Niacin, also known as vitamin B3, is an important nutrient. In fact, every part of your body needs it to function properly. As a supplement, niacin may help lower cholesterol, ease arthritis and boost brain function, among other benefits. However, it can also cause serious side effects if you take large doses.
What foods are high in vitamin b3?
8 Foods That Are High in Niacin (Vitamin B3)
Liver. Liver is one of the best natural sources of niacin. …
Chicken Breast. Chicken, especially the breast meat, is a good source of both niacin and lean protein. …
Tuna. Tuna is a good source of niacin and a great option for people who eat fish but not meat. …
What are the symptoms of vitamin b3 deficiency?
thick, scaly pigmented rash on skin exposed to sunlight.
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Even in environments with low air pollution, long term exposure to traffic exhaust near people’s homes may heighten their risk of stroke, according to a new study from Sweden. The culprit appears to be a fine particle air pollutant called black carbon.
The researchers came to this conclusion after investigating links between exposure to different types of particulate matter and rates of heart disease and stroke in three cities in Sweden.
The authors write that they observed “few consistent associations” between heart disease and stroke and different types of particulate matter and their sources.
Black carbon and particulate matter
Black carbon is a sooty material that comes from burning fossil fuels. According to the United States Environmental Protection Agency (EPA), it is a significant component of fine particle air pollution.
Vehicle and other engines that run on gas and diesel and power plants that run on coal and other fossil fuels emit black carbon along with other particulate matter.
Road traffic is the primary source of black carbon emissions in cities.
Scientists have tied black carbon inhalation to respiratory conditions, cancer, cardiovascular disease, and birth abnormalities.
Dr. Ljungman and colleagues from Karolinska Institutet and other research centers in Sweden used data on 114,758 people who were participants in other studies that had collected information about cardiovascular risk factors from examinations and questionnaires.
The participants, who lived in three cities in Sweden, were healthy and middle-aged at recruitment. The study period started in 1990 and lasted for around 20 years. The dataset included the history of the participants‘ residential addresses over the period.
Over the 20 years of follow-up, 5,166 individuals developed ischemic heart disease, and 3,119 experienced strokes.
Using emissions databases and dispersion models, the team estimated how much each type of emission source contributed to particulate matter, including black carbon, at specific residential addresses.
The sources that they included in the analysis were traffic exhaust, road wear, and residential heating. They included data for two grades of particulate matter: coarse, which includes particles under 10 micrometers (10μm) in diameter (PM10), and fine, which includes particles under 2.5 μm in diameter (PM2.5). Black carbon counts as PM2.5.
Black carbon and raised stroke risk
The analysis revealed that the risk of stroke went up by 4% for every additional 0.3 micrograms per cubic meter (μg/m3) of black carbon air pollutant from traffic exhaust.
The researchers found no link to stroke for black carbon emissions from residential heating.
Also, they observed no links between total levels of PM10 and PM2.5 particulate matter and either heart disease or stroke.
“There was some evidence,” note the authors, “of an association between PM2.5 specifically from local emissions of residential heating and incidence of [ischemic heart disease] that warrant further investigation.”
In their study background, the authors refer to research that has linked long term exposure to PM2.5 particles and atherosclerosis, the clogged artery condition that raises the risk of heart disease and stroke.
The residential areas that the new study covered were in the cities of Gothenburg, Stockholm, and Umeå. The annual averages during the study period for PM2.5 particulate matter in these cities ranged from 5.8 to 9.2 μg/m3. This range is below the 25 μg/m3 threshold in current EU standards.
Although the EU mention black carbon as a component of PM2.5 particulate air pollution, they have no specific threshold for black carbon.
“Black carbon from traffic exhaust could be an important measure to consider when assessing air quality and health consequences.”
New research suggests it is possible to slow or even reverse aging, at least in mice, by undoing changes in gene activity—the same kinds of changes that are caused by decades of life in humans.
By tweaking genes that turn adult cells back into embryoniclike ones, researchers at the Salk Institute for Biological Studies reversed the aging of mouse and human cells in vitro, extended the life of a mouse with an accelerated-aging condition and successfully promoted recovery from an injury in a middle-aged mouse, according to a study published Thursday in Cell.
The study adds weight to the scientific argument that aging is largely a process of so-called epigenetic changes, alterations that make genes more active or less so. Over the course of life cell-activity regulators get added to or removed from genes. In humans those changes can be caused by smoking, pollution or other environmental factors—which dial the genes’ activities up or down. As these changes accumulate, our muscles weaken, our minds slow down and we become more vulnerable to diseases.
The new study suggests the possibility of reversing at least some of these changes, a process researchers think they may eventually get to work in living humans. “Aging is something plastic that we can manipulate,” says Juan Carlos Izpisua Belmonte, the study’s senior author and an expert in gene expression at Salk. In their study Belmonte and his colleagues rejuvenated cells by turning on, for a short period of time, four genes that have the capacity to convert adult cells back into an embryoniclike state.
In living mice they activated the four genes (known as “Yamanaka factors,” for researcher Shinya Yamanaka, the Nobelist who discovered their combined potential in 2006). This approach rejuvenated damaged muscles and the pancreas in a middle-aged mouse, and extended by 30 percent the life span of a mouse with a genetic mutation responsible for Hutchinson–Gilford progeria syndrome, which causes rapid aging in children.
Because the Yamanaka factors reverse changes made to gene regulators, some scientists see the study as further evidence that aging is driven by epigenetic changes. “I do think that epigenetic reprogramming is the ultimate way to reverse aging,” says David Sinclair, a Harvard University geneticist and anti-aging researcher who was not involved in the study but is doing similar work. “My lab has a lot of evidence that the primary driver of what we call the hallmarks of aging is the epigenetic change.” Sinclair says his lab is preparing a paper explaining what causes these changes as we age.
The Salk study was conducted on middle-aged mice. But in theory, reprogramming epigenetics should work on mice and people at any age, says first author Alejandro Ocampo, adding that even cells from human centenarians could eventually be rejuvenated. He and Belmonte say they think they can improve the efficiency and results of the technique with more research—and that they can undo the epigenetic changes responsible for aging by using easier-to-handle chemicals instead of the Yamanaka factors, hopefully moving toward the possibility of treatment for people.
Matt Kaeberlein, a molecular biologist at the University of Washington who studies aging but was not part of the work, says other researchers have found that the Yamanaka factors can rejuvenate cells—so in some ways this study is not surprising. But Kaeberlein says no one else had yet shown that the factors can treat age-related diseases in an animal by making the same changes. “That’s the wow factor,” he explains.
Kaeberlein says the study suggests it may be possible not just to slow aging but to actually reverse it. “That’s really exciting—that means that even in elderly people it may be possible to restore youthful function,” he says. Plus, it is easier to imagine a treatment that makes changes to the epigenome than to consider going into every cell and changing its genes. He also notes that the results of the new study are very similar to those seen when senescent cells—those that have lost function due to aging—are removed from an organism. It is not yet clear, he says, whether “this is another way to shut down or maybe reprogram senescent cells.”
Manuel Serrano, an expert on senescence at the Spanish National Cancer Research Center in Madrid, was not associated with the new research but says he is impressed with the study and its results. “I fully agree with the conclusions. This work indicates that epigenetic shift is in part responsible for aging, and reprogramming can correct these epigenetics errors,” he wrote in an e-mail. “This will be the basis for future exciting developments.”
The study also showed how fine the line can be between benefit and harm. When the researchers treated mice continually, some developed tumors and died within a week. When the scientists cut the treatment to two days out of seven, however, the mice benefited significantly. Sinclair says this should be taken as a note of caution by anyone trying to increase the human life span. “We’ve all been playing with fire,” he says, adding that this fine line will make it challenging to get a drug approved by regulatory agencies. “This is going to be what we spend the next 10 years figuring out: how to reprogram cells to be young again without taking it too far so they become tumors.”
Both Sinclair and Kaeberlein say they wish Belmonte’s lab had shown that a normal mouse could live longer after the gene tinkering—instead of just reversing an aging-related illness.
Belmonte, like some other anti-aging researchers, says his initial goal is to increase the “health span”—the number of years that someone remains healthy. Extending life span, the number of years someone remains alive, will likely take longer to achieve. Most major killers, including heart disease, cancer and Alzheimer’s, are diseases of aging that become far more common past middle age. “This is not just a matter of how many years we can live but how well we can live the rest of our life,” Ocampo says.
Belmonte says his team is also trying to determine if aging is a process that occurs simultaneously throughout the body. Or, as he puts it, “Is there some tissue that regulates aging—and when that goes bad, the entire organism goes bad?” He says they currently think the brain’s hypothalamus—known as the seat of control for hormones, body temperature, mood, hunger and circadian rhythms—may also act as a regulator of aging.
Other approaches that have been discovered to have anti-aging benefits in animals include calorie restriction, the drug rapamycin and parabiosis—the practice of giving old mice a blood supply from younger ones. The fact that these diverse strategies all seem to work suggests there may be more than one way to age, and that multiple complementary therapies may be needed to significantly extend longevity, Kaeberlein says.
Some compounds such as resveratrol, a substance found in red wine that seems to have anti-aging properties in high concentrations, appear to delay epigenetic change and protect against damage from epigenetic deterioration, Sinclair says. These approaches can reverse some aspects of aging, such as muscle degeneration—but aging returns when the treatment stops, he adds. With an approach like the one Belmonte lays out in the new study, theoretically “you could have one treatment and go back 10 or 20 years,” he says. If aging starts to catch up to you again, you simply get another treatment.
“This work is the first glimmer that we could live for centuries,” Sinclair says, adding that he would happily do so himself: “Forty-seven years went by pretty quickly.”
Scars form when the dermis (deep, thick layer of skin) is damaged. The body forms new collagen fibers (a naturally occurring protein in the body) to mend the damage, resulting in a scar. The new scar tissue will have a different texture and quality than the surrounding tissue. Scars form after a wound is completely healed.
There are different kinds of scars. Most scars are flat and pale. However, in cases when the body produces too much collagen, scars can be raised. Raised scars are called hypertrophic scars or keloid scars. Both of these kinds of scars are more common in younger and dark-skinned people.
Some scars can have a sunken or pitted appearance. This kind of scarring occurs when underlying structures supporting the skin (for example, fat or muscle) are lost. Some surgical scars have this appearance, as do some scars from acne.
Scars also can appear as stretched skin. Such scars result when the skin stretches rapidly (for example, as in growth spurts or during pregnancy). In addition, this type of scar can occur when the skin is under tension (near a joint, for example) during the healing process.
How Can Scars Be Treated?
Although scars cannot be completely removed, their appearance can be improved to some extent. Methods for improving the appearance of scars include:
Topical treatments, such as vitamin E, cocoa butter cream, and several commercial skin care products sold over the counter may be somewhat effective in helping to heal scars.
Surgery. Although it will not remove a scar, surgery can be used to alter a scar’s shape or make it less noticeable. Surgery is not recommended in cases of hypertrophic or keloid scarring (raised scars) because there is a risk of recurring scars as well as more severe scarring that results from the treatment.
Steroid injections. A course of steroid injections into a scar may help flatten it. Injections may help to soften the appearance of keloid or hypertrophic scars.
Radiotherapy. Low-dose, superficial radiotherapy is used to prevent recurrence of severe keloid and hypertrophic scarring. This treatment is used only in extreme cases because of potential long-term side effects.
Dermabrasion. This treatment involves the removal of the surface of the skin with special equipment. Dermabrasion is useful to blend in the irregularities of a scar whether it is raised or depressed.
Microdermabrasion is a much less invasive form of dermabrasion but is minimally useful for very superficial scars.
Laser resurfacing. This procedure, similar to dermabrasion, removes the surface layers of the skin using different types of lasers. Newer types of lasers may achieve more subtle results by working on the collagen in the dermis without removing the upper layers of skin. This advancement results in little down time as opposed to traditional laser resurfacing and dermabrasion, which requires a longer recovery.
Filler injections. These treatments can be used to raise sunken scars to the level of surrounding skin. The effects of these injections are only temporary, however, and the procedures may need to be regularly repeated. Newer forms of injectable fillers are now on the market and may be an option for some people.
Microneedling. Many small puncture holes are made into the superficial skin to stimulate collagen production and even introduce collagen stimulators or other products to try to reduce the appearance of scars.