ยืดอายุให้ยืนยาวด้วย ‘ทูน่า’

bangkokbiznews140307_001โรคหัวใจและหลอดเลือดเป็นปัญหาสุขภาพที่มีแนวโน้มสูงขึ้นทุกปี จากข้อมูลของสำนักงานหลักประกันสุขภาพแห่งชาติ (สปสช.) ในปี 2556 พบว่า โรคหัวใจเป็นโรคที่มีอัตราการเสียชีวิตติดอันดับ 1 ใน 10 ของโรคที่มีอัตราการตายสูงสุดในประเทศไทย และยังส่งผลให้เกิดความสูญเสียทางเศรษฐกิจถึงปีละประมาณ 50,000 ล้านบาท จากการวิจัยและคำแนะนำของแพทย์เพื่อยืดอายุให้ยืนยาวพร้อมกับลดความเสี่ยงจากโรคหัวใจนั้นสามารถเริ่มต้นง่ายๆ ด้วยการรับประทานปลา โดยเฉพาะปลาทะเลน้ำลึกที่อุดมไปด้วยกรดไขมันโอเมก้า 3 ที่เต็มเปี่ยมด้วยคุณค่าทางโภชนาการและมากประโยชน์ต่อสุขภาพ

กรดไขมันโอเมก้า 3 เป็นกรดไขมันไม่อิ่มตัวที่ร่างกายสร้างเองไม่ได้ จำเป็นต้องได้รับจากอาหาร ซึ่งพบได้มากในปลาทะเลน้ำลึกทั้งในปลาแซลมอน ปลาซาร์ดีน ปลาแมคเคอเรล และปลาทูน่า ที่มีไขมัน โอเมก้า 3 สูงถึง 1 – 4 กรัม ต่อเนื้อปลา 100 กรัม กรดไขมันโอเมก้า 3 ที่สำคัญมี 2 ชนิด ได้แก่ EPA (EICOSAPENTAENOIC ACID) และ DHA (DOCOSAHEXAENOIC ACID) ที่เป็นประโยชน์ต่อผู้สูงอายุ ซึ่งจะช่วยลดความเสี่ยงของการเกิดโรคหลอดเลือดหัวใจได้ เนื่องจากโอเมก้าไปช่วยลดการเกาะตัวของเกล็ดเลือดและการหดตัวของหลอดเลือด จึงส่งผลให้เกิดลิ่มเลือดอุดตันได้ยากขึ้น อีกทั้งยังช่วยลดอัตราเสี่ยงโรคหัวใจล้มเหลว และช่วยลดระดับไขมันไตรกลีเซอไรด์ในเลือดจึงลดความเสี่ยงการเกิดโรคหลอดเลือดได้

ผลการศึกษาวิจัยของนักวิทยาศาสตร์จากคณะสาธารณสุขมหาวิทยาลัยฮาร์วาร์ดในสหรัฐ พบว่าผู้ใหญ่อายุ 65 ปีขึ้นไปที่กินปลาเป็นประจำมีโอเมก้า 3 ในปริมาณสูง ทำให้มีอายุเฉลี่ยยืนยาวมากกว่าผู้ที่ไม่บริโภคกรดไขมันโอเมก้า 3 ถึง 2 ปี ทั้งนี้ พบความเชื่อมโยงว่าผู้ที่มีระดับโอเมก้า 3 ในร่างกายในปริมาณสูงมีความเสี่ยงเสียชีวิตด้วยโรคหัวใจเพียงร้อยละ 35 น้อยกว่าผู้มีระดับความดันโลหิตต่ำ นอกจากนั้นทางสมาคมแพทย์โรคหัวใจอเมริกันยังแนะนำเพิ่มเติมว่าวิธีที่ดีที่สุดในการเพิ่มกรดโอเมก้า 3 ในร่างกาย คือ เพิ่มการรับประทานปลาทะเลสัปดาห์ละ 2-3 ครั้ง เพื่อช่วยลดความเสี่ยงโรคหัวใจและหลอดเลือด

ที่มา : กรุงเทพธุรกิจ 7 มีนาคม 2557

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Credit: better4you.mbooth.com

Credit: better4you.mbooth.com

Ask the Expert: Omega-3 Fatty Acids

The Expert

Dr. Frank Sacks

Professor of Cardiovascular Disease Prevention, Department of Nutrition, Harvard School of Public Health

1. What are omega-3 fatty acids, and why should I make sure to include them in my diet?

Omega-3 fatty acids (also known as n-3 fatty acids) are polyunsaturated fatty acids that are essential nutrients for health. We need omega-3 fatty acids for numerous normal body functions, such as controlling blood clotting and building cell membranes in the brain, and since our bodies cannot make omega-3 fats, we must get them through food. Omega-3 fatty acids are also associated with many health benefits, including protection against heart disease and possibly stroke. New studies are identifying potential benefits for a wide range of conditions including cancer, inflammatory bowel disease, and other autoimmune diseases such as lupus and rheumatoid arthritis.

2. What foods are good sources of omega-3 fatty acids? How much do I need to eat of these foods to get enough omega-3s?

There are two major types of omega-3 fatty acids in our diets: One type is alpha-linolenic acid (ALA), which is found in some vegetable oils, such as soybean, rapeseed (canola), and flaxseed, and in walnuts. ALA is also found in some green vegetables, such as Brussels sprouts, kale, spinach, and salad greens. The other type, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), is found in fatty fish. The body partially converts ALA to EPA and DHA.

We do not know whether vegetable or fish omega-3 fatty acids are equally beneficial, although both seem to be beneficial. Unfortunately, most Americans do not get enough of either type. For good health, you should aim to get at least one rich source of omega-3 fatty acids in your diet every day. This could be through a serving of fatty fish (such as salmon), a tablespoon of canola or soybean oil in salad dressing or in cooking, or a handful of walnuts or ground flaxseed mixed into your morning oatmeal.

3. What are omega-6 fatty acids? Should I be concerned about the ratio of omega-6 fatty acids to omega-3 fatty acids in my diet?

