Abstract

The age spectrum of human populations is shifting toward the older with larger proportions suffering physical decline. Mitochondria influence the pace of aging as the energy they provide for cellular function in the form of adenosine triphosphate (ATP) declines with age. Mitochondrial density is greatest in photoreceptors, particularly cones that have high energy demands and mediate color vision. Hence, the retina ages faster than other organs, with a 70% ATP reduction over life and a significant decline in photoreceptor function. Mitochondria have specific light absorbance characteristics influencing their performance. Longer wavelengths spanning 650–>1,000 nm improve mitochondrial complex activity, membrane potential, and ATP production. Here, we use 670-nm light to improve photoreceptor performance and measure this psychophysically in those aged 28–72 years. Rod and cone performance declined significantly after approximately 40 years of age. 670-nm light had no impact in younger individuals, but in those around 40 years and older, significant improvements were obtained in color contrast sensitivity for the blue visual axis (tritan) known to display mitochondrial vulnerability. The red visual axis (protan) improved but not significantly. Rod thresholds also improved significantly in those >40 years. Using specific wavelengths to enhance mitochondrial performance will be significant in moderating the aging process in this metabolically demanding tissue.

https://academic.oup.com/biomedgerontology/article/75/9/e49/5863431

Extract:

This pilot study has limitations due to its sample size, but the results reveal significant improvement in both rod and cone function in an aged cohort but not in younger individuals. This difference is presumably because age-related mitochondrial decline has not yet affected the younger individuals. Widespread positive results using long-wavelength light in aging and disease in animals have provided an impetus for their clinical application in full-scale clinical trials for diabetic retinopathy (NCT03866473) and age related macular degeneration (NCT02725762, 03878420). However, a recently published study on AMD patients has failed to show any improvement in retinal function in this disease (25). Consequently, there is much that we still need to understand regarding the advantages and limits of this therapeutic route. 

The post Optically Improved Mitochondrial Function Redeems Aged Human Visual Decline appeared first on EMFSA.

Depending on cellular demand or oxidative stress, mitochondria produce adenosine triphosphate (ATP) or reactive oxygen species (ROS), thereby controlling the entire scale of cellular energy supply or disease, respectively. While deficiency in ROS can compromise the immune system, excessive ROS levels contribute to a large number of pathological conditions, including retinal, neurodegenerative and cardiovascular disease as well as cancer. Aging is also a process accelerated by ROS. There is one noninvasive tool allowing us to precisely control both mitochondrial ATP and ROS: red-to-near infrared (R-NIR) light. The understanding why and how R-NIR light interacts with mitochondria was missing so far in the literature. Here we present a unified model for the interaction of R-NIR photons with three mitochondrial key players involved in ATP and ROS generation: ATP synthase, cytochrome c (CYTc) and cytochrome c oxidase (COX). The new model allows us to predictably control ATP and ROS generation in mitochondria by R-NIR light. Furthermore, comparison of the action spectrum of R-NIR light related to mitochondrial ATP and ROS generation with the spectral solar irradiance on Earth, puts us in the position to propose an evolutionary model describing the coordinated interplay of solar irradiation and water on the development of mitochondria on Earth. It accurately predicts which wavelengths of light provides maximum benefit for any desired clinical application and provides valuable hints regarding a time point for the evolutionary provenance of the mitochondrion.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7154450/

The post Mitochondrial solar sensitivity: evolutionary and biomedical implications appeared first on EMFSA.

Abstract

Many physiological processes are regulated with a 24-h periodicity to anticipate the environmental changes of daytime to nighttime and vice versa. These 24-h regulations, commonly termed circadian rhythms, among others control the sleep–wake cycle, locomotor activity and preparation for food availability during the active phase (daytime for humans and nighttime for nocturnal animals). Disturbing circadian rhythms at the organ or whole-body level by social jetlag or shift work, increases the risk to develop chronic metabolic diseases such as type 2 diabetes mellitus. The molecular basis of this risk is a topic of increasing interest. Mitochondria are essential organelles that produce the majority of energy in eukaryotes by converting lipids and carbohydrates into ATP through oxidative phosphorylation. To adapt to the ever-changing environment, mitochondria are highly dynamic in form and function and a loss of this flexibility is linked to metabolic diseases. Interestingly, recent studies have indicated that changes in mitochondrial morphology (i.e., fusion and fission) as well as generation of new mitochondria are dependent on a viable circadian clock. In addition, fission and fusion processes display diurnal changes that are aligned to the light/darkness cycle. Besides morphological changes, mitochondrial respiration also displays diurnal changes. Disturbing the molecular clock in animal models leads to abrogated mitochondrial rhythmicity and altered respiration. Moreover, mitochondrial-dependent production of reactive oxygen species, which plays a role in cellular signaling, has also been linked to the circadian clock. In this review, we will summarize recent advances in the study of circadian rhythms of mitochondria and how this is linked to the molecular circadian clock.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5854864/?fbclid=IwAR3m8t_O0RMjcGx5o48Nnn1SStI4mcTmRJV5cw2e0EjuMvgQdkCbNlYhUAY

The post Circadian rhythms in mitochondrial respiration appeared first on EMFSA.

Prof. Paul Héroux is Professor of Toxicology and Health Effects of Electromagnetism at the McGill University. Faculty of Medicine (Department of Surgery, McGill University Health Center and InVitroPlus Laboratory).

His area of expertise:

General toxicology, in vitro toxicology of metals.

Health effects of electricity and electromagnetic fields.

His department website: http://www.invitroplus.mcgill.ca/ 

Available at the above link: Some of Prof Héroux’s  research plus a free textbook and curriculum. (A powerful and compelling read.)

He still has plenty of works not published on the site but they are highlighted in the interview.

In summary:

Prof Héroux developed a Unified Theory of Weak Magnetic Field Action that proposes A Radical New Outlook. His work has been developed, is replicable and is a total eye-opener. I will confess, when I read it months ago, I had to take many double takes because the truth of the data seems totally unbelievable to what industry literature describes. Again, all of this is true and replicable with a standard laboratory.

Additionally, we discuss how research to date has met the deterministic merit requirements for nnEMF to be labelled as a WHO IARC Type 1 carcinogen substance.

We discuss how literature tends to discriminate between non-native electromagnetic fields (nnEMF), blue light, low frequency and high frequency. Essentially, they have something in common and therefore can be lumped together in terms of their biological reaction. In this example, I will refer to how extra-low-frequency magnetic fields interact with unstable molecular structures such as hydrogen bridges, altering the ability of protons to tunnel from one molecule to another. How this plays out in practice is that the reaction rates of certain enzymes can be altered by magnetic fields at very low intensities such as 25 nT, comfortably within the range of everyday exposures. This is replicable easily in biophysics studies (nnEMF although disruptive to the cell), does not increase quickly with field intensity (power density), and drives an adaptation of the cell to the radiation. Metabolism is altered because one enzyme, ATP Synthase, is particularly vulnerable: the ratio between glycolysis and redox metabolism is changed. The mechanism also extends to RF frequencies, implicating all broadcasting and radiating telecommunications systems. Hence, why nnEMF impacts chronic disease rates such as cancer, obesity diabetes, neurological disorders and autoimmune diseases (basically everything epigenetic).

The simpler explanation:

We are taught to believe 100% that everything is tied to diet and exercise. However, it is exactly the opposite. We are taught to think about obesity as excess calories. Yet, when using Albert Einstein’s equations, and in this example E = MC2 (number 2 must be super scripted), when reading his equation in reverse, it says obesity is a disease of a loss of electrons. Stop thinking of food as carbs, proteins, and fats, and instead think of them as electrons that move protons across membranes in cells. The brain is a quantum computer and processes food as such.

Think of your body as a car, if it were a Porche, what is more important, ensuring how the car performing under the hood or worrying if 93 or 95 octane is going into it? nnEMFs puts your car’s performance and function out of whack.

Additionally, with genetic tests into nnEMF reactions to the body, a 2014 study by De Luca et al. found a large percentage of the population lacking the enzyme to detox nnEMF effectively, and even with those that do, persons would have different efficiency rates.

Based on the above, there is a syndrome of symptoms and diseases experienced by the population with the associated score of Neolithic diseases. Quantum biology uses the principles of physics to explain the biological processes. This is demonstrable when using mitigation options from the understanding of biophysics that results are very noticeable. For example, being able to lose 35kg in 3 months without any exercise and calorie counting, or seeing massive improvements in diabetes or thyroid issues.

The problems with nnEMF exposures is that it is not like engineering where we can flick off a switch and therefore the problem. The effects can be permanent and evident. A well-conducted epidemiology study in California assessed pregnant mothers with exposures greater than 2.5 millGauss.

The results showed:

  3 times increased risk incidence for, miscarriage, asthma in offspring, ADHD, abnormal thyroid function

  5 times increased the risk of obesity in offspring. 

However, the WHO IARC assessment found the incidence of childhood leukaemia in as low as 1 mG.

Super Dads – Prof. Paul Héroux

Note to our readers: EMFSA added the video below to the notes about the podcast.

Dr. Paul Heroux Testifies at Michigan’s 5G Small Cell Tower Legislation Hearing October 4, 2018

The post Super Dads – Prof. Paul Héroux appeared first on EMFSA.