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

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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.

Magnesium rich foods: mushrooms, sweet potatoes, cauliflower, corn, asparagus, swiss chard, lentils, spinach, beet greens, red beans, black-eyed peas, brocolli, carrot, onions, tomatoes, green pepper

“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.”

Ginty and his colleagues study how the nervous system develops and is wired. In trying to understand how touch-responsive nerve cells develop, they set out to build new tools that enable them to look at individual nerve cells. According to Ginty, there are more than 20 broad classes of so-called mechanosensory nerve cells in the skin — of which only six account for light touch — that sense everything from temperature to pain. But until now, the only way to tell one cell from another was to take electrical recordings as each type of cell generates a different current based on what it senses.

The team first genetically engineered mice to make a fluorescent protein in one type of nerve cell — called the C-type low-threshold mechanosensory receptor or C-LTMR. C-LTMR cells stretch from the spinal cord to the skin, and those cells containing fluorescent protein could be seen in their entirety under a microscope. The team found that each C-LTMR cell branched to send projections to as many as 30 different hair follicles.

Mice have three different types of hair: a thick, long guard hair that accounts for only about 1 percent of total hairs on the body; a shorter hair called the awl/auchene that constitutes about 23 percent of body hair; and a fine hair called the zigzag that makes up 76 percent of body hair. The team found that most of the C-LTMR cell endings — about 80 percent — associate with zigzag hair follicles, the rest with the awl/auchene and none with the guard hair follicles.

The researchers then similarly marked two other types of touch nerve cells and found that each hair type has a different and specific set of nerve endings associated with it. “This makes every hair a unique mechanosensory organ,” says Ginty. Moreover, with their new marking tools, they found that each hair type is evenly spaced and patterned throughout the skin.

The team then wondered how all the input from these individual hairs is collected and sent to the brain. Using a different dying technique, the researchers were able to stain the other end of the cell, in the spinal cord. They found that the nerves connecting each patch of skin containing one guard hair and other associated smaller hairs line up in columns in the spinal cord — neighboring columns correspond to neighboring patches of skin. They estimate that there are about 3,000 to 5,000 columns in the spinal cord, with each column accounting for 100 to 150 hair follicles.

So how does the brain interpret what each hair follicle experiences? “How this happens is remarkable and we’re fairly clueless about it,” says Ginty. But he suspects that the organization of the columns is key to how all the various inputs are processed before a message goes to the brain. And while people are not as hairy as mice, Ginty believes that many of the same structures are shared. This study and the new cell-marking tools they developed, he says, open a lot of doors for new research in understanding touch and other senses.

This study was funded by the National institutes of Health, the Johns Hopkins NINDS core imaging facility and the Howard Hughes Medical Institute.

Authors on the paper are Lishi Li, Michael Rutlin, Victoria Abraira, Wenqin Luo and David Ginty of Johns Hopkins; Colleen Cassidy and C. Jeffery Woodbury of University of Wyoming; Laura Kus, Shiaoching Gong and Nathaniel Heintz of the Howard Hughes Medical Institute and The Rockefeller University; and Michael Jankowski and H. Richard Koerber of University of Pittsburgh School of Medicine.


When we start aging at 40 , we must up our intake of whole foods rich in Vitamins C, A, D, E, calcium-magnesium and B complex which are essential for the health of our skin and nervous system.

For quality supplementation, visit:

http://www.clubalthea.pxproducts.com

 

Folate – Vit B9 deficiency or MTHFR gene mutation

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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 amino acid and breakdown product of protein metabolism that, when present in high concentrations, has been linked to an increased risk of heart attacks and strokes. Elevated homocysteine levels are thought to contribute to plaque formation by damaging arterial walls.

Homocysteine is an amino acid thought to damage the lining of your arteries and other cells of the body. It is naturally formed in the body, but gets broken down (recycled) by 5-MTHF.  Elevated homocysteine levels in the blood is an independent risk factor for heart disease, stroke and other forms of cardiovascular disease.  It has also been linked with a wide range of other health problems including macular degeneration, Alzheimer’s disease, hearing loss, depression and cancer.