Omega-6 fatty acids (also known as n-6 fatty acids) are also polyunsaturated fatty acids that are essential nutrients, meaning that our bodies cannot make them and we must obtain them from food. They are abundant in the Western diet; common sources include safflower, corn, cottonseed, and soybean oils.

Omega-6 fatty acids lower LDL cholesterol (the “bad” cholesterol) and reduce inflammation, and they are protective against heart disease. So both omega-6 and omega-3 fatty acids are healthy. While there is a theory that omega-3 fatty acids are better for our health than omega-6 fatty acids, this is not supported by the latest evidence. Thus the omega-3 to omega-6 ratio is basically the “good divided by the good,” so it is of no value in evaluating diet quality or predicting disease.

4. Is it better to get omega-3 fatty acids from food or from supplements?

Certainly foods, since the plants and fish that contain omega-3 fats have other good nutrients, such as protein, vitamins and minerals. People who do not eat fish or other foods rich in omega-3 fatty acids should consider taking an omega-3 supplement of 500 mg per day; fish oil is used in supplements, but there are also vegetarian supplements that have ALA. Studies suggest that people who have already had a heart attack may benefit from higher doses of omega-3 supplements (basically, double the 500 mg), so if you do have heart disease, consult your healthcare provider about whether taking a higher dose of omega 3s makes sense for you.

5. I am a vegetarian, so I do not consume any fish. But I get plenty of ALA in my diet, from canola and soybean oil, ground flax seed, and walnuts. How efficiently does the body convert ALA to DHA and EPA? Should I take an algal DHA supplement?

If you are getting adequate ALA in your diet from oils and nuts, I am not sure you really need to take an algal DHA supplement. As I mentioned above, the body partially converts ALA to EPA and DHA; it is not known if ALA has substantial health benefits as is, or whether it must be converted to EPA and DHA to produce most of the benefits. My current interpretation of the science is that ALA is important to nutrition because it is an essential fatty acid, and that at least part of its benefits come from its conversion to EPA and DHA. I don’t advocate that vegans take n-3 supplements if they are getting ALA from vegetable oils, vegetables, walnuts, and other vegetarian sources as described above.

6. Can omega-3 fatty acids be destroyed by high-heat cooking?

Not if the oil is fresh. In fact, even in frying oil that is used for days, you still can find ALA in it.

SOURCE : www.hsph.harvard.edu

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นักวิจัยอเมริกันชี้ว่าเกลือในอาหารมีผลให้เกิดโรคแพ้ภูมิตนเอง

voathai130320_001ทีมนักวิทยาศาสตร์อเมริกันหลายทีมพบว่าเกลือที่ผสมในอาหารมีผลให้เกิดกลุ่มโรคแพ้ภูมิตนเองหรือกลุ่มโรคออโต้อิมมูน เป็นอาการที่เกิดจากระบบภูมิต้านทานของร่างกายไปต่อต้านและทำลายเนื้อเยื่อที่เเข็งแรงในร่างกายและอวัยวะต่างๆ

นักวิทยาศาสตร์สามารถระบุยีนที่มีความแตกต่างจากยีนปกติได้ราวหนึ่งร้อยตัว ที่ปรับเปลี่ยนไปจากเดิมหลังจากสลับโมเลกุลของยีนภายในเซลล์ของสิ่งมีชีวิต โดยเชื่อว่ายีนที่แตกต่างจากยีนปกติเหล่านี้น่าจะมีส่วนก่อให้เกิดกลุ่มโรคแพ้ภูมิตนเอง รวมทั้งโรคปลอกประสาทอักเสบ หรือโรคมัลติเพิล สเคลอโรซีส (Multiple Sclerosis) ที่เรียกสั้นๆว่าเอ็มเอส (MS)

นักวิทยาศาสตร์พบหลักฐานยืนยันว่าการปรับเปลี่ยนลักษณะของยีนเหล่านี้ไม่สืบทอดมาจากพันธุกรรมพ่อแม่แต่น่าจะเกิดจากปัจจุยกระตุ้นจากสภาพแวดล้อมภายนอก ผู้เชี่ยวชาญเชื่อว่าสาเหตุที่กระตุ้นให้เกิดโรคภูมิต้านตนเองอาจมาจากการติดเชื้อ การขาดวิตามินดี การสูบบุหรี่และความอ้วน การวิจัยชิ้นล่าสุดในเรื่องนี้พบว่าเกลือที่ผสมในอาหารรับประทานอาจเป็นปัจจัยที่กระตุ้นให้ยีนเกิดการเปลี่ยนแปลงในเซลล์ทำให้ภูมิต้านทานเกิดความสับสนและหันไปทำลายเนื่อเยื่อที่แข็งแรงแทนที่จะไปทำลายเชื้อโรคและสิ่งแปลกปลอมที่เข้าสู่ร่างกาย

ในรายงานผลการวิจัยอย่างน้อยสองชิ้นที่เพิ่งตีพิมพ์ไปเมื่อเร็วๆนี้ ทีมนักวิทยาศาสตร์ที่มหาวิทยาลัย Harvard Medical School และที่สถาบัน Broad Insitute ในรัฐ Massachusetts อธิบายลักษณะความเป็นไปได้ของการเปลี่ยนแปลงทางโมเลกุลในยีนในหลายลักษณะที่เกิดจากอาการภูมิต้านอันเกิดจากการบริโภคเกลือ

และในผลการศึกษาชิ้นที่สาม ทีมนักวิจัยที่มหาวิทยาลัยเยลเปิดเผยผลการทดลองผลกระทบของเกลือต่อร่างกายหนูทดลอง โดยนักวิจัยแบ่งกลุ่มหนูทดลองเป็นสองกลุ่ม กลุ่มแรกเลี้ยงด้วยอาหารที่มีเกลือผสมอยู่ในปริมาณต่ำ กลุ่มที่สองเลี้ยงด้วยอาหารที่มีเกลือผสมอยู่ในปริมาณสูง แต่หนูทดลองทั้งหมดได้รับการเพาะพันธุ์ให้พัฒนาโรคที่คล้ายกับโรคปลอกประสาทอักเสบหรือเอ็มเอส

