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vitamin pp 50 mg

บทความที่เกี่ยวข้อง vitamin pp 50 mg

เปิดตัว MG5 EV และ MG HS Plug-in ก่อนในอังกฤษ ไทยจะตามมาสิ้นปี

MG Motor ค่ายรถยนต์ที่กำลังมาแรงในขณะนี้ กำลังขยับขยายการผลิตด้วยการเพิ่มโมเดลรถยนต์ไฟฟ้าที่ราคาจับต้องได้

เสียงวิจารณ์โลกโซเชียลไม่ระคาย ทำไม MG ทำยอดขายผงาดผู้นำ

ความสำเร็จของรถอเนกประสงค์ค่าย MG ทั้ง MG ZS (เอ็มจี แซดเอส) และ MG HS (เอ็มจี เอชเอส) แสดงให้เห็นว่าค่ายรถยนต์น้องใหม่สามารถโค่นแบรนด์ยักษ์อันเก่าแก่ลงได้หากเดินถูกทางยอดขายสะสมของรถอเนกประสงค์ขนาดซับคอมแพ็กต์อย่าง

เทียบรถยนต์ไฟฟ้า MG EP หรือว่า ZS EV ได้ส่วนลด 100,000 บาท นำเข้าจีนทั้งคู่ แล้วต่างกันยังไง

2021 MG EP (2021 เอ็มจี อีพี) รถแวกอนเปิดตัวอย่างเป็นทางการด้วยราคา 988,000 บาท ส่วนทางด้าน MG ZS EV

เปิดสเปก 2020 Proton X50 หวังเดินตามความสำเร็จ MG ZS ในประเทศไทย

2020 Proton X50 (โปรตอน เอ็กซ์50) เปิดตัวอย่างเป็นทางการแล้วในประเทศมาเลเซีย พร้อมกับกระแสข่าวว่าคอรถยนต์ชาวไทยจะได้ใช้กันแน่นอนภายในอีก

เผยสเปก 2020 MG Gloster รถพีพีวีบนพื้นฐาน Extender โอกาสทำตลาดเมืองไทยมากน้อยแค่ไหน?

หลังจาก 2020 MG Gloster (เอ็มจี กลอสเตอร์) ได้รับการเผยโฉมรุ่นต้นแบบโปรโตไทพ์ในอินเดียไปตั้งแต่เดือนกุมภาพันธ์ที่ผ่านมา

2021 MG5 ความหวังใหม่ MG ไทย คาดเปิดตัวปลายปีนี้ ด้วยราคาไม่เกิน 7 แสน

ว่า MG5 (เอ็มจี5) ใหม่อาจจะเข้ามาในไทย หรือที่ฮือฮากันใน Facebook ที่มีการปล่อยภาพโทรศัพท์พร้อมตรา MG

ใครจะซื้อควรรอก่อนไหม? 2021 MG ZS EV โฉมใหม่จะมีระยะทางขับขี่ด้วยไฟฟ้าไกลขึ้น

2020 MG ZS EV ในเมืองไทย2021 MG ZS EV (2021 เอ็มจี แซดเอส อีวี) รถพลังงานไฟฟ้าโฉมใหม่จ่อเปิดตัวในประเทศไทย

แบบนี้ถล่มตลาด 2021 MG Marvel R รถเอสยูวีไฟฟ้ารุ่นใหม่ ขับขี่ได้ไกล ภายในสวยล้ำ

2021 MG Marvel R (2021 เอ็มจี มาร์เวล อาร์) รถเอสยูวีไฟฟ้ารุ่นใหม่เตรียมเปิดตัวออกสู่ตลาดยุโรปเป็นแห่งแรก

รู้ข้อดีข้อเสีย MG V80 ก่อนเป็นเจ้าของ

MG V801.ภายใน MG V80 กว้างขวางจุดเด่น MG V80 ก็คือด้านความกว้างขวาง เนื่องจากตัวถังที่ค่อนข้างใหญ่ ถ้าเทียบกับคู่แข่งก็จะเห็นว่าความกว้างความยาวความสูงล้วนแต่มากกว่าแทบทุกจุด2

