How to have healthy blood flow to your heart?

blood flowI believe that a healthy blood flow to the heart starts with clean alkaline blood processed by a healthy liver free from toxins such as drugs, alcohol and toxic medications (narcotics).  Consumption of foods rich in nutrients such as folate, Vitamin C and B and L-arginine amino acid can prevent mitochondrial damage.  Example of foods rich in these nutrients are cage-free eggs, dairy products like cultured yogurtkefir and raw cheeses (choose organic and raw dairy whenever possible) Grass-fed beef or meat and pasture-raised poultry (including turkey and chicken) Liver and organ meats (such as chicken liver pate).

And the most important factors for a healthy heart are deep cleansing breath from calm mind, sleep, stress-free and healthy lifestyle with positive energies from sunshine, massage and grounding (walking barefoot on the beach or ground).

Connie


Sun, Earth and the Human Touch — 3 Key Principles for Healthy Blood Flow

Pollack has also clearly demonstrated there are three natural energies that result in separation of charges that create flow:

1.Sunlight charges up your blood vessels, which increases the flow of blood. When the sun’s rays penetrate your skin, it causes a massive increase of nitric oxide that acts as a vasodilator. As much as 60 percent of your blood can be shunted to the surface of your skin through the action of nitric oxide. This helps absorb solar radiation, which then causes the water in your blood to capture the energy and become structured.

This is a key component for a healthy heart. The ideal is to be exposed to the sun while grounding, meaning walking barefoot. This forms a biological circuit that makes it work even better.

2.Negative ions from the Earth, also known as earthing or grounding. This also charges up your blood vessels, creates a separation of charges, creates more positive ions and allows the blood to flow upward, against gravity.

3.The field effect or touch from another living being, such as laying on of hands.


Mitochondrial encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) is one of the family of mitochondrial cytopathies, which also include MERRF, and Leber’s hereditary optic neuropathy.

Most people with MELAS have a buildup of lactic acid in their bodies, a condition called lactic acidosis. Increased acidity in the blood can lead to vomiting, abdominal pain, extreme tiredness (fatigue), muscle weakness, loss of bowel control, and difficulty breathing. Less commonly, people with MELAS may experience involuntary muscle spasms (myoclonus), impaired muscle coordination (ataxia), hearing loss, heart and kidney problems, diabetes, epilepsy, and hormonal imbalances.

MELAS is a condition that affects many of the body’s systems, particularly the brain and nervous system (encephalo-) and muscles (myopathy). In most cases, the signs and symptoms of this disorder appear in childhood following a period of normal development.[3]Early symptoms may include muscle weakness and pain, recurrent headaches, loss of appetite, vomiting, and seizures. Most affected individuals experience stroke-like episodes beginning before age 40. These episodes often involve temporary muscle weakness on one side of the body (hemiparesis), altered consciousness, vision abnormalities, seizures, and severe headaches resembling migraines. Repeated stroke-like episodes can progressively damage the brain, leading to vision loss, problems with movement, and a loss of intellectual function (dementia). The stroke-like episodes can be mis-diagnosed as epilepsy by a doctor not aware of the MELAS condition.

Patients are managed according to what areas of the body are affected at a particular time. Enzymesamino acidsantioxidants and vitamins have been used.

Also the following supplements may help:

  • CoQ10 has been helpful for some MELAS patients.[7] Nicotinamide has been used because complex l accepts electrons from NADH and ultimately transfers electrons to CoQ10.
  • Riboflavin has been reported to improve the function of a patient with complex l deficiency and the 3250T-C mutation.[8]
  • The administration of L-arginine during the acute and interictal periods may represent a potential new therapy for this syndrome to reduce brain damage due to impairment of vasodilation in intracerebral arteries due to nitric oxide depletion

Brain Immune System is Key to Recovery from Motor Neuron Degeneration

Brain Immune System is Key to Recovery from Motor Neuron Degeneration

Summary: Researchers report microglia is critical for neuronal survival in ALS.

Source: University of Pennsylvania.

The selective demise of motor neurons is the hallmark of Lou Gehrig’s disease, also known as amyotrophic lateral sclerosis (ALS). Yet neurologists have suspected there are other types of brain cells involved in the progression of this disorder — perhaps protection from it, which could light the way to treatment methods for the incurable disease. To get to the bottom of this question, researchers in the Perelman School of Medicine at the University of Pennsylvania engineered mice in which the damage caused by a mutant human TDP-43 protein could be reversed by one type of brain immune cell. TDP-43 is a protein that misfolds and accumulates in the motor areas of the brains of ALS patients.

First author Krista J. Spiller, PhD, a postdoctoral fellow, and senior author Virginia M-Y. Lee, PhD, director of the Center for Neurodegenerative Disease Research and a professor of Pathology and Laboratory Medicine, published their findings this week in Nature Neuroscience.

They found that microglia, the first and primary immune response cells in the brain and spinal cord, are essential for dealing with TDP-43-associated neuron death. This study is the first to demonstrate how healthy microglia respond to pathological TDP-43 in a living animal.

“The prevailing view in the field has been that immune system inflammation contributes to the death of neurons in ALS, but this study shows the opposite – that microglia are actually critical for neuronal survival,” Lee said.

The number of microglia cells remained stable in mice with ALS symptoms. However, after the researchers chemically suppressed expression of pathological human TDP-43 in the mice, microglia dramatically proliferated and changed their shape and what genes they expressed.

The researchers were perplexed as to why the microglia did not react automatically to the presence of mutant TDP-43 and how subduing its expression incited microglia to react. “This is still a mystery, but one that we’d very much like to figure out in future studies,” Spiller said.

The normally branched microglia retracted their extensions and expanded the size of their main cell bodies. (This rapid change in shape is fairly unique to microglia in the central nervous system, although macrophages, microglia’s immune-system counterpart in peripheral parts of the body, are similarly dynamic in their shape shifting.)

neurons

The now abundant, remade microglia multiplied by 70 percent after one week and selectively cleared accumulated human TDP-43 from motor neurons. Microglia surround TDP-43-filled neurons and turned on genes to make proteins that help them attach to the sick cells and induce a process called phagocytosis that envelops the mutant proteins for disposal. After the mop up, mice stopped exhibiting motor dysfunction symptoms such as leg clasping and tremors, and they regained their ability to walk and gain weight.

Conversely, TDP-43 was not fully cleared in mice with no microglia. When proliferation of microglia was blocked, the mice failed to regain full muscle function, revealing how important microglia are for cleaning up clumps of misfolded proteins.

“The way reactive microglia protect neurons points us towards new ideas for ALS therapies,” Spiller said. “For example, we want to know if we can encourage the expansion of microglia in early-stage ALS patients to save their motor neurons.”

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

Funding: This work was supported by the Judith and Jean Pape Adams Charitable Foundation, the ALS Association, the National Institutes of Health (PO1-017586), and gifts from the Koller and Pottruck families.

Source: Karen Kreeger – University of Pennsylvania
Publisher: Organized by NeuroscienceNews.com.
Image Source: NeuroscienceNews.com image is credited to Virginia M-Y. Lee, PhD and Krista J. Spiller, PhD, Perelman School of Medicine at the University of Pennsylvania.
Original Research: Abstract in Nature Neuroscience.
DOI:10.1038/s41593-018-0083-7

CITE THIS NEUROSCIENCENEWS.COM ARTICLE
University of Pennsylvania “Brain Immune System is Key to Recovery from Motor Neuron Degeneration.” NeuroscienceNews. NeuroscienceNews, 20 February 2018.
< http://neurosciencenews.com/als-immune-system-8524/&gt;.

Abstract

Microglia-mediated recovery from ALS-relevant motor neuron degeneration in a mouse model of TDP-43 proteinopathy

Though motor neurons selectively degenerate in amyotrophic lateral sclerosis, other cell types are likely involved in this disease. We recently generated rNLS8 mice in which human TDP-43 (hTDP-43) pathology could be reversibly induced in neurons and expected that microglia would contribute to neurodegeneration. However, only subtle microglial changes were detected during disease in the spinal cord, despite progressive motor neuron loss; microglia still reacted to inflammatory triggers in these mice. Notably, after hTDP-43 expression was suppressed, microglia dramatically proliferated and changed their morphology and gene expression profiles. These abundant, reactive microglia selectively cleared neuronal hTDP-43. Finally, when microgliosis was blocked during the early recovery phase using PLX3397, a CSF1R and c-kit inhibitor, rNLS8 mice failed to regain full motor function, revealing an important neuroprotective role for microglia. Therefore, reactive microglia exert neuroprotective functions in this amyotrophic lateral sclerosis model, and definition of the underlying mechanism could point toward novel therapeutic strategies.

Anti-aging blend of thirty vitamins and minerals

A dietary supplement containing a blend of thirty vitamins and minerals—all natural ingredients widely available in health food stores—has shown remarkable anti-aging properties that can prevent and even reverse massive brain cell loss, according to new research from McMaster University.

It’s a mixture scientists believe could someday slow the progress of catastrophic neurological diseases such as Alzheimer’s, ALS and Parkinson’s.

“The findings are dramatic,” says Jennifer Lemon, research associate in the Department of Biology and a lead author of the study. “Our hope is that this supplement could offset some very serious illnesses and ultimately improve quality of life.”

The formula, which contains common ingredients such as vitamins B, C and D, folic acid, green tea extract, cod liver oil and other nutraceuticals, was first designed by scientists in McMaster’s Department of Biology in 2000.

A series of studies published over the last decade and a half have shown its benefits in mice, in both normal mice and those specifically bred for such research because they age rapidly, experiencing dramatic declines in cognitive and motor function in a matter of months.

The mice used in this study had widespread loss of more than half of their brain cells, severely impacting multiple regions of the brain by one year of age, the human equivalent of severe Alzheimer’s disease.

The mice were fed the supplement on small pieces of bagel each day over the course of several months. Over time, researchers found that it completely eliminated the severe brain cell loss and abolished cognitive decline.

“The research suggests that there is tremendous potential with this supplement to help people who are suffering from some catastrophic neurological diseases,” says Lemon, who conducted the work with co-author Vadim Aksenov, a post-doctoral fellow in the Department of Biology at McMaster.

“We know this because mice experience the same basic cell mechanisms that contribute to neurodegeneration that humans do. All species, in fact. There is a commonality among us all.”

In addition to looking at the major markers of aging, they also discovered that the mice on the supplements experienced enhancement in vision and most remarkably in the sense of smell—the loss of which is often associated with neurological disease—improved balance and motor activity.

The next step in the research is to test the supplement on humans, likely within the next two years, and target those who are dealing with neurodegenerative diseases.

The research is published online in the journal Environmental and Molecular Mutagenesis.

Explore further: ‘Silver bullet’ supplement could slow brain aging

Provided by: McMaster University


Keywords:

  • aging;
  • neurodegeneration;
  • multi-ingredient dietary supplement;
  • oxidative stress;
  • neuroprotectant

Abstract

Transgenic growth hormone mice (TGM) are a recognized model of accelerated aging with characteristics including chronic oxidative stress, reduced longevity, mitochondrial dysfunction, insulin resistance, muscle wasting, and elevated inflammatory processes. Growth hormone/IGF-1 activate the Target of Rapamycin known to promote aging. TGM particularly express severe cognitive decline.

We previously reported that a multi-ingredient dietary supplement (MDS) designed to offset five mechanisms associated with aging extended longevity, ameliorated cognitive deterioration and significantly reduced age-related physical deterioration in both normal mice and TGM.

Here we report that TGM lose more than 50% of cells in midbrain regions, including the cerebellum and olfactory bulb. This is comparable to severe Alzheimer’s disease and likely explains their striking age-related cognitive impairment.

We also demonstrate that the MDS completely abrogates this severe brain cell loss, reverses cognitive decline and augments sensory and motor function in aged mice. Additionally, histological examination of retinal structure revealed markers consistent with higher numbers of photoreceptor cells in aging and supplemented mice.

We know of no other treatment with such efficacy, highlighting the potential for prevention or amelioration of human neuropathologies that are similarly associated with oxidative stress, inflammation and cellular dysfunction.

Environ. Mol. Mutagen., 2016. © 2016 Wiley Periodicals, Inc.