คุณเดวิด ฮัฟเฟล่อ หัวหน้าแผนกประสาทวิทยาที่มหาวิทยาลัยเลย กล่าวว่าหนูทดลองที่กินเกลือเข้าไปในปริมาณน้อยกว่ายังเดินได้ดีแต่ควบคุมการทำงานของหางไม่ได้ดีเท่าที่ควร

คุณฮัฟเล่อร์ หัวหน้าทีมวิจัยกล่าวกับผู้สื่อข่าววีโอเอว่าหนูทดลองที่ได้รับเกลือในปริมาณสูงกลายเป็นอัมพาต ไม่สามารถเคลื่อนไหวไปรอบๆกรงได้ เขาคิดว่าผลการทดลองสร้างภาพที่ชัดเจนถึงผลกระทบของเกลือต่อการกำเริบของโรคปลอกประสาทอักเสบในหนูทดลอง

คุณฮัฟเล่อร์กล่าวว่าทีมนักวิจัยของเขาพบหลักฐานความเกี่ยวโยงนี้โดยบังเอิญ ขณะทำการศึกษาชนิดของเชื้อเเบคทีเรียหลายพันธุ์ที่อาศัยอยู่ในลำใส้ของคนอย่างน้อยหนึ่งร้อยตัวอย่าง นักวิจัยพบว่าคนที่บริโภคอาหารฟ้าสฟู้ดมีปริมาณทีเซลล์ที่เเสดงว่ามีอาการอักเสบในกระแสเลือดสูง อาการอักเสบดังกล่าวเป็นสัณญาณว่าระบบภูมิต้านทานเริ่มต้นทำงานแล้ว กลุ่มโรคภูมิต้านตนเองนี้รวมทั้งโรคเอ็มเอส เบาหวานประเภทที่หนึ่ง ลูปุส โรครูมาตอยด์ มีคนป่วยด้วยโรคเหล่านี้เพิ่มมากขึ้นในปัจจุบัน แม้แต่อัตราการเกิดโรคหัวใจ ที่เกิดจากการทำงานผิดพลาดของระบบภูมิต้านทานนี้ก็เิ่พิ่ม ขึ้นอย่างมาก และผลการศึกษาได้เเสดงให้เห็นว่าเกลืออาจจะเป็นปัจจัยทางสิ่งแวดล้อมที่ก่อให้เกิดกลุ่มโรคเหล่านี้ ซึ่งเป็นการค้นพบที่ใหม่ที่ไม่มีใครรู้มาก่อนหน้านี้

Jessica Berman
20.03.2013

ที่มา : www.voathai.com

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foxnews130307_001

Too much salt may trigger autoimmune diseases, studies find

Published March 07, 2013
Reuters

Increased salt consumption may be a key culprit behind rising rates of autoimmune diseases such as multiple sclerosis, researchers reported on Wednesday in a trio of papers looking at the role of a specific class of cells linked with inflammation.

Reporting in the journal Nature, the researchers said high-salt diets increased levels of a type of immune cell linked with autoimmune disease. And mice genetically engineered to develop multiple sclerosis (MS) got much worse when they ate what amounted to a high-salt Western diet compared with mice who had more moderate salt intake.

The findings suggest that salt may play a previously unknown role in triggering autoimmune diseases such as MS or type 1 diabetes in individuals who are already genetically predisposed.

“It’s not bad genes. It’s not bad environment. It’s a bad interaction between genes and the environment,” said Dr. David Hafler, a professor of immunobiology at Yale University in New Haven, Connecticut, and senior author of one of the three papers.

High salt intake is already a known culprit in increasing the risk of heart disease and hypertension. The new study now implicates high-salt diets in increasing rates of autoimmune disease. “It can’t be just salt. We know vitamin D probably plays a small component. We know smoking is a risk factor. This now suggests that salt is also a risk factor,” Hafler said.

“How much? We don’t know,” he added.

Hafler became interested in studying the link between salt and autoimmunity through studies of the gut microbiome – a census of gut microbes and cell function of 100 healthy individuals.

The team noticed that when people in the study visited fast food restaurants more than once a week, they saw a marked increase in levels of destructive inflammatory cells, which the immune system produces to respond to injury or foreign invaders, but which attack healthy tissues in autoimmune diseases.

He shared these findings with colleagues at Harvard Medical School and the Broad Institute of Harvard and the Massachusetts Institute of Technology and others who were working out what factors induce the activity of a type of autoimmune cell known as a T helper 17 or a Th17 cell.

Th17 cells can promote inflammation that is important for defending against pathogens, but they have also been linked to diseases like multiple sclerosis, psoriasis, rheumatoid arthritis, and ankylosing spondylitis. Treatment options for some of these diseases, such as psoriasis, include manipulating T cell function.

“The question we wanted to pursue was: How does this highly pathogenic, pro-inflammatory T cell develop?” said Vijay Kuchroo of the Harvard-affiliated Brigham and Women’s Hospital and a member of the Broad Institute.

“Once we have a more nuanced understanding of the development of the pathogenic Th17 cells, we may be able to pursue ways to regulate them or their function.”

Hafler said Kuchroo’s team worked on tracing how these immune cells were wired, and what triggered their development. They identified a specific gene known as SGK1 that plays an important role in the cells’ development. This gene had not been seen in T cells before, but it has been known to play a role in absorbing salt in the gut and kidneys.

“We put the two together and went after this,” Hafler said.

Researchers at Harvard and Yale and colleagues in Germany led by Dominik Mueller looked to see whether a high-salt diet could induce the destructive immune system response that is the hallmark of autoimmunity.

They found that adding salt to the diet of mice induced the production of Th17 cells and that mice genetically engineered to develop a form of MS had more severe disease than mice fed a normal mouse diet.

Hafler says the findings now need to be studied in people. He has already gotten permission to test the effects of lowering the salt intake in the diets of individuals with multiple sclerosis to see if their symptoms improve.

It likely be years before this link is confirmed, but Hafler says for patients already at risk of autoimmune disease, reducing dietary salt may be a good idea.

“If I had MS, I would think very much about not eating processed foods and really cutting down my salt intake,” he said.

