoQ10? Here are the medications that can deplete your body of CoQ10 and how much CoQ10 you need to take to restore your body’s supply of this vital heart vitamin.
  • To Get the Right CoQ10 Dosage You Can’t Always Trust the Label: Years ago, when I first started to put patients on CoQ10 some patients didn’t have the expected benefits. So, I sent the CoQ10 supplements they were taking out to a lab for testing, and what I found is that it contained just a fraction of the CoQ10 stated on the label. Here’s how to find a high-quality CoQ10 supplement.
  • Taking the Right CoQ10 Dosage for Energy Can Keep You Feeling Young: With many people, the fatigue they chalk up to “aging” is actually a lack of CoQ10. Once people begin supplementing with this important heart vitamin, they often tell me they feel years younger. Here’s why CoQ10 can make such a huge difference in your quality of life.
  • The Right DHA and CoQ10 Dosage for Healthy Blood Pressure: Did you know that DHA omega-3s and CoQ10 are among my top recommended heart vitamins for supporting healthy blood pressure? Here’s why, along with the DHA and CoQ10 dosages I recommend for healthy blood pressure.

Ubiquinone or Ubiquinol: Which Is The Best Form of CoQ10?

The Important Benefits of CoQ10 with Statin Medications

CoQ10 & “The Awesome Foursome” Heart Vitamins

Irregular heartbeat or long QT syndrome and energy drinks do not mix

energyLong QT or Irregular heartbeat, Energy Drinks Do not Mix

As they report in the International Journal of Cardiology, the researchers found that the patients given the caffeinated energy drinks had increased blood pressure levels and that a portion of patients also had prolonged QT intervals, which could led to dangerously irregular heartbeats.

Long QT syndrome (LQTS) is a congenital disorder characterized by a prolongation of the QT interval on electrocardiograms (ECGs) and a propensity to ventricular tachyarrhythmias, which may lead to syncope, cardiac arrest, or sudden death.

“Some individual patients may be at a higher risk,” says senior author Christopher Semsarian in a statement. “We therefore suggest caution in allowing the consumption of energy drinks in young patients with LQTS.”

In an editorial also appearing in the International Journal of Cardiology, IRCCS Istituto Auxologico Italiano’s Peter Schwartz and Federica Dagradi note that many long QT syndrome patients don’t exhibit symptoms until after their teenage years. “[This] implies that a significant number of youngsters with LQTS will help themselves to energy drinks without knowing their real condition and thus endangering themselves,” Schwartz says in a statement.

About QT Syndrome

Long QT syndrome (LQTS) is a rare congenital and inherited or acquired heart condition in which delayed repolarization of the heart following a heartbeat increases the risk of episodes of torsades de pointes (TdP, a form of irregular heartbeat that originates from the ventricles). These episodes may lead to fainting and sudden death due to ventricular fibrillation. Episodes may be provoked by various stimuli, depending on the subtype of the condition.[1]

The condition is named for the appearance of the electrocardiogram (ECG/EKG) on which a prolongation of the QT interval occurs. Normally, the QT interval duration is between 350 and 440 milliseconds.[2] In some individuals, the QT prolongation occurs after the administration of certain medications, which may be dangerous.[1] In addition to medications, long QT syndrome can be acquired from too low blood potassium or low blood magnesium, as in anorexia nervosa.