MTHFR mutation/gene variation can impact how well your body metabolizes folate and folic acid. Both are forms of vitamin B9, required for numerous critical bodily functions.  A fault in this metabolic cycle is linked to many serious health problems (neck pain,others).

MTHFR, short for Methylenetetrahydrofolate Reductase, is a very important enzyme in the body.  It’s necessary for Methylation to occur, a metabolic process that switches genes on and off, repairs DNA and many other important things.  Methylation is also essential to convert both folate and folic acid – each a form of Vitamin B9 – into its active, usable form called 5-MTHF.

One reader, a Rehab, Nutrition and Lifestyle Coach, Josh Rubin from California notes:

“…Folic acid def[initely] leads to catabolism of histadine. Low levels of histadine creates catabolism in the body and has been shown to be as a marker to arthritic and RA conditions.

“Low folate levels can lead to inhibition of DNA synthesis, impaired cell division, and alterations in protein synthesis.”

Histidine can even help protect tissues from damage caused by radiation or heavy metals. High histidine foods include beef, lamb, cheese, chicken, turkey, soy, fish, nuts, seeds, eggs, beans, and whole grains. The recommended daily intake for histidine is 10mg per kilogram of body weight, or 4.5mg per pound.

Diet

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Diet should include greens, whole foods, lemon, Vit B and Vit C rich whole foods, potassium and iron-rich foods) and vinegar (to aid in absorbtion of nutrients). Vit C and vinegar help in the absorption of nutrients from whole foods.

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What is folic acid/vitamin B9?

Vitamin B9, more commonly known as folate or folic acid, is a water-soluble vitamin that is part of the B vitamin family. B vitamins/folate help support adrenal function, help calm and maintain a healthy nervous system, and are necessary for key metabolic processes. Folate occurs naturally in foods, while folic acid is the synthetic form of folate.

Why is vitamin B9 necessary?

Vitamin B9 is essential for human growth and development, encourages normal nerve and proper brain functioning, and may help reduce blood-levels of the amino acid homocysteine (elevated homocysteine levels have been implicated in increased risk of heart disease and stroke). Folic acid or folate may also help protect against cancers of the lung, colon, and cervix, and may help slow memory decline associated with aging.

Pregnant women have an increased need for folic acid: it supports the growth of the placenta and fetus, and helps to prevent several types of birth defects, especially those of the brain and spine. Pregnant women and women of child-bearing age should take extra caution to get enough folic acid (see below for recommended amounts).

What are the signs of a folic acid deficiency?

Deficiency has been linked to birth defects, low birth weight, pregnancy loss, depression, memory loss, and cervical dysplasia. Alcoholics, pregnant women, and people living in institutional settings are at a higher risk of vitamin B9 or folate deficiency.


Folate and Depression

Many studies, going back to the 1960s, show an elevated incidence of folate deficiency in patients with depression.2 Studies vary depending on the criteria used to define folate deficiency, but often, about one-third of depression patients were deficient. Given that depression is often accompanied by decreased appetite and weight loss, the high incidence of folate deficiency in depression patients is not surprising. However, there is some evidence, though not conclusive, that folate deficiency may be involved in the etiology of depression in a minority of patients. Alternatively, depressed mood may decrease appetite, lower folate levels and thereby help to prevent recovery from depression. A recent review and metaanalysis looked at the results from the limited number of studies that investigated the effect of giving folate to depression patients and concluded that “there is some evidence that augmentation of antidepressant treatment with folate may improve patient outcome.”3 Whether the putative beneficial effect of folate is limited to those with folate deficiency is not clear.1,3

If folate deficiency can contribute to depressed mood and folate supplementation is beneficial in patients, a plausible mechanism implicates serotonin. In most,4–8 but not all,9,10 studies on patients with neuropsychiatric disorders, folate deficiency was associated with low levels of the serotonin metabolite 5-hydroxyindoleacetic acid (5-HIAA) in the cerebrospinal fluid (CSF). In one study, supplementation with folate restored CSF 5-HIAA levels to normal.8

There is also a decrease in serotonin synthesis in patients with 5,10-methylenetetrahydrofolate reductase (MTHFR) deficiency, a disorder of folate metabolism.11,12

While the mechanism relating folate deficiency to low serotonin is not known, it may involve S-adenosylmethionine (SAMe). SAMe is a major methyl donor formed from methionine. Folate is involved in a cycle that regenerates methionine from homocysteine after SAMe is demethylated to S-adenosylhomocysteine, with subsequent conversion to homocysteine. Folate deficiency decreases SAMe in the rat brain.13 In humans, SAMe is an antidepressant14,15 and increases CSF 5-HIAA levels.16 Thus, there is some consistency in what is known about the interrelations of folate, SAMe and depression.

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 which cancer accounts for 1.5 percent of global gross domestic product (GDP) losses. The AICR estimates Americans lost 83 million years of healthy life because of cancer deaths and disabilities in 2008.

More than half a million Americans die of cancer, the second-leading cause of death in the U.S., every year.

To breakdown the direct healthcare costs, the Agency for Healthcare Research and Quality (AHRQ) estimated cancer cost Americans $88.7 billion in 2011. Of that cost:

  • 50% came from hospital outpatient or doctor office visits
  • 35% came from inpatient hospital stays
  • 11% came from prescription drugs

And it’s getting more expensive.

A 2011 study in the Journal of the National Cancer Institute determined the cost of all cancer care in the U.S. totaled $124.5 billion in 2010. The researchers projected the total cost would rise to $157.7 billion by 2020. The projected cost increase by phase of treatment is displayed in the table below.

Cost of Cancer Care in Billions of 2010 Dollars
Initial Continuing Last
2010 $40.46 $46.64 $37.45
2020 $48.31 $61.37 $48.07
Increase 19.4% 31.6% 28.3%

There doesn’t seem to be a good reason for the increase in cost though.

A 2015 National Bureau of Economic Research study found anticancer drug prices at launch increased by 10% ever year between 1995 and 2013, about an $8,500 annual increase. That’s after an adjustment for inflation and survival benefits.

When calculating the average cost for one extra year of life, the researchers determined patients and insurers paid $54,100 in 1995. The price for one year of life increased to $139,100 in 2005 and $207,000 in 2013.

Another study (2014) published in The Lancet found the costs of cancer are already unaffordable in many countries. In the U.S., even those with very good insurance coverage incur out-of-pocket costs or experience overexposure to harmful treatments.

Many people have no idea what to expect financially when their doctor gives them or a loved one the heartbreaking diagnosis.

Total Cost of Cancer Treatment

On an individual level, a cancer diagnosis isn’t limited to physical and emotional hardship. It can put someone in a hard spot financially too.

People may have to choose between more successful expensive treatments and less effective, affordable treatments.

Each person’s cost to treat cancer is different. According to the American Cancer Society (ACS), factors to treat cancer include:

  • The type of treatment.
  • The length of treatment.
  • The location of the treatment.
  • The type of insurance coverage.

For people with health insurance, the concern might not be as great. But some insurance plans won’t cover the most expensive, sometimes most-necessary treatments.

Sadly, many cancer patients have to spend time and energy working out financial issues before treatment even begins. Others face financial struggles during treatment, and almost everyone spends precious energy trying to manage their money while recovering from treatment.

Major healthcare costs to consider include:

  • Hospital and clinic visits.
  • Medicine and prescription drugs.
  • Lab tests.
  • Treatments.
  • Surgeries.
  • Home health services.