Review: MG Extender กระบะยักษ์พันธุ์แกร่ง

MG Extender 2.0 Giant Cab D 6MT ราคา 619,000 บาท- MG Extender 2.0 Giant Cab GRAND D 6MT ราคา 659,000

ดูเพิ่มเติม

2021 MG EP ไมเนอร์เชนจ์ใหม่ ใช้มอเตอร์เร็วฟ้าแล่บ 184 แรงม้า ชมภาพและราคาจริงจากจีน

2021 MG EP (เอ็มจี อีพี) เปิดตัวโฉมไมเนอร์เชนจ์ในประเทศจีน ขายแล้วในชื่อ Roewe ei5 เปลี่ยนหน้าตาครั้งใหญ่

อ่านก่อนซื้อ! MG EXTENDER มีข้อดีกับข้อเสียอย่างไร

และต้องบอกเลยว่า MG กล้าหาญชาญชัยมากที่นำรถกระบะ MG EXTENDER (เอ็มจี เอกซ์เทนเดอร์) เข้ามาขายในประเทศไทย

เปิดตัว 2021 New MG EP รถพลังงานไฟฟ้ารุ่นใหม่สุดประหยัด วิ่งกิโลเมตรละ 50 สตางค์

2021 MG EPNew 2021 MG EP (2021 เอ็มจี อีพี) เปิดตัวอย่างเป็นทางการแล้ว มาพร้อมระบบขับเคลื่อนพลังงานไฟฟ้าชาร์จเต็มหนึ่งครั้งวิ่งได้ไกลประมาณ

รู้ข้อดีข้อด้อยก่อนซื้อ MG HS ตัวท็อป

MG HS (เอ็มจี เอชเอส) ถือเป็นรถอเนกประสงค์อีกรุ่นที่ได้รับความนิยมไม่แพ้ MG ZS ของค่ายเอ็มจีเลย ด้วยความโดดเด่นในด้านเทคโนโลยี

ไม่ง้อรัฐ! MG ตัดงบตัวเอง ลุยขยายสถานีประจุไฟ 500 แห่ง เอาใจลูกค้า EV และ PHEV

MG (เอ็มจี) ผู้นำด้านรถยนต์ไฟฟ้าในประเทศไทย ประกาศเดินหน้าแผนงานขยายสถานีประจุไฟฟ้า 500 แห่งทั่วประเทศ

MG คว้ารางวัลแบรนด์รถยนต์คุ้มค่ายอดเยี่ยม – MG ZS EV รับรางวัลรถใหม่คุ้มค่าสูงสุด

MG (เอ็มจี) ได้รับรางวัลแบรนด์รถยนต์ที่ความคุ้มค่ายอดเยี่ยม (Best Value Brand 2020) จากการประกาศผลรางวัล

2021 New MG EP กับค่าตัว 988,000 บาท มีรถพลังงานทางเลือกรุ่นอื่นใดอีกบ้าง?

รถพลังงานไฟฟ้า New 2021 MG EP (2021 เอ็มจี อีพี) มาพร้อมกับราคาค่าตัวที่ 988,000 บาท คำถามคือเงินก้อนประมาณ

2020 MG HS PHEV ปะทะ Honda CR-V คุณจะเลือกชื่อชั้นแบรนด์หรือคุณสมบัติตัวรถ?

2020 MG HS PHEV (เอ็มจี เอชเอส พีเอชอีวี) เปิดตัวอย่างเป็นทางการด้วยราคาที่เรียกเสียงฮือในงานแถลงข่าวที่

ไขข้อสงสัยข้อดีข้อเสียก่อนซื้อ MG HS

หลังจาก MG HS รถสไตล์รถครอบครัวจากแบรนด์จีนเปิดตัวก็ได้รับความสนใจล้นหลาม และก็กลายเป็น Compact SUV ที่มียอดขายดีในกลุ่มได้อย่างรวดเร็วด้วยชื่อ