SOURCE: www.foxnews.com

———————————————————————————————-

Salt link to multiple sclerosis unproven

Thu, 07 Mar 2013 13:33:00 EST

News that high-salt diets have been linked to autoimmune conditions has hit the headlines today, with BBC News reporting that “The amount of salt in our diet could be…leading to diseases such as multiple sclerosis.”

However, the BBC’s story is not based on trials of how much salt people eat and whether they go on to develop multiple sclerosis (MS), as you might expect. The story is actually based on studies looking at the impact salt has on immune cells, and how it affects the development of a condition similar to MS in mice.

MS is an autoimmune disease. These are diseases that occur when the immune system malfunctions, creating antibodies that attack the body’s own cells. In MS, the immune system attacks the cells that make up nerve fibres.

This study found that mice fed a high-salt diet produced more immune cells called T-helper 17 (TH17) cells, which are involved in some autoimmune diseases.

These results are food for thought about the role high-salt diets play in the development of autoimmune diseases. But because the study was carried out in animals, it is unclear if similar results would be found in people.

We can’t conclude that a high-salt diet causes MS from the results of this study. However, we do know that a high-salt diet is unhealthy and too much salt can cause high blood pressure.

Where did the story come from?

The study was carried out by researchers from Harvard Medical School, the Massachusetts Institute of Technology and the University of Salzburg, and was funded by the US National Institutes of Health and other research foundations in the US and Austria.

It was published in the peer-reviewed journal Nature.

The BBC report on the research was measured and accurate, emphasising that the findings were from early laboratory studies.

What kind of research was this?

This was a series of laboratory and animal studies investigating possible environmental triggers for autoimmune activity.

Experts suggest that genetics and gender play a key role in autoimmune diseases, but that environmental triggers are also a factor in the development of these disorders. The current research looked at the impact of salt on the production (or overproduction) of a specific type of immune cell, T-helper 17 (TH17) cells, which promote inflammation as part of an immune response.

One experiment moved beyond cells in a laboratory and looked at the effect of a high-salt diet on the development of a condition similar to MS, called experimental autoimmune encephalomyelitis (EAE), in mice.

As laboratory and animal studies, this series of experiments can provide clues about how salt may impact immune cell responses. However, they cannot tell us whether it directly affects the development of autoimmune diseases in people.

What did the research involve?

Several teams of researchers first looked into the molecular mechanisms that produce TH17 cells. This series of experiments suggested that a gene responsible for regulating salt levels in cells is involved in the TH17 cells signalling network (the series of molecular activity that enables communication between cells).

They found that when cells were exposed to increased concentrations of salt, this gene (SGK1) was activated and increased the development of TH17 cells. This finding led to the researchers conducting experiments using mice with EAE.

The researchers took three groups of mice:

  • group 1 lacked the SGK1 gene and was fed a normal diet
  • group 2 lacked the SGK1 gene and was fed a high-salt diet for three weeks
  • group 3 had the SGK1 gene and was fed the same high-salt diet as group 2

The researchers then determined whether the mice developed EAE so they could look at the role played in the disease by the SGK1 gene and salt exposure.

What were the basic results?

The researchers found differences between the groups in the number of TH17 cells produced, as well as the likelihood of the mice developing EAE, and the severity of the condition:

  • group 1 (which lacked the SGK1 gene and was fed a normal diet) had fewer TH17 cells and less severe EAE
  • group 2 (which lacked the SGK1 gene and was fed a high-salt diet) appeared to be protected against the development of EAE
  • group 3 (which had the SGK1 gene and was fed a high-salt diet) had more frequent and severe EAE than mice fed a normal diet, and more TH17 cells than group 2

How did the researchers interpret the results?

The researchers say that this data suggests that high salt intake allows for an increase in TH17 cells in a way that relies on the SGK1 gene activating. They feel this “therefore has the potential to increase the risk of promoting autoimmunity.”

Conclusion

This early stage research suggests that increased salt consumption may play a role in the production of a certain type of immune cell (TH17). The study further suggests that a high-salt diet can increase the rate and severity of an MS-like condition in mice (EAE).

These experiments are an interesting insight into the possible interplay between the genetic and environmental factors involved in autoimmune diseases. However, at this stage what this means for human autoimmune disease is not clear.

This research should certainly not be interpreted as meaning that a high-salt diet causes multiple sclerosis in people (although it can cause high blood pressure).

While the term ‘autoimmune diseases’ may seem to imply a similar set of conditions, there are in fact a variety of different autoimmune conditions. The different factors involved in these conditions is unlikely to be the same across all conditions.

The researchers say that while their results indicate that the gene SGK1 plays a key role in autoimmune responses, “it is likely that other immune cells and pathways are also influenced by increased salt intake,” and that their results “do not exclude additional alternative mechanisms by which an increase in NaCl [salt] affects TH17 cells.”

This means that these experiments outlined a possible way that a single environmental trigger (salt) could interact with a single gene (SGK1), and how this could influence the production of a type of immune cell (TH17 cells) that has been implicated in autoimmune disorders.

Other complex processes are likely to be involved, because many other cells also produce proteins that are involved in autoimmune disorders.

As the researchers themselves say, their results raise “the important issue of whether increased salt in westernised diets and in processed foods contributes to an increased generation of pathogenic [disease causing] TH17 cells and for an unprecedented increase in autoimmune disorders.”

A great deal more research is needed to find out whether, and how, salt consumption impacts on both the development and severity of autoimmune diseases in people. Such research could involve cohort or case control studies to establish whether or not there is a link between dietary salt intake and multiple sclerosis, or other autoimmune diseases.

Randomised controlled trials would be needed to firmly establish the role that salt plays in autoimmune conditions. Commentators point out that “the risks of limiting dietary salt intake are not great, so it is likely that several such trials will be starting soon.”