Cost of Surgery

Physically removing a tumor during surgery is one of the top ways to treat cancer. Doctors can use surgery to prevent, diagnose, remove, or debulk (remove as much as possible) cancer. They have a variety of methods to do so too, according to the MayoClinic. Surgery methods include:

  • Cryosurgery: freezing cancer cells to destroy them.
  • Electrosurgery: killing cancer cells with high-frequency current.
  • Laser surgery: killing cancer cells with beams of intense light.
  • Mohs surgery: removing cancer cells layer by layer.
  • Laparoscopic surgery: minimally-invasive surgery using small incisions.
  • Robotic surgery: use of 3-D imaging and computers to operate surgical tools.

The costs per surgery vary greatly, depending on the hospital, insurance coverage and type of procedure.

A 2014 study examining the costs of surgery involving various types of cancer found average costs ranging from $14,161 to $56,587. The costs included admissions, readmissions, physician services and other costs (outpatient visits, hospice care, home health agencies or medical equipment).

Average Cost of Cancer Surgery
Procedure Cost
Colectomy (colon) $31,738
Cystectomy (bladder) $42,386
Pancreatectomy (pancreas) $56,587
Proctectomy (rectum) $33,759
Prostatectomy (prostate) $14,161
Pulmonary lobectomy $39,412

Cost of Chemotherapy

Chemotherapy is another way to treat cancer. It involves chemicals that kill fast-growing cells. Since cancer cells grow more quickly than other body cells, doctors often use chemotherapy to treat the disease.

According to an Avalere Health study which analyzed three years of data, the adjusted (based on age, sex and prior cancer history) cost of chemotherapy differed depending on location – in a doctor’s office or hospital’s outpatient department (HOPD).

Average Cost of Chemotherapy
Office HOPD
1 Month $10,764 $13,828
6 Months $49,062 $61,661
12 Months $66,826 $102,395

The costs also differed depending on the type of cancer. The most expensive was colon cancer, which cost $45,997 in an office and $46,220 in an HOPD. The average costs for all lengths of treatment (averaging 3.8 months in an office and 3.4 months in an HOPD) ranged from $28,177 in an office to $34,973 in an HOPD.

Cost of Radiation Therapy

Radiation therapy is another form of expensive cancer treatment. It involves the use of intense energy beams, usually X-rays, to kill genetic material. The radiation kills both healthy cells and cancer cells, so the length of treatment is usually shorter than chemotherapy.

The Avalere Health study also analyzed the adjusted cost of radiation therapies at different locations.

Average Cost of Radiation Therapy
Office HOPD
1 Month $11,472 $13,209
2 Months $23,305 $24,150
3 Months $38,732 $35,761

The costs of radiation therapy also differed by cancer type. The most expensive was prostate cancer, which cost $37,472 in an office and $29,800 in an HOPD. The average costs for all lengths of treatment (averaging 2.1 months in an office and 1.9 months in an HOPD) ranged from $25,144 in an office to $23,756 in an HOPD.

Most people think of healthcare costs when they think of the cost of cancer, but there are other costs that many don’t consider.


Dr Mercola on Melanoma

  • The rising rates of melanoma documented over the last three decades are not due to sun exposure as often stated; researchers instead believe they are due to an increase in diagnoses of non-cancerous lesions classified, misleadingly, as “stage 1 melanoma”
  • Exposure to sunlight, particularly UVB, is protective against melanoma — or rather, the vitamin D your body produces in response to UVB radiation is protective
  • Optimizing your vitamin D levels through proper sun exposure or use of a safe tanning bed can reduce your risk of skin cancer and as many as 16 different types of cancer
  • The sun is your source of vitamin D because when you expose your skin to sunshine, your skin synthesizes vitamin D3 sulfate. This form of vitamin D is water-soluble and can travel freely in your bloodstream, unlike oral vitamin D3 supplements.

Diagnostic drift, according to the study, refers to a hefty increase in disease that is being fueled by non-cancerous lesions.

In fact, during the study period from 1991 to 2004, there were nearly 4,000 cases of melanoma included in the report, with an annual increase of 9.39 to 13.91 cases per 100,000 per year.

The researchers revealed that, rather than being fueled by increasing exposure to sunlight as is commonly suggested, the increased incidence was almost entirely due to minimal, stage 1 disease.