MG ประกาศขึ้นแท่นผู้นำตลาดเอสยูวีในครึ่งปีแรกของปี 2563

MG (เอ็มจี) แบรนด์รถยนต์น้องใหม่ประเทศไทย ประกาศขึ้นแท่นผู้นำตลาดเอสยูวีในครึ่งแรกของปี 2563 ด้วยยอดจำหน่ายรวม

ไฟเขียว! MG เตรียมเปิดตัวรถสปอร์ตพลังไฟฟ้าปลายปีนี้ รอลุ้นราคาจำหน่าย

รถต้นแบบ MG E-Motionรถสปอร์ตพลังงานไฟฟ้ารุ่นแรกของ MG (เอ็มจี) ยุคใหม่เตรียมเปิดตัวครั้งแรกในโลกภายในช่วงปลายปีนี้

2020 MG ZS ผ่าน 5 ดาวเต็มความปลอดภัย แต่ยังตามหลัง Toyota Corolla Cross

2020 MG ZS (เอ็มจี แซดเอส) รถเอสยูวีโฉมใหม่ได้รับรองมาตรฐานความปลอดภัยระดับ 5 ดาวจาก Asean NCAP แต่คะแนนการทดสอบยังด้อยกว่า

รีวิว 2019 MG HS พิสูจน์ตำแหน่งผู้นำตลาดรถคอมแพ็กต์เอสยูวี มีดีที่ความคุ้มค่า?

เอ็มจี บริษัทรถยนต์ลูกครึ่งอังกฤษ-จีน นำเสนอ 2019 เอ็มจี เอชเอส (2019 MG HS) รถอเนกประสงค์เอสยูวีออกทำตลาดประเทศไทยทั้งหมด

รู้ก่อนซื้อ MG V80 รถตู้ 11 ที่นั่ง ราคาไม่ถึงล้าน!

MG V80 (เอ็มจี วี80)เป็นรถตู้โดยสารขนาด 11 ที่นั่งของค่าย MG ที่มีจุดเด่นในการวางเครื่องยนต์ด้านหน้า

MG ZS EV รถพลังงานไฟฟ้าล้วน ที่ตอบโจทย์ทุกไลฟ์สไตล์คนเมือง ราคา 1.19 ล้านบาท

MG ZS EV รถอเนกประสงค์พลังงานไฟฟ้าล้วน ที่ออกแบบเพื่อตอบโจทย์การใช้ชีวิตสไตล์คนเมือง ด้วยความจุแบตเตอรี่

MG เผยคอนเซปท์สปอร์ตไฟฟ้าคันใหม่ MG Cyberster วิ่งไกล 800 กม.

MG (เอ็มจี) ลอนดอน ได้ทำการเปิดคอนเซปท์รถสปอร์ตคันใหม่ในนาม MG Cyberster แบบเปิดประทุน ก่อนที่จะมีรายละเอียดออกมาในงาน

7 เรื่องควรรู้ก่อนซื้อ MG HS 2019

ตอนนี้ตลาดรถอเนกประสงค์อย่าง SUV กำลังมาแรงมากขึ้นเรื่อยๆ และค่าย MG (เอ็มจี) ก็ถือเป็นอีกค่ายหนึ่งที่คนให้ความสนใจ

MG เล็งไทยเป็นฮับอาเซียน ผลิต MG ZS พวงมาลัยซ้าย ส่งออกอินโดนีเซีย-เวียดนาม-มาเลเซีย

MG (เอ็มจี) ประเทศไทย ขยับสายการผลิตเพิ่มการผลิต MG ZS (เอ็มจี แซดเอส) พวงมาลัยซ้าย เพื่อเริ่มการส่งออกไปยังตลาดเวียดนามภายในสิ้นปีนี้

ลองของแท่นชาร์จไฟ 50 kW ที่ EGAT ประทับใจทั้งความไว สถานที่และเจ้าหน้าที่ที่ดีเยี่ยม

แล้วตู้ชาร์จไฟในศูนย์การเรียนรู้แห่งนี้ถือว่าหลากหลายและมีความพร้อมมากที่สุดแห่งหนึ่ง โดยมีตู้ที่ผมเห็น 3 ตู้ ปล่อยกระแสไฟ 90, 50

โวลั่น Proton X50 ปลอดภัยกว่า BMW X1 เทียบชั้น Tesla (ในราคาเท่า MG?)