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Salt linked to immune rebellion in study. BBC News, March 7 2013

Could junk food increase your risk of MS, asthma and eczema? Scientists link salt to autoimmune diseases for first time. Mail Online, March 6 2013

Links To Science

Wu C, Yosef N, Thalhamer T, et al. Induction of pathogenic TH17 cells by inducible salt-sensing kinase SGK1. Nature. Published online March 6 2013

SOURCE :   www.ncbi.nlm.nih.go

ถูกแดดกันโรคข้ออักเสบ อาบมากไปเข้าใกล้มะเร็ง

thairath130211_001แพทย์ผู้เชี่ยวชาญแนะนำว่า คนเราควรหาถิ่นฐานที่อยู่ในที่ซึ่งมีแสงแดดส่อง เพราะมันจะช่วยป้องกันไม่ให้เป็นโรคข้ออักเสบง่าย ๆ

วารสารการแพทย์ “โรคข้ออักเสบแห่งอังกฤษ” แจ้งว่า นักวิจัยของโรงเรียนสาธารณสุขฮาร์วาร์ด ได้ศึกษากับผู้หญิงไม่ต่ำกว่า 2 แสนคน เพื่อหาความเกี่ยวพันของแสงแดดกับโรคข้ออักเสบ เพราะเชื่อว่าวิตามินดีในแสงแดดอาจจะให้คุณ ช่วยปกป้องร่างกายได้ แต่บอกไว้ก่อนว่า ไม่ควรจะไปตากแดดหัวแดงตลอดทั้งวัน เพราะอาจจะล่อแหลมกับการเป็นมะเร็งผิวหนังได้

โรคข้ออักเสบ มักจะเป็นกันมากในหมู่สตรี เกิดจากระบบภูมิคุ้มโรคของตัวเองกลับหันไปทำร้ายข้อต่อ ทำให้เกิดอาการเจ็บปวดอย่างรุนแรง.

ที่มา :ไทยรัฐ 11 กุมภาพันธ์ 2556

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Women regularly exposed to sunlight reduced their risk of developing rheumatoid arthritis by a fifth

Women regularly exposed to sunlight reduced their risk of developing rheumatoid arthritis by a fifth

Soaking up the sun can reduce the risk of rheumatoid arthritis

  • Women regularly exposed to sunlight reduced their risk of developing the condition by a fifth
  • But using sun creams or covering up to avoid the sun could lessen the protective effects

 

By DAILY MAIL REPORTER

PUBLISHED: 00:57 GMT, 5 February 2013

Soaking up the sun may reduce a woman’s risk of rheumatoid arthritis.

New research has shown that those regularly exposed to sunlight reduced their risk of developing the condition by a fifth.

But using sun creams or covering up to avoid the sun could lessen the protective effects.

And in younger women who have heeded the calls to protect themselves from the harmful effects of the sun, the effect of UVB exposure was less evident.

Rheumatoid arthritis is an autoimmune disease that causes inflammation in joints and the main symptoms are joint pain and swelling. The condition is the second most common form of arthritis in the UK.

 

There are an estimated 300,000 sufferers in the UK with women three times more likely to suffer from the disease than men.

The long term study looked at participants in two phases of the US Nurses’ Health Study, the first of which has tracked the health of more than 120,000 nurses since 1976, when they were aged between 30 and 55, until 2008.

The second phase tracked the health of a further 115,500 nurses since 1989, when they were aged between 25 and 42, until 2009.

Rather than simply relying on geography to quantify likely levels of UVB exposure, the researchers used a more sensitive assessment, known as UV-B flux, which is a composite measure of UVB radiation, based on latitude, altitude, and cloud cover.

Exposure was then estimated according to where they lived in the US and ranged from an annual average of 93 in Alaska and Oregon to 196 in Hawaii and Arizona where they get the most sunshine.

Likely estimates of UV exposure at birth and by the age of 15 were also included.

Over the period, 1,314 women developed rheumatoid arthritis.

Among nurses in the first phase, higher cumulative exposure to UVB was associated with a reduced risk of developing the disease.

Those with the highest levels of exposure were a fifth less likely to develop rheumatoid arthritis than those with the least.

This confirms the findings of other studies, showing a link between geography and the risk of rheumatoid arthritis as well as other autoimmune conditions, including type 1 diabetes, inflammatory bowel disease, and multiple sclerosis.

But no such association for UV-B exposure was found among women in the second phase because these women were younger than those in the first study, and so might have been more aware about the potential hazards of acquiring a tan.

The authors added: ‘Differences in sun protective behaviours, for example greater use of sun block in younger generations, may explain the disparate results’.

But they conclude: ‘Our study adds to the growing evidence that exposure to UV-B light is associated with decreased risk of rheumatoid arthritis. The mechanisms are not yet understood, but could be mediated by the cutaneous production of vitamin D and attenuated by use of sunscreen or sun avoidant behaviour.’

The findings are published online in the Annals of the Rheumatic Diseases.

SOURCE: dailymail.co.uk

การทำสมาธิสามารถบรรเทาอาการปวดที่เกี่ยวข้องจากความเครียดเช่นโรค IBS และโรคข้ออักเสบ

The study suggests gaining 'inner peace' can have a very real outward effect

The study suggests gaining ‘inner peace’ can have a very real outward effect

การทำสมาธิสามารถบรรเทาอาการปวดที่เกี่ยวข้องจากความเครียด เช่น โรคลำไส้แปรปรวน IBS และโรคข้ออักเสบ

Meditation can ease pain from stress-related conditions like IBS and arthritis

  • Mindfulness meditation involves ‘being present’ by focusing on the breath and bodily sensations
  • Study compared a group practising mindfulness with another using alternative relaxation methods
  • Only mindfulness reduced inflammation caused by an irritating cream

By CLAIRE BATES

PUBLISHED: 16:01 GMT, 17 January 2013

People who suffer from painful conditions such as rheumatoid arthritis could ease their symptoms using a form of meditation, say researchers.

They added that the treatment, known as mindfulness, could prove a cheaper alternative to prescription medicines.

Mindfulness meditation involves ‘being present’ by focusing on breathing patterns and bodily sensations. This reduces worrying about the past and future and has been shown to be effective at alleviating depression.

The latest study suggested its calming effect could help those with stress-related chronic inflammatory conditions – such as bowel disease and asthma.

It is also a convenient technique as people can do the meditation exercises while sitting down or walking, according to the authors from the University of Wisconsin.

It comes as family doctors in the UK are being told to slash prescriptions of painkillers and sleeping pills amid concerns that patients are becoming addicted.

New guidelines now urge doctors  to consider alternative treatments such as physiotherapy and counselling.

Study leader Melissa Rosenkranz, said some people don’t benefit from regular medicines with many suffering from negative side effects of drugs or failing to respond to standard treatment.

Ms Rosenkranz said: ‘Our study shows that there are specific ways mindfulness (meditation) can be beneficial and that there are specific people who may be more likely to benefit from this approach than other interventions.

‘The mindfulness-based approach to stress reduction may offer a lower-cost alternative or complement standard treatment and it can be practised easily by patients in their own homes, whenever they need.’

The study compared two different methods of reducing stress, one related to meditation and the other involving exercise and musical therapy.

The content of the program was meant to match aspects of the mindfulness instruction in some way. For example, physical exercise was meant to match walking meditation, without the mindfulness component.

‘In this setting, we could see if there were changes that we could detect that were specific to mindfulness,’ Rosenkranz said.

Cream containing heat from chilli peppers was used to inflame the skin of participants in both groups. Although both groups felt calmer after therapy, only mindfulness proved effective at reducing the inflammation.

Ms Rosenkranz added: ‘The study suggests that mindfulness techniques may be more effective in relieving inflammatory symptoms than other activities that promote well-being.

‘This is not a cure-all, but our study does show that – there are specific people who may be more likely to benefit from this approach than other interventions.’

Significant portions of the population do not benefit from available pharmaceutical treatment options. Some of these patients suffer from negative side effects of the drugs, or simply do not respond to the standard-of-care for treatment of the disorder.

More information about mindfulness can be found at http://www.bemindful.co.uk/

SOURCE: dailymail.co.uk

กินลูกเชอร์รี่ตีโรคเกาต์เพลาลงทันตา ยิ่งกินกับยาจะป้องกันได้เกือบหมด

Credit: blueheronhealthnews.com

วารสารวิชาการ “โรคข้ออักเสบและข้อบวม” แจ้งว่า กินผลเชอร์รี่ช่วยสกัดโรคเกาต์ที่ทำให้ปวดบวมตามข้อ จากการมีกรดยูริกมากได้ เมื่อกินติดกัน 2 วัน ถ้าเทียบกับคนที่ไม่ได้กิน ป้องกันได้ถึงร้อยละ 35

โรคเกาต์เป็นโรคสามัญโรคหนึ่ง ทำให้ปวดบวมตามข้อมาก ใน 100 คน จะต้องมีผู้ป่วยสักรายหนึ่ง เป็นกับผู้ชายมากกว่าผู้หญิง 2-3 เท่า

นักวิจัยมหาวิทยาลัยบอสตันของสหรัฐฯได้ศึกษากับคนไข้ 633 คน อายุเฉลี่ย 54 ปี และได้ติดตามทางออนไลน์อยู่ 1 ปี ทดลองให้คนไข้บางส่วนกินลูกเชอร์รี่ 10-12 ลูก หรือน้ำสกัดเชอร์รี่ดู

ผลการศึกษาสรุปได้ว่า คนไข้ที่กินลูกเชอร์รี่ โอกาสที่จะเกิดจะลดน้อยลงไปร้อยละ 37 เมื่อเทียบกับคนที่ไม่ได้กิน แต่จะเห็นผลก็ต่อเมื่อได้กินวันละ 3 หน เป็นเวลาติดกัน 2 วัน ยิ่งกินเชอร์รี่รวมทั้งกินยากันไว้ด้วย จะป้องกันไม่ให้เป็นขึ้นมาได้มากถึงร้อยละ 75

ผู้อำนวยการงานวิจัยโรคข้ออักเสบของอังกฤษกล่าวชื่นชมว่า “เคยคิดว่าต้องมีผลไม้บางอย่างที่กันโรคเกาต์และโรคข้อบวมได้ ผลการศึกษาแสดงว่าลูกเชอร์รี่ต้องมีสารประกอบที่มีฤทธิ์ต่อต้านอนุมูลอิสระอยู่”.

ที่มา: ไทยรัฐ 1 ตุลาคม 2555

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Eating cherries ‘could cut gout’

28 September 2012

Eating cherries can reduce the risk of gout attacks, a study has suggested.

US researchers found patients with gout who ate cherries over a two-day period had a 35% lower risk of attacks compared to those who did not.

The study in Arthritis & Rheumatism said cherries contain anthocyanins, antioxidants which contain anti-inflammatory properties.

UK experts said the research offered “good evidence” of the benefits of eating cherries for people with gout.

Gout is a common type of arthritis that can cause sudden and very severe attacks of pain and swelling in the joints, particularly in the feet.

It is caused by too much uric acid in the bloodstream, which causes urate crystals to start to form in and around the joints and under the skin.

Cherry intake

Gout affects about one in 100 people, with men two to three times more likely to be affected than women.

In this study, researchers from Boston University recruited 633 gout patients with an average age of 54, who were followed online for one year. Most were male.

People were asked to record gout attacks including symptoms, the drugs they used and their diet and drinking patterns in the two days prior to the attack, including whether or not they had eaten cherries or cherry extract intake.

Ten to 12 cherries was counted as one serving.


“Eating cherries, in fact, is not dissimilar to taking ibuprofen on a daily basis”

Prof Alan Silman,Arthritis Research UK

During the period the patients were studied, they had a total of 1,247 gout attacks.

Some 42% of those studied ate cherries or cherry extract.

These patients had a 37% lower risk of gout attacks than those who did not eat the fruit – in any form.

However, the benefit was only seen when eating up to three servings over the two days prior to an attack. Further cherry consumption provided no extra benefit.

But when patients ate cherries or cherry extract and took the common anti-gout drug allopurinol, the risk of attacks was 75% less than if they were doing neither.

Writing in the journal, the team led by Dr Yuqing Zhang, said: “Our findings indicate that consuming cherries or cherry extract lowers the risk of gout attack.”

Prof Alan Silman, medical director of Arthritis Research UK welcomed the research: “It has been thought for some time that some fruits, in particular cherries, may have benefits for diseases such as gout and rheumatoid arthritis which are characterised by chronic inflammation.

“It has been suggested that antioxidant compounds found in cherries may be natural inhibitors of enzymes which are targeted by common anti-inflammatory medications such as ibuprofen.”

Prof Silman added: “This study provides good evidence to suggest that cherry intake, combined with traditional uric-acid reducing drugs, can significantly reduce the risk of painful gout attacks.

“Eating cherries, in fact, is not dissimilar to taking ibuprofen on a daily basis.

“However, we’d like to see additional clinical trials are necessary to further investigate and provide confirmation of this effect.”

SOURCE: bbc.co.uk

Immunologists find a molecule that puts the brakes on inflammation

Christopher Hunter and Aisling O’Hara Hall

(Medical Xpress) September 28, 2012—We couldn’t live without our immune systems, always tuned to detect and eradicate invading pathogens and particles. But sometimes the immune response goes overboard, triggering autoimmune diseases like lupus, asthma or inflammatory bowel disease.

A new study led by University of Pennsylvania researchers has now identified a crucial signaling molecule involved in counterbalancing the immune system attack.

“The immune response is like driving a car,” said Christopher Hunter, professor and chair in the Department of Pathobiology in Penn’s School of Veterinary Medicine. “You hit the accelerator and develop this response that’s required to protect you from a pathogen, but, unless you have a brake to guide the response, then you’ll just careen off the road and die because you can’t control the speed of the response.”

The research to characterize this immune system “brake” was led by Hunter and Aisling O’Hara Hall, a doctoral candidate in the Immunology Graduate Group. Additional Penn collaborators included scientists from the Penn Genome Frontiers Institute’s Department of Biology and the Perelman School of Medicine’s Department of Medicine.Researchers from Merck Research Laboratories, the National Institute of Allergy and Infectious Disease, Harvard Medical School and Janssen Research and Development also contributed to the work, which was published in the journal Immunity.

“Healthy people have these cells—you have them, I have them—that are called Tregs,” or regulatory T cells, Hunter said. “If you don’t have them you develop spontaneous inflammation and disease.”

Different forms of regulatory T cells operate as the brakes on various kinds of inflammation, but, until now, scientists hadn’t been certain of how these Tregs became specialized to do their particular jobs.

Hall, Hunter and colleagues decided to follow up on a molecule called IL-27. Scientists used to think IL-27 played a role in causing inflammation, but, in 2005, a team of Penn researchers, including Hunter, found the opposite; it was actually involved in suppressing inflammation. Thus, when mice that lack IL-27 are challenged with the parasite Toxoplasma gondii, they develop overwhelming inflammation. ”

We never worked out how it did that, but it was a paradigm change at the time,” Hunter said.

In the new study, the researchers delved deeper into IL-27’s role. They found that exposing regulatory T cells to IL-27 promoted their ability to suppress a particular type of inflammation. The Penn-led team also demonstrated that they could rescue infected IL-27-deficient mice by giving them a transfusion of regulatory T cells. This finding suggests that IL-27 is required to produce the Treg cells that normally keep inflammatory responses in check during infection.

“Very surprisingly, we were able to show that the Tregs could ameliorate the pathology in this system,” Hall said. “We don’t think this is the only mechanism by which IL-27 limits immune pathology, but it sheds light on one mechanism by which it could be functioning.”

Further experiments showed that Tregs express a different suite of genes in the presence of IL-27 as compared to another molecule that has been implicated in this process, interferon gamma, or IFN-γ. The researchers’ findings indicate that the two molecules have division of labor when it comes to suppressing inflammation: IL-27 seems to be important in helping control inflammation at the site of inflammation, whereas IFN-γ appears more significant in the peripheral tissues.

“At the site of inflammation, where you’re getting your pathology, that’s where IL- 27 is important,” Hall said.

With a new understanding of how IL-27 may cause a class of Tregs to become specialized inflammation fighters, researchers have a new target for ameliorating the unwanted inflammation associated with all kinds of autoimmune conditions.

“Now we have a molecular signature that may be relevant in inflammatory bowel disease, in multiple sclerosis, in colitis and Crohn’s disease, in rheumatoid arthritis, in lupus,” Hunter said.

Next on tap, the team plans to study IL-27 in the context of asthma , lupus and arthritis.

More information: dx.doi.org/10.1016… .2012.06.014 J
Journal reference: Immunity
Provided by University of Pennsylvania

SOURCE: medicalxpress.com

Delivery System for Gene Therapy May Help Treat Arthritis

ScienceDaily (May 15, 2012) — A DNA-covered submicroscopic bead used to deliver genes or drugs directly into cells to treat disease appears to have therapeutic value just by showing up, researchers report.

Within a few hours of injecting empty-handed DNA nanoparticles, Georgia Health Sciences University researchers were surprised to see increased expression of an enzyme that calms the immune response.

In an animal model of rheumatoid arthritis, the enhanced expression of indoleomine 2,3 dioxygenase, or IDO, significantly reduced the hallmark limb joint swelling and inflammation of this debilitating autoimmune disease, researchers report in the study featured on the cover of The Journal of Immunology.

“It’s like pouring water on a fire,” said Dr. Andrew L. Mellor, Director of the GHSU’s Medical College of Georgia Immunotherapy Center and the study’s corresponding author. “The fire is burning down the house, which in this case is the tissue normally required for your joints to work smoothly,” Mellor said of the immune system’s inexplicable attack on bone-cushioning cartilage. “When IDO levels are high, there is more water to control the fire.”

Several delivery systems are used for gene therapy, which is used to treat conditions including cancer, HIV infection and Parkinson’s disease. The new findings suggest the DNA nanoparticle technique has value as well for autoimmune diseases such as arthritis, type 1 diabetes and lupus. “We want to induce IDO because it protects healthy tissue from destruction by the immune system,” Mellor said.

