What are the symptoms of low vitamin E?

The body needs vitamin E to function, making it an essential vitamin. It is fat-soluble, meaning that it requires fat from the diet to be properly absorbed. Vitamin E is mainly stored in the liver before being released into the blood stream for use.

Deficiency is uncommon and typically the result of an underlying condition. Some premature infants also have low levels.

Vitamin E occurs in eight chemical forms. With a blood test, a doctor can learn how much of one form, alpha-tocopherol, a person has. Using this information, they can determine whether a person's overall level of vitamin E.

A normal level is usually with the range of 5.5–17 milligrams per liter (mg/L). The normal range may be different for premature infants and children under 17. Normal ranges can also vary slightly among labs.

When an adult has less than 4 mg/L of vitamin E in their blood, they usually require supplementation.

Signs and symptoms of deficiency

Vitamin E deficiency may cause disorientation and vision problems.

Low levels of vitamin E can lead to:

• Muscle weakness: Vitamin E is essential to the central nervous system. It is among the body's main antioxidants, and a deficiency results in oxidative stress, which can lead to muscle weakness.
• Coordination and walking difficulties: A deficiency can cause certain neurons, called the Purkinje neurons, to break down, harming their ability to transmit signals.
• Numbness and tingling: Damage to nerve fibers can prevent the nerves from transmitting signals correctly, resulting in these sensations, which are also called peripheral neuropathy.
• Vision deterioration: A vitamin E deficiency can weaken light receptors in the retina and other cells in the eye. This can lead to loss of vision over time.
• Immune system problems: Some research suggests that a lack of vitamin E can inhibit the immune cells. Older adults may be particularly at risk.

Muscle weakness and difficulties with coordination are neurological symptoms that indicate damage to the central and peripheral nervous systems.

The peripheral system is the network of nerves located beyond the brain and spinal cord. These neurons pass messages throughout the body.

The central nervous system communicates between the brain and the spinal cord.

The sheaths of neurons are mostly composed of fats. When the body has too little vitamin E, it contains fewer antioxidants that protect these fats, and the function of the nervous system breaks down.

Causes of vitamin E deficiency

- Genetics

Vitamin E deficiency often runs in families.

Learning about family history can make diagnosing certain rare, inherited diseases easier. Two of these diseases, congenital abetalipoproteinemia and familial isolated vitamin E deficiency, are chronic and result in extremely low vitamin E levels.

- Medical conditions

Vitamin E deficiency can also result from diseases that severely reduce the absorption of fat. This is because the body requires fat to absorb vitamin E correctly.

Some of these diseases include:

• chronic pancreatiti
• celiac disease
• cholestatic liver disease
• cystic fibrosis.

Deficiency is also common in newborns and babies born prematurely who have lower birth weights and less fat.

Premature infants are at particular risk because an immature digestive tract can interfere with fat and vitamin E absorption.

Vitamin E deficiencies in these infants can also lead to hemolytic anemia, which destroys red blood cells.

When to see a doctor

When a person has no history of genetic disease but experiences any symptoms of a vitamin E deficiency, they should contact a doctor.

An extremely low level of vitamin E in the blood can indicate an underlying health issue. Further testing will help to determine the cause and treatment options.

What are the treatment options?

Newborns and premature babies may be given a vitamin E supplement via a tube in the stomach.

Vitamin E supplementation is often effective.

Newborns and premature babies

Current practice involves providing vitamin E supplementation through a tube in the stomach. When necessary, it can also be administered intravenously.

While one dose can sufficiently raise blood levels of vitamin E, multiple doses may be required.

Children and adults

Children and adults with deficiencies caused by inherited conditions require supplementation with high doses of vitamin E.

Supplementation can stop the progression of the disease. When the deficiency is detected early, it may prevent neurological symptoms.


source : Medical News Today

Hidden Secret of Immortality Enzyme Telomerase .Can we stay young forever, or even recapture lost youth?

Research from the laboratory of Professor Julian Chen in the School of Molecular Sciences at Arizona State University recently uncovered a crucial step in the telomerase enzyme catalytic cycle. This catalytic cycle determines the ability of the human telomerase enzyme to synthesize DNA "repeats" (specific DNA segments of six nucleotides) onto chromosome ends, and so afford immortality in cells. Understanding the underlying mechanism of telomerase action offers new avenues toward effective anti-aging therapeutics. illustration depicting the enzyme telomerase This figure depicts the enzyme telomerase as well as telomeres relative to a chromosome.

Typical human cells are mortal and cannot forever renew themselves. As demonstrated by Leonard Hayflick a half-century ago, human cells have a limited replicative lifespan, with older cells reaching this limit sooner than younger cells. This "Hayflick limit" of cellular lifespan is directly related to the number of unique DNA repeats found at the ends of the genetic material-bearing chromosomes. These DNA repeats are part of the protective capping structures, termed "telomeres," which safeguard the ends of chromosomes from unwanted and unwarranted DNA rearrangements that destabilize the genome.

Each time the cell divides, the telomeric DNA shrinks and will eventually fail to secure the chromosome ends. This continuous reduction of telomere length functions as a "molecular clock" that counts down to the end of cell growth. The diminished ability for cells to grow is strongly associated with the aging process, with the reduced cell population directly contributing to weakness, illness, and organ failure.

The fountain of youth at molecular level

Counteracting the telomere shrinking process is the enzyme, telomerase, that uniquely holds the key to delaying or even reversing the cellular aging process. Telomerase offsets cellular aging by lengthening the telomeres, adding back lost DNA repeats to add time onto the molecular clock countdown, effectively extending the lifespan of the cell. Telomerase lengthens telomeres by repeatedly synthesizing very short DNA repeats of six nucleotides -- the building blocks of DNA -- with the sequence "GGTTAG" onto the chromosome ends from an RNA template located within the enzyme itself. However, the activity of the telomerase enzyme is insufficient to completely restore the lost telomeric DNA repeats, nor to stop cellular aging.

The gradual shrinking of telomeres negatively affects the replicative capacity of human adult stem cells, the cells that restore damaged tissues and/or replenish aging organs in our bodies. The activity of telomerase in adult stem cells merely slows down the countdown of the molecular clock and does not completely immortalize these cells. Therefore, adult stem cells become exhausted in aged individuals due to telomere length shortening that results in increased healing times and organ tissue degradation from inadequate cell populations.

Tapping the full potential of telomerase

Understanding the regulation and limitation of the telomerase enzyme holds the promise of reversing telomere shortening and cellular aging with the potential to extend human lifespan and improve the health and wellness of elderly individuals. Research from the laboratory of Chen and his colleagues, Yinnan Chen, Joshua Podlevsky and Dhenugen Logeswaran, recently uncovered a crucial step in the telomerase catalytic cycle that limits the ability of telomerase to synthesize telomeric DNA repeats onto chromosome ends.

"Telomerase has a built-in braking system to ensure precise synthesis of correct telomeric DNA repeats. This safe-guarding brake, however, also limits the overall activity of the telomerase enzyme," said Professor Chen. "Finding a way to properly release the brakes on the telomerase enzyme has the potential to restore the lost telomere length of adult stem cells and to even reverse cellular aging itself."

This intrinsic brake of telomerase refers to a pause signal, encoded within the RNA template of telomerase itself, for the enzyme to stop DNA synthesis at the end of the sequence 'GGTTAG'. When telomerase restarts DNA synthesis for the next DNA repeat, this pause signal is still active and limits DNA synthesis. Moreover, the revelation of the braking system finally solves the decades-old mystery of why a single, specific nucleotide stimulates telomerase activity. By specifically targeting the pause signal that prevents restarting DNA repeat synthesis, telomerase enzymatic function can be supercharged to better stave off telomere length reduction, with the potential to rejuvenate aging human adult stem cells.

Human diseases that include dyskeratosis congenita, aplastic anemia, and idiopathic pulmonary fibrosis have been genetically linked to mutations that negatively affect telomerase activity and/or accelerate the loss of telomere length. This accelerated telomere shortening closely resembles premature aging with increased organ deterioration and a shortened patient lifespan from critically insufficient cell populations. Increasing telomerase activity is the seemingly most promising means of treating these diseases.

While increased telomerase activity could bring youth to aging cells and cure premature aging-like diseases, too much of a good thing can be damaging for the individual. Just as youthful stem cells use telomerase to offset telomere length loss, cancer cells employ telomerase to maintain their aberrant and destructive growth. Augmenting and regulating telomerase function will have to be performed with precision, walking a narrow line between cell rejuvenation and a heightened risk for cancer development.

Distinct from human stem cells, somatic cells constitute the vast majority of the cells in the human body and lack telomerase activity. The telomerase deficiency of human somatic cells reduces the risk of cancer development, as telomerase fuels uncontrolled cancer cell growth. Therefore, drugs that increase telomerase activity indiscriminately in all cell types are not desired. Toward the goal of precisely augmenting telomerase activity selectively within adult stem cells, this discovery reveals the crucial step in telomerase catalytic cycle as an important new drug target. Small molecule drugs can be screened or designed to increase telomerase activity exclusively within stem cells for disease treatment as well as anti-aging therapies without increasing the risk of cancer.

Source : Arizona State University

Largest study of its kind finds alcohol use biggest risk factor for dementia

Alcohol use disorders are the most important preventable risk factors for the onset of all types of dementia, especially early-onset dementia. This according to a nationwide observational study, published in The Lancet Public Health journal, of over one million adults diagnosed with dementia in France.

This study looked specifically at the effect of alcohol use disorders, and included people who had been diagnosed with mental and behavioural disorders or chronic diseases that were attributable to chronic harmful use of alcohol.

Of the 57,000 cases of early-onset dementia (before the age of 65), the majority (57%) were related to chronic heavy drinking.

The World Health Organization (WHO) defines chronic heavy drinking as consuming more than 60 grams pure alcohol on average per day for men (4-5 Canadian standard drinks) and 40 grams (about 3 standard drinks) per day for women.

As a result of the strong association found in this study, the authors suggest that screening, brief interventions for heavy drinking, and treatment for alcohol use disorders should be implemented to reduce the alcohol-attributable burden of dementia.

"The findings indicate that heavy drinking and alcohol use disorders are the most important risk factors for dementia, and especially important for those types of dementia which start before age 65, and which lead to premature deaths," says study co-author and Director of the CAMH Institute for Mental Health Policy Research Dr. Jürgen Rehm. "Alcohol-induced brain damage and dementia are preventable, and known-effective preventive and policy measures can make a dent into premature dementia deaths."

Dr. Rehm points out that on average, alcohol use disorders shorten life expectancy by more than 20 years, and dementia is one of the leading causes of death for these people.

For early-onset dementia, there was a significant gender split. While the overall majority of dementia patients were women, almost two-thirds of all early-onset dementia patients (64.9%) were men.

Alcohol use disorders were also associated with all other independent risk factors for dementia onset, such as tobacco smoking, high blood pressure, diabetes, lower education, depression, and hearing loss, among modifiable risk factors. It suggests that alcohol use disorders may contribute in many ways to the risk of dementia.

"As a geriatric psychiatrist, I frequently see the effects of alcohol use disorder on dementia, when unfortunately alcohol treatment interventions may be too late to improve cognition," says CAMH Vice-President of Research Dr. Bruce Pollock. "Screening for and reduction of problem drinking, and treatment for alcohol use disorders need to start much earlier in primary care." The authors also noted that only the most severe cases of alcohol use disorder -- ones involving hospitalization -- were included in the study. This could mean that, because of ongoing stigma regarding the reporting of alcohol-use disorders, the association between chronic heavy drinking and dementia may be even stronger.

Source :  Centre for Addiction and Mental Health. 

SKIN CARE THAT PROTECTS YOU FROM THE TECH WORLD AND POLLUTION

Every day, your skin goes to battle with the environment. UV rays, pollution, blue light from laptops, and harsh ingredients do a number on our skin—which is why the next wave of skin-care products is working to support it in the modern world. Think “skin-barrier-supporting” and “microbiome-enhancing” serums that help fuel optimal skin function and, of course, a healthy glow.

“Especially now, there are lots of impacts from pollutants in the environment and ozone to UV rays, and all of these can have a negative impact on the [skin’s] lipid barrier,” explains Jim Hammer, a cosmetic chemist, such as redness, acne, or dryness. “So, proper skin barrier function is really key to maintaining healthy, hydrated skin.”

Beauty brands are rising to the occasion with new products designed to nourish and support this important ecosystem of the skin, says Cindy DiPrima Morisse, co-founder of CAP Beauty. “Instead of stripping away layers of the skin, products are helping build up its own defenses.”

Launches from companies like Marie Veronique, Biossance, Allies of Skin, and microbiome-protecting Mother Dirt are anticipating the environmental stressors your skin might encounter over the day, and the imbalances they could cause.

They’re using ingredients like lipids, ceramides, adaptogens, and even live bacteria to help fortify your skin’s natural functioning, so it can do its thing—and be your first natural line of defense against technology and the pollutants of the modern world.

Source : www.wellandgood.com

IF YOU LIKE TURMERIC, YOU’RE GOING TO LOVE MORINGA

Buzz about turmeric’s anti-inflammatory powers dominated 2017, but 2018 is all about moringa. North American healthy food companies have discovered this super-green from south of the equator, and it’s being touted as an even more powerful inflammation fighter.

Called the “world’s most useful tree” by scientists, moringa’s healing history in India, Chile, and Africa has been little known in this part of the world. But its nutrition profile is now becoming super brag-worthy on the wellness scene: It has twice the protein of spinach and three times as much iron, says nutritionist (and Well+Good Council member) Kimberly Snyder. According to the journal Ecology of Food and Nutrition, it has impressive amounts of calcium, potassium, and vitamin A. So this is pretty much a Survivor Island superfood of choice.

Fortunately, the buzzy veggie has a likable taste—its seeds are slightly sweet, and its ground leaves are nutty and grassy like tea. So food companies are not wasting a minute adding moringa into everything from nutrition bars and protein powders (Kuli Kuli) to juices (Pressed Juicery) and kombucha (as in,Suja’s new adaptogenic brew). Moringa’s even entering the chip aisle, where you can grab a bag of Vegan Rob’s Moringa Puffs for your next Netflix girls’ night in.

Oh, and in 2018 expect beauty brands featuring super-nourishing moringa oil (which can be a fair-trade ingredient) to make a point of telling you how great it is for your skin. Based on our research, they might be right.

source : www.wellandgood.com