2020 Proton X50 (โปรตอน เอ็กซ์50) กำลังถูกพูดถึงอย่างมากในมาเลเซีย ด้วยความเพียบพร้อมทั้งคุณภาพตัวรถ

รูปภาพที่เกี่ยวข้อง vitamin pp 50 mg

วิดีโอรถยนต์ที่เกี่ยวข้อง vitamin pp 50 mg

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รีวิวโพสต์ vitamin pp 50 mg

Vitamin C 500 mgVitamin B1 10 mgVitamin B2 50 mgVitamin B3 60 mgVitamin B12 30 mgFolic 200 mg อย. 10-1-01949-1-0313#มัลติซีพลัส #วิตามินซี #วิตามินรวม1 ซอง 50 บาท #ต้องลอง

Vitamin B complex 2 ml 10 ampoules: 10 mg (5 mg/ml) thiamine hydrochloride (vit. B1), riboflavine sodium phosphate - 2 mg (1 mg/ml) riboflavin (vit. B2), 10 mg (5 mg/ml) pyridoxine hydrochloride (vit. B6), 100 mg (50 mg/ml) nicotinamide (vit. PP).

ของแท้ เราพรีมาจาก Official shop Korea Eundun Vitamin C 1000 mg. วิตามินซีอึนดัน 1 แพ็ค มี 60 เม็ด 150฿วันหมดอายุ 12/12/2022ค่าส่ง ลทบ 30/Ems 50 ชิ้นต่อไป +10 Kerry 40*มีอยู่ 9 แพ็คนะคะ #วิตามินซีอึนดัน #วิตามินซีเกาหลี

Vitamin B6 diberikan dengan dosis 25 mg perhari atau 50 mg selang sehari atau 2 hari sekali untuk mengurangi efek samping INH.Pemantauan pengobatan PP INH ini dilakukan selama dan setelah pemberian PP-INH dengan tujuan untuk memastikan kepatuhan ODHA #MateriByOBS

dan ODHA yang memiliki kontak erat dengan pasien TB harus diobati sebagai infeksi TB laten dengan INH 300mg/hari selama 6 bulan. Isoniazid dosis 300 mg untuk PP INH diberikan setiap hari selama 6 bulan (total 180 dosis). #MateriByOBS

รีวิว Q&A vitamin pp 50 mg

Does oats cause diabetes? What is the truth in words of some people who say oats cause diabetes and are not healthy?