They noted:

“There was no change in the combined incidence of the other stages of the disease, and the overall mortality only increased from 2.16 to 2.54 cases per 100,000 per year … We therefore conclude that the large increase in reported incidence is likely to be due to diagnostic drift, which classifies benign lesions as stage 1 melanoma.”

In other words, people are being diagnosed with melanoma skin cancer even when they have only a minimal, non-cancerous lesion, and these diagnoses appear to be skewing disease rates significantly. Further, adding even more credence to the growing body of evidence showing sun exposure is not the primary cause of melanoma, the researchers noted that the distribution of the lesions reported did not correspond to the sites of lesions caused by sun exposure.

They concluded:

“These findings should lead to a reconsideration of the treatment of ‘early’ lesions, a search for better diagnostic methods to distinguish them from truly malignant melanomas, re-evaluation of the role of ultraviolet radiation and recommendations for protection from it, as well as the need for a new direction in the search for the cause of melanoma.”

Vitamin D is a steroid hormone that influences virtually every cell in your body, and is easily one of nature’s most potent cancer fighters. So I want to stress again that if you are shunning all sun exposure, you are missing out on this natural cancer protection.

Your organs can convert the vitamin D in your bloodstream into calcitriol, which is the hormonal or activated version of vitamin D. Your organs then use it to repair damage, including damage from cancer cells and tumors. Vitamin D’s protective effect against cancer works in multiple ways, including:

  • Increasing the self-destruction of mutated cells (which, if allowed to replicate, could lead to cancer)
  • Reducing the spread and reproduction of cancer cells
  • Causing cells to become differentiated (cancer cells often lack differentiation)
  • Reducing the growth of new blood vessels from pre-existing ones, which is a step in the transition of dormant tumors turning cancerous

This applies not only to skin cancer but other types of cancer as well. Theories linking vitamin D to certain cancers have been tested and confirmed in more than 200 epidemiological studies, and understanding of its physiological basis stems from more than 2,500 laboratory studies, according to epidemiologist Cedric Garland, DrPH, professor of family and preventive medicine at the UC San Diego School of Medicine.

Here are just a few highlights into some of the most noteworthy findings:

  • Some 600,000 cases of breast and colorectal cancers could be prevented each year if vitamin D levels among populations worldwide were increased, according to previous research by Dr. Garland and colleagues.
  • Optimizing your vitamin D levels could help you to prevent at least 16 different types of cancer including pancreatic, lung, ovarian, prostate, and skin cancers.
  • A large-scale, randomized, placebo-controlled study on vitamin D and cancer showed that vitamin D can cut overall cancer risk by as much as 60 percent. This was such groundbreaking news that the Canadian Cancer Society has actually begun endorsing the vitamin as a cancer-prevention therapy.
  • Light-skinned women who had high amounts of long-term sun exposure
    • had half the risk of developing advanced breast cancer (cancer that spreads beyond your breast) as women with lower amounts of regular sun exposure, according to a study in the American Journal of Epidemiology.
    • A study by Dr. William Grant, Ph.D., internationally recognized research scientist and vitamin D expert, found that about 30 percent of cancer deaths — which amounts to 2 million worldwide and 200,000 in the United States — could be prevented each year with higher levels of vitamin D.
  • In 2007 the recommended level was between 40 to 60 nanograms per milliliter (ng/ml). Since then, the optimal vitamin D level has been raised to 50-70 ng/ml, and when treating cancer or heart disease, as high as 70-100 ng/ml.
  • Melanoma skin cancer is the deadliest form, but far more common are non-melanoma skin cancers, which impact millions of Americans every year.

    If you or someone you love is affected, a cream containing eggplant extract, known as BEC and BEC5, appears to cure and eliminate most non-melanoma skin cancers in several weeks time. Unlike conventional skin-cancer treatment, which is often surgery, the eggplant-extract cream leaves no scarring and no visible sign a tumor or lesion was ever present. The eggplant extract appears to be exceptionally safe and only kills cancerous cells, leaving healthy cells untouched, and causes only minor side effects, such as itching and burning.

    The leading researcher in this area today is Dr. Bill E. Cham, who reported as early as 1991 in Cancer Letters that:

    “A cream formulation containing high concentrations (10%) of a standard mixture of solasodine glycosides (BEC) has been shown to be effective in the treatment of malignant and benign human skin tumors.

    We now report that a preparation … which contains very low concentrations of BEC (0.005%) is effective in the treatment of keratoses, basal cell carcinomas (BCCs) and squamous cell carcinomas (SCCs) of the skin of humans. In an open study, clinical and histological observations indicated that all lesions (56 keratoses, 39 BCCs and 29 SCCs) treated with [the preparation] had regressed.”

    Dr. Cham’s latest study was published in the International Journal of Clinical Medicine this year. The paper includes two impressive case reports of 60-something men who were suffering from large basal cell carcinoma (BCC) or squamous cell carcinoma (SCC), which had plagued them for years.  The results upon treatment with a cream formulation of BEC (eggplant extract) twice a day are astounding, and you can view the pictures here.

    Unfortunately, simply eating eggplant, tomatoes, peppers or similar veggies, while beneficial for many reasons, will not induce this same effect because the active components are not able to effectively penetrate your cells. This requires the addition of glycosides, molecules with various simple sugars attached to them that can latch on to receptors found on skin cancer cells.

  • What’s even better than an inexpensive, safe and natural cure for skin cancer is, of course, preventing it in the first place. Your body is made to be in the sun, and, when done properly, sun exposure will be one of the best ways you can help reduce your risk of skin, and many other forms of, cancer. Along with optimizing your vitamin D levels, the carotenoid astaxanthinhas also piqued the interest of researchers due to its ability to reduce signs of aging by helping protect your skin from sun damage. I personally take 8 mg every day to help limit any potential damage from sun exposure as most of the year I am able to spend one to two hours a day in the sun.

    Consuming a healthy diet full of natural antioxidants is another useful strategy to avoid sun damage to your skin, as fresh, raw, unprocessed foods deliver the nutrients that your body needs to maintain a healthy balance of omega-6 and omega-3 oils in your skin, which is your first line of defense against sunburn.

    Fresh, raw vegetables also provide your body with an abundance of powerful antioxidants that will help you fight the free radicals caused by sun damage that can lead to burns and cancer.

  • ————-
  • Connie’s comments: Lessen alcohol intake, avoid fungus and molds and eat whole foods rich in Vit A, D, C and E (for the skin).

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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Is grinding up naproxen for migraines safe (mixing in water)?

Is grinding up naproxen for migraines safe (mixing in water)? by Connie b. Dellobuono

Answer by Connie b. Dellobuono:

Naproxen as an NSAID is acidic. It maybe safe but long term but can be acidic to the cells causing ulceration. Reduce dosage for safety reasons. For migraines, visit http://www.clubalthea.com. Migraines can be a sign of lack of magnesium and Vit C and presence of stress, lack of sleep and other unknowns.
From Wiki:
Naproxen (brand names: Aleve, Naprosyn, and many others) is a nonsteroidal anti-inflammatory drug (NSAID) of the propionic acid class (the same class as ibuprofen) that relieves pain, fever, swelling, and stiffness.[2][3]:665,673 It is a nonselective COX inhibitor, usually sold as the sodium salt.
It is the preferred NSAID for long-term use in people with a high risk of cardiovascular complications (for example, heart attacks or strokes),[3]:665 due to its relatively low risk of such complications. Naproxen poses an intermediate risk of stomach ulcers compared to ibuprofen, which is low-risk, and indometacin, which is high-risk.[4] To reduce stomach ulceration risk, it is often combined with a proton-pump inhibitor (a medication that reduces stomach acid production) during long-term treatment of those with pre-existing stomach ulcers or a history of developing stomach ulcers while on NSAIDs

Is grinding up naproxen for migraines safe (mixing in water)?