The researchers were exploring IDO’s autoimmune treatment potential by inserting the human IDO gene into DNA nanoparticles. They hoped to enhance IDO expression in their arthritis model when Dr. Lei Huang, Assistant Research Scientist and the paper’s first author, serendipitously found that the DNA nanoparticle itself produced the desired result. Exactly how and why is still being pursued. Early evidence suggests that immune cells called phagocytes, white blood cells that gobble up undesirables like bacteria and dying cells, start making more IDO in response to the DNA nanoparticle’s arrival. “Phagocytes eat it and respond quickly to it and the effect we measure is IDO,” Mellor said.

Dr. Tracy L. McGaha, GHSU immunologist and a co-author on the current study, recently discovered that similar cells also prevented development of systemic lupus erythematosus in mice.

Follow-up studies include documenting all cells that respond by producing more IDO. GHSU researchers already are working with biopolymer experts at the Massachusetts Institute of Technology, the University of California, Berkeley and the Georgia Institute of Technology to identify the optimal polymer.

The polymer used in the study is not biodegradable so the researchers need one that will eventually safely degrade in the body. Ideally, they’d also like it to target specific cells, such as those near inflamed joints, to minimize any potential ill effects.

“It’s like a bead and you wrap the DNA around it,” Mellor said of the polymer. While the DNA does not have to carry anything to get the desired response in this case, DNA itself is essential to make cells express IDO. To ensure that IDO expression was responsible for the improvements, they also performed experiments in mice given an IDO inhibitor in their drinking water and in mice genetically altered to not express IDO. “Without access to the IDO pathway, the therapy no longer works,” Mellor said.

Drs. Andrew Mellor and David Munn reported in 1998 in the journal Science that the fetus expresses IDO to help avoid rejection by the mother’s immune system. Subsequent studies have shown tumors also use IDO for protection and clinical trials are studying the tumor-fighting potential of an IDO inhibitor. On the flip side, there is evidence that increasing IDO expression can protect transplanted organs and counter autoimmune disease.

Mellor is the Bradley-Turner and Georgia Research Alliance Eminent Scholar in Molecular Immunogenetics at MCG. The research was funded by the Carlos and Marguerite Mason Trust and the National Institutes of Health and a patent is pending on the findings.

Story Source:

The above story is reprinted from materials provided byGeorgia Health Sciences University. The original article was written by Toni Baker.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.


Journal Reference:

  1. L. Huang, H. P. Lemos, L. Li, M. Li, P. R. Chandler, B. Baban, T. L. McGaha, B. Ravishankar, J. R. Lee, D. H. Munn, A. L. Mellor. Engineering DNA Nanoparticles as Immunomodulatory Reagents that Activate Regulatory T CellsThe Journal of Immunology, 2012; 188 (10): 4913 DOI: 10.4049/jimmunol.1103668
Drs. Andrew L. Mellor (left) and Lei Huang at Georgia Health Sciences University have shown a system called DNA nanoparticles, used to deliver genes or drugs directly into cells to treat a variety of diseases, may help arthritis without delivering anything. (Credit: Image courtesy of Georgia Health Sciences University)

Data from: sciencedaily.com

‘Mindfulness’ exercises help curb stress and fatigue associated with arthritis

การฝึก “เจริญสติ” ช่วยลดความเครียดและความเหนื่อยล้าที่เกี่ยวข้องกับโรคข้ออักเสบอักเสบต่าง ๆ  เช่น โรคขออักเสบรูมาตอยด (Rheumatoid Arthritis), โรคข้อสันหลังอักเสบติดยึด (Ankylosing Spondylitis) , โรคขออักเสบสะเก็ดเงิน. (Psoriatic Arthritis)

“Mindfulness” exercises, which focus on experiencing the present moment, no matter how difficult, can help curb the stress and fatigue associated with painful rheumatoid joint disease, indicates a small study published online in the Annals of Rheumatic Diseases.

The authors base their findings on 73 patients between the ages of 20 and 70, all of whom had had painful joint disease, caused by rheumatoid arthritis, ankylosing spondylitis, or psoriatic arthritis for at least a year.
Half of them were randomly allocated to scheduled “mindfulness” exercises, which took place in 10 group sessions over a period of 15 weeks, plus a booster session around six months after the course had completed.

The sessions, which were facilitated by healthcare professionals trained in mindfulness techniques, addressed particular topics, such as recognising individual limitations, and strong emotions, such as anger, joy, and sorrow.
The exercises, which were part of the Vitality Training Programme of VTP, encouraged participants to become aware of, and deliberately concentrate on their feelings, thoughts and bodily experiences, including pain, without judging or trying to avoid them.

Participants were also given creative exercises, such as guided imagery, music and drawing, and shared their experiences with other members of the group.

The rest of the volunteers randomly allocated to the comparison group were given standard care plus a CD containing similar exercises for use at home, as and when they wanted.

Stress levels, coping abilities, and symptom control, including pain and fatigue, were assessed, using validated scores, immediately after all 10 sessions had finished, and again 12 months later.

In total, 67 participants completed all the assessments. These showed no differences in pain levels, disease activity or the ability to talk about feelings.
But there were significant differences in levels of stress and fatigue.
The number of participants with a high stress score of above 23 in the GHQ-20 questionnaire fell from 13 at the start of the study to two, just 12 months after the sessions had finished. Comparable figures in the comparison group were 10 and eight, respectively.

There was, however, a tangible fall in measured levels of fatigue in the intervention group: no such change was evident in the comparison group.
There have been previous attempts to use psychological and educational tactics to help people with arthritis cope better with the distressing aspects of the disease, but they have tended to be short term, say the authors.
The lasting improvements found with the VTP course “indicate that the participants may have incorporated some mindfulness strategies into their daily lives and that these strategies have strengthened their ability to respond to their stressful experience in a more flexible way,” they say.

The authors emphasise that while the treatment of rheumatoid arthritis has improved greatly, it is less effective in those with more established disease, and that ultimately the disease can only be partly controlled, forcing many patients to make very demanding lifestyle changes.

“There is therefore a need for complementary interventions that enhance individuals’ health-promoting resources and help them adjust to their disease,” they conclude.

More information: To be published at http://ard.bmj.com

Data from: medicalxpress.com

 

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