No, The effects of oats are listed below. Oats - an annual crop plant from the family of grasses, with a powerful root. Useful properties of oats are known a long time and, therefore, it is quite popular in folk medicine. Most of the oats grown in the countries of the Old World. It includes about 40 different species. The benefits of oatmeal are undeniable for people who are overweight or who have problems with the gastrointestinal tract. Oatmeal contains a lot of minerals and vitamins. Calorie oats are 300 kcal, while it is a food rich in carbohydrates (which contain about 60%). The composition of oat includes vitamins A, E, PP, H, a group B. In addition, it is rich in the elements of the periodic table such as silicon (1000mg) and potassium (421 mg), phosphorus (361mg), magnesium (135mg), choline ( 110mg), chlorine (119mg), calcium (117 mg). Substances such as sulfur, tungsten, boron, iodine, manganese, copper, molybdenum, fluorine, tin, selenium, titanium, zinc, zirconium and strontium are also part of oats. Because most of all the vitamins in it is vitamin B3, also known as pantothenic acid. This acid affects the body's metabolism and digestion. Lack of this vitamin causes weakness, fatigue, numbness in the toes. This vitamin is sensitive to heat and when its temperature rises loss could be 50%. Useful properties of oats are quite extensive. For example, it is rich in silicon. Silicon plays an important role in the body's livelihood or as a structural element of the connective tissue. Deficiency of silicon can cause the development of atherosclerosis. Compounds of silicon powerful catalysts of redox processes. With age, the concentration decreases, which sometimes results in time for the violation of bone strength. In addition, silicon improves the immune system, strengthens the vascular wall, and supports the health of the musculoskeletal system. Apart from silicon contained in oats also potassium. It regulates the acid-base balance in the blood. In addition, potassium improves heart function, is involved in the transmission of nerve impulses, has beneficial effects on the kidneys and skin. It is often used for edema and poisoning, as it can increase urine output. It helps and pressure. The phosphorus content, which is part of oats, a great benefit. Phosphorus is part of the protein, its compounds are involved in the exchange of energy with transformations which involve mental and muscular activity. Also, phosphorus affects the activity of the kidneys and the heart. Magnesium is also a part of the oat elderly important as it enhances the work of the heart muscle, it regulates the nervous tissue is involved in the metabolism of carbohydrates. Often oat products used in dietary nutrition. They do not irritate the stomach, displays all the toxins and harmful substances from the body, reduce cholesterol, it is a very beneficial effect on digestion. Oats improves the pancreas and liver and promotes the absorption of fat in the intestine. Oat broths and accept anemia. It can be used also as anti-TB drugs, and after myocardial infarction is recommended to drink a decoction of oats, it strengthens the heart muscle. Doctors recommend it and at the initial stage of hypertension. Even for colds oats comes in because of the ability to increase immunity. Cases where it is necessary to use, it is possible to list almost indefinitely: it's diabetes, and allergies and hives, and asthma, and insomnia, and diathesis, and thrombophlebitis, and nephrolithiasis, and skin diseases. With such huge benefits to the human body, what is the harm of oatmeal? Harm porridge obvious to people suffering from celiac disease (intolerance to grains). Upotreblenie cereals in unlimited quantities and will cause that harm oatmeal exceeds a positive impact on the human body. Porridge contained in phytic acid accumulating in its body in a large amount leads to leaching of calcium from bone. Fast Food harm oatmeal compared to oat flakes is that after special processing vitamins it becomes much less. In addition, oatmeal loses thus its ability to regulate metabolism and provide the human body with energy in the right quantity. Before use, it should be noted that oats are contraindicated in patients with renal and heart failure, as well as if you are hypersensitive. In case of overdose, it can cause headaches. Benefits and harms of oatmeal fully investigated by physicians. This is one of the few products virtually no contraindications. Eat oatmeal every day if the main do not overeat.

Is it safe to eat jaggery during pregnancy?

