Tag: Alzheimer’s Disease

bookmark_borderHow to Protect Yourself From Air Pollution

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By Daniel Brouse

Climate change is a primarily caused by air pollution.

Air pollution is a primary cause of death.

The health impacts of air pollution are both cumulative and irreversible. The more polluted the air, the more severe the effects. The more polluted air you breathe over time, the more severe the effects. That is to say breathing “Moderate” quality air for 3 days might be similar to breathing “Unhealthy for Sensitive Group” quality air for 1 day. In both cases, your respiratory, circulatory, neurological, and immune systems have been damaged.

You can (and should) check your local air quality several times a day at AirNow.gov. The air quality index (AQI) goes from 0 to 500. An AQI value of 50 or below represents good air quality, while an AQI value over 300 represents hazardous air quality.

Particulate Matter (PM)

The EPA defines particulate matter (also called particle pollution): the term for a mixture of solid particles and liquid droplets found in the air. Some particles, such as dust, dirt, soot, or smoke, are large or dark enough to be seen with the naked eye. Others are so small they can only be detected using an electron microscope.

Particle pollution is similar to smoking cigarettes. The more you inhale, the worse it is for you. Also, the more particles in the air you breath, the worse it is for you. Breathing air on a day with an AQI that is unhealthy is similar to smoking a half-pack of cigarettes. If you go running instead of walking, it might be equivalent to smoking 2 packs of cigarettes.

The more particulate matter you breathe in over time, the greater the cumulative effect. The impact on your health will depend on your predisposition. In all cases your risk increases for nasal and upper respiratory tract health problems, heart attacks, strokes, asthma, and bronchitis, as well as premature death from heart ailments, lung disease, and cancer. Studies show that exposure can impair brain development in children and are significantly associated with the development of dementia and Alzheimer’s disease.

Some of the impacts of particle pollution may be reversed overtime if further exposure to particle pollution is eliminated. After five years of quitting smoking, the risk of developing complications decreases by up to 50%.

The best lifestyle is to avoid particulate matter. Exercise outside only on days with a “Good” AQI under 50. If you must go out on days with an AQI over 50, wear an N95 mask. Indoors build and run a Corsi-Rosenthal Box filter.

Ground-level Ozone

Tropospheric ozone is low level ozone caused by humans. Tropospheric ozone is “bad ozone” that causes health problems in humans, plants to die and other destructive results. (Stratospheric ozone, the good ozone, is the ozone layer in the stratosphere that keeps 95-99% of the suns ultraviolet radiation from striking the earth.)

“Tropospheric ozone is formed by the interaction of sunlight, particularly ultraviolet light, with hydrocarbons and nitrogen oxides, which are emitted by automobiles, gasoline vapors, fossil fuel power plants, refineries, and certain other industries.” — National Center for Atmospheric Research

Ozone primarily affects the respiratory and immune systems. The damage is permanent, untreatable and often results in death. The Santa Barbara County Air Pollution Control District reports, “Roughly one out of three people in the U.S. is at risk of experiencing ozone-related health effects.”

The best lifestyle is to avoid ozone exposure. Since heat and ultraviolet light are needed to create ozone, staying indoors offers the best protection. Neither masks nor air purifiers protect from ozone exposure. (Ozone is O3 and almost the same size as Oxygen O2)

REFERENCES
Death by Ozone
COVID-19 and Air Pollution
Ozone Know Zone
Air Pollution Kills
Indoor Air Pollution: How to Purify the Air, Aromatic Plants, and Phytoncides
Corsi-Rosenthal Box filter
The Human Induced Climate Change Experiment

bookmark_borderCopper Connected to Alzheimer’s Disease

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Proceedings of the National Academy of Sciences of the United States of America has conducted a study linking the consumption of copper to Alzheimer’s:

Significance
The causes of the sporadic form of Alzheimer’s disease (AD) are unknown. In this study we show that copper (Cu) critically regulates low-density lipoprotein receptor-related protein 1–mediated Aβ clearance across the blood–brain barrier (BBB) in normal mice. Faulty Aβ clearance across the BBB due to increased Cu levels in the aging brain vessels may lead to accumulation of neurotoxic Aβ in brains. In a mouse model of AD low levels of Cu also influences Aβ production and neuroinflammation. Our study suggests that Cu may also increase the severity of AD.

Abstract
Whereas amyloid-β (Aβ) accumulates in the brain of normal animals dosed with low levels of copper (Cu), the mechanism is not completely known. Cu could contribute to Aβ accumulation by altering its clearance and/or its production. Because Cu homeostasis is altered in transgenic mice overexpressing Aβ precursor protein (APP), the objective of this study was to elucidate the mechanism of Cu-induced Aβ accumulation in brains of normal mice and then to explore Cu’s effects in a mouse model of Alzheimer’s disease. In aging mice, accumulation of Cu in brain capillaries was associated with its reduction in low-density lipoprotein receptor-related protein 1 (LRP1), an Aβ transporter, and higher brain Aβ levels. These effects were reproduced by chronic dosing with low levels of Cu via drinking water without changes in Aβ synthesis or degradation. In human brain endothelial cells, Cu, at its normal labile levels, caused LRP1-specific down-regulation by inducing its nitrotyrosination and subsequent proteosomal-dependent degradation due in part to Cu/cellular prion protein/LRP1 interaction. In APPsw/0 mice, Cu not only down-regulated LRP1 in brain capillaries but also increased Aβ production and neuroinflammation because Cu accumulated in brain capillaries and, unlike in control mice, in the parenchyma. Thus, we have demonstrated that Cu’s effect on brain Aβ homeostasis depends on whether it is accumulated in the capillaries or in the parenchyma. These findings should provide unique insights into preventative and/or therapeutic approaches to control neurotoxic Aβ levels in the aging brain.

In a separate study, playing a musical instrument was found to and years to the life of the brain.