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Skin and nerves need Vit C, A, D, E, calcium-magnesium and B complex

Neuroscientists at the Johns Hopkins University School of Medicine have discovered how the sense of touch is wired in the skin and nervous system. The new findings, published Dec. 22 in Cell, open new doors for understanding how the brain collects and processes information from hairy skin.

“You can deflect a single hair on your arm and feel it, but how can you tell the difference between a raindrop, a light breeze or a poke of a stick?” says David Ginty, Ph.D., professor of neuroscience at Johns Hopkins. “Touch is not yes or no; it’s very rich, and now we’re starting to understand how all those inputs are processed.”

Folate – Vit B9 deficiency or MTHFR gene mutation

Folate – Vit B9 or MTHFR deficiency has a frequency of 1 in 1.9 . Those with potentially “severe” mutations should check homocysteine with their doctor. Folate deficiency: A deficiency in folic acid (folate) could be linked to MTHFR mutation and is worth checking out. Common symptoms include extreme fatigue, light-headedness, and forgetfulness. Homocysteine is an […]

Cancer costs $895 billion annually, Vit D from sun as anti-cancer

Cancer costs $895 billion annually. Comparatively, heart disease costs $753 billion. Nothing else comes close, with traffic accidents and diabetes each costing about $204 billion. “The price for one year of life increased to $139,100 in 2005 and $207,000 in 2013.” The biggest financial impact is in terms of loss of life and productivity, in […]

Macular degeneration dietary supplementation

By Dr Mercola

The human retina is about the size of a postage stamp andthe macula only about the size of a pencil tip. Yet hundreds of millions of light-receptor cellsare employed. Cone cells produce color vision and are located in the macula.Rod cells produce black and white for night vision. The cone cells arelocated in the center of the retina and are used for reading and finecentral vision. The rods are in the periphery of the retina and are usedfor night and side vision. Degeneration of the rods results in night blindness(retinitis pigmentosa). Degeneration of the cones results in macular degeneration.

From back to front, the maculais nourished by the choroid or blood layer of the retina. Poor circulationwould then affect vision. The choroid has extensions into the retina.If the capillaries (connectors) become leaky, then the chorio-capillaruswill ooze some blood serum behind the retina, called subretinal swelling.If the capillaries become even more leaky, then red blood cells will oozebehind the retina and become a sub-retinal hemorrhage.

VitaminC and bioflavonoids (bilberry, cranberry, blueberry, others) help to keep strong capillaries.

Furthermore, the back of theretina is protected from sunlight damage by brown melanin pigment. Asmelanin pigment dissipates with age, macular degeneration accelerates.Plant pigments like bilberry mimic the light-absorption of melanin.

The blood and its nutrients(oxygen, vitamins, lutein) must pass a membrane, called Bruch’s membrane,which may become calcified over time, blocking nutrient entry and theexit of cellular debris. This can be remedied by taking magnesium, a calcium-antogonist(natural calcium blocker).

Once nutrients have passedBruch’s membrane, they go thru a single-cell layer of cells called theretinal pigment epithelium (RPE). The RPE are garbage-cleaning cells.They digest used-up portions of vitamin A shed from the rod cells everymorning. The RPE accomplishes this by producing an antioxidant calledglutathione peroxidase, which is generated from vitamin E and selenium.

Without Vitamin E and selenium, the RPE will build up cellular garbage deposits.

If nutrients pass through thechoroid, Bruch’s membrane, and the RPE, then they finally reach the retinallight-receptor cells, the rod and cones. These cells are lined with fat– – omega-3 fat called DHA. Studies show that people who consume morefish, which is rich in DHA-fish fat, are less likely to develop maculardegeneration. Vitamin B12 is the glue that keeps the DHA in place. VitaminE protects the DHA-fat from turning rancid.

In front of the photoreceptorsis the nerve layer of the retina. These nerve cells transmit visual signalsvia the optic nerve to the brain. It is in this nerve layer thay luteinand zeaxanthin reside. These are two yellow dietary pigments that worklike sunglass filters to protect the underlying macula from solar radiation.Blue-eyed adults have far less lutein and zeaxanthin in their retinas.

A recent study shows that 60-yearolds who had adequate retinal levels of lutein and zeaxanthin retainedthe ability to see faint light as well as 20-year old adults!! How’s thatfor anti-aging. Lutein and zeaxanthin are acquired from spinachand kale, and from food supplements as extracts of marigoldflower petals. At least 6 milligramsof lutein and zeaxanthin should be consumed daily. (Centrum multivitaminonly provide 1/4th of one milligram!.)

A nutritional regimen for macular degeneration should include:

1. Habitual wearing of UV-blueblocking sunglasses when outdoors in daylight.

2. Consumption of spinach andkale

3. A daily food supplementregimen that include lutein (6-12 mg), vitamin E (200-400 IU), selenium (organic, nor selenate or selenite) 200 mcg; vitamin B12, 300 mcg; magnesium 400 mg; vitamin C 500-2000 mg; bilberry 120-240 mg; DHA-rich fish oil providing 1000 mg of DHA; sulfur-bearing nutrients (glutathione, lipoicacid, N-acetyl cysteine or taurine).

4. Avoid high-dose calcium supplements without balancing magnesium (60:40 ratio).

5. Avoid hydrogenated fats that interfere with the omega-3 fats.

6. Avoid very low-fat diets, that rob the retina of omega-3 fats.

7. Eat sulfur-rich foods, such as garlic, eggs, asparagus, onions.

 

Depression is a brain disease

In a genome-wide study, Perlis and colleagues found 17 genetic variations linked to depression at 15 genome locations. In addition to hinting at a link between depression and brain gene expression during development, there was also evidence of overlap between the genetic basis of depression and other mental illnesses. While the genome sites identified still account for only a fraction of the risk for depression, the researchers say the results support the strategy of complementing more traditional methods with crowd-sourced data.

To increase their odds of detecting these weak genetic signals, the researchers adopted a strategy of studying much larger samples than had been used in the earlier genome-wide studies. They first analyzed common genetic variation in 75,607 people of European ancestry who self-reported being diagnosed or treated for depression and 231,747 healthy controls of similar ethnicity. These data had been shared by people who purchased their own genetic profiles via the 23 and Me website and agreed to participate in the company’s optional research initiative, which makes data available to the scientific community, while protecting privacy.

The researchers integrated these data with results from a prior Psychiatric Genomic Consortium  genome-wide-association study, based on clinician-vetted diagnoses of more than 20,000 patients and controls of European ancestry. They then followed-up with a closer look at certain statistically suspect sites from that analysis in an independent 23 and Me “replication” sample of 45,773 cases and 106,354 controls.

“We hope these findings help people understand that depression is a brain disease, with it’s own biology,” said Perlis. “Now comes the hard work of using these new insights to try to develop better treatments.”

Hyde CL, Nagle MW, Tian C, Chen X, Paciga SA, Wendland JR, Tung J, Hinds DA, Perlis RH, Winslow AR. Identification of 15 genetic loci associated with risk of major depression in individuals of European descent. Nature Genetics, Aug 1., 2016. doi:10.1038/ng.3623

About the National Institute of Mental Health (NIMH): The mission of the NIMH is to transform the understanding and treatment of mental illnesses through basic and clinical research, paving the way for prevention, recovery and cure. For more information, visit the NIMH website.

Five Major mental disorders share genetic roots

Prior to the study, researchers had turned up evidence of shared genetic risk factors for pairs of disorders, such as schizophenia and bipolar disorder, autism and schizophrenia and depression and bipolar disorder. Such evidence of overlap at the genetic level has blurred the boundaries of traditional diagnostic categories and given rise to research domain criteria, or RDoC, an NIMH initiative to develop new ways of classifying psychopathology for research based on neuroscience and genetics as well as observed behavior.

To learn more, the consortium researchers analyzed the five key disorders as if they were the same illness. They screened for evidence of illness-associated genetic variation across the genomes of 33,332 patients with all five disorders and 27,888 controls, drawing on samples from previous consortium mega-analyses.

For the first time, specific variations significantly associated with all five disorders were among several suspect genomic sites that turned up. These included variation in two genes that code for the cellular machinery for regulating the flow of calcium into neurons. Variation in one of these, called CACNA1C, which had previously been implicated in susceptibility to bipolar disorder, schizophrenia and major depression, is known to impact brain circuitry involved in emotion, thinking, attention and memory – functions disrupted in mental illnesses. Variation in another calcium channel gene, called CACNB2, was also linked to the disorders.

Alterations in calcium-channel signaling could represent a fundamental mechanism contributing to a broad vulnerability to psychopathology, suggest the researchers.

They also discovered illness-linked variation for all five disorders in certain regions of chromosomes 3 and 10. Each of these sites spans several genes, and the specific causal factors within them remain elusive. However, one region, called 3p21, which produced the strongest signal of illness association, harbors suspect variations identified in previous genome-wide studies of bipolar disorder and schizophrenia.

Source: Jordan Smoller, M.D., Massachusetts General Hospital

CACNA1c 3CACNA1C 2CACNA1 1

References

Cross-Disorder Group of the Psychiatric Genomics Consortium. Identification of risk loci with shared effects on five major psychiatric disorders: a genome-wide analysis. The Lancet, February 28, 2013

 

CACNA1C,

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