Before I give a straight answer to this question, let me answer the fundamental question - Is jaggery healthy or not? Jaggery has a host of goodness and benefits to it. Jaggery is the best bet for a natural sugar substitute. It is raw and concentrated sugarcane juice; it contains sugars, iron and other minerals in traces. Since it is a non-processed form of sugar, it is considered healthy and safe for pregnancy. Here is the breakdown of the nutritional composition of jaggery: According to the Journal of Food Processing and Technology per 100g of jaggery contains Calcium - 40 to 100mg Potassium - 1056mg Magnesium - 70 to 90mg Sodium - 19 to 30mg Iron - 10 to 13mg Phosphorus - 20 to 90mg Zinc - 0.2 to 0.4mg Manganese - 0.2 to 0.5mg Copper - 0.1 to 0.9mg and Chloride - 5.3mg Protein - 280mg Traces of vitamins - Vitamin A-3.8 mg, Vitamin B1-0.01 mg, Vitamin B2- 0.06 mg, Vitamin B5-0.01 mg, Vitamin B6-0.01 mg, Vitamin C-7.00 mg, Vitamin D2-6.50 mg, Vitamin E-111.30 mg, Vitamin PP-7.00 mg The above numbers are pretty impressive and a reason why jaggery is a “Superfood” sweetener. Consuming jaggery can help in many ways, and during pregnancy, it can help in: Maintaining a healthy blood pressure: Jaggery can reduce the body's sodium levels and help maintain a healthy blood pressure reading. High blood pressure during pregnancy is dangerous as it can lead to preeclampsia and affect the developing baby. Jaggery also provides the much needed TLC to the kidneys and your heart, in turn keeping them healthy. Control oedema: Water retention is one severe and irritating pregnancy discomfort of pregnancy. Jaggery can help in countering the problem. A rich source of potassium, it helps to curb water retention. Prevent anaemia: Jaggery is also a rich source of iron. It can help to up your iron intake during pregnancy. Did you know that around 50% of pregnant women are anaemic in India as per the NFHS-4 (National Family Health Survey) data published in 2016? Consuming jaggery can improve the red blood cell count, thereby preventing the risk of anaemia. It also acts as an excellent source of energy. Purification of blood: Jaggery helps to flush out toxins from the body as it also acts as a detox. Lower joint pains: The traces of vitamins and minerals found in jaggery also helps to keep your bones healthy and act as pain relievers from aching joints. It also reduces joint stiffness in pregnant women. Should you make jaggery a staple in your diet during pregnancy? The thumb rule is moderation. Having things in moderation will maximise the benefits of any food ingredient. So, don't go overboard, there can be consequences. Remember, even though it is a raw form of sugar, it is still sugar. If it is taken in excess, it can cause trouble. It is especially not recommended for expectant mothers who have gestational diabetes mellitus (GDM). Mothers with GDM are advised to have foods with a low glycemic index and jaggery’s glycemic index is very high. So, stay away from any sugar - raw or unprocessed if you have GDM. The takeaway message: Have jaggery in moderation. Don't eat blocks of jaggery directly, as it could affect your blood sugar levels. Instead, add jaggery to your: Cup of tea Include it in desserts and kheer Mix with peanuts and dates to make energy balls Add it to curries or dals to enhance the taste Don’t go overboard with it: Just consuming one or half a block of jaggery per day should be enough. I hope you enjoyed reading this answer. If you found this information helpful, please don’t forget to upvote & follow.

Why does Crest market six different types of toothpaste, aren't they all really the same thing?

No they are all the same the most important thing is that they contain fluoride Joakim Fluoride This article is about the fluoride ion. For a review of fluorine compounds, see Compounds of fluorine. For the fluoride additive used in toothpaste, see Fluoride therapy. Not to be confused with Floride or Fluorite. Fluoride F- crop.svg Fluoride ion.svg Names IUPAC name Fluoride[1] Identifiers CAS Number 16984-48-8 ☑ 3D model (JSmol) Interactive image ChEBI CHEBI:17051 ChEMBL ChEMBL1362 ☑ ChemSpider 26214 ☑ Gmelin Reference 14905 KEGG C00742 ☑ MeSH Fluoride PubChem CID 28179 CompTox Dashboard (EPA) DTXSID9049617 Edit this at Wikidata InChI[show] SMILES[show] Properties Chemical formula F− Molar mass 18.998403163 g·mol−1 Conjugate acid Hydrogen fluoride Thermochemistry Std molar entropy (So298) 145.58 J/mol K (gaseous)[2] Std enthalpy of formation (ΔfH⦵298) −333 kJ mol−1 Related compounds Other anions Chloride Bromide Iodide Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa). Infobox references Fluoride (/ˈflʊəraɪd, ˈflɔːr-/)[3] is an inorganic, monatomic anion with the chemical formula F− (also written [F]− ), whose salts are typically white or colorless. Fluoride salts typically have distinctive bitter tastes, and are odorless. Its salts and minerals are important chemical reagents and industrial chemicals, mainly used in the production of hydrogen fluoride for fluorocarbons. Fluoride is classified as a weak base since it only partially associates in solution, but concentrated fluoride is corrosive and can attack the skin. Fluoride is the simplest fluorine anion. In terms of charge and size, the fluoride ion resembles the hydroxide ion. Fluoride ions occur on earth in several minerals, particularly fluorite, but are present only in trace quantities in bodies of water in nature. Contents 1 Nomenclature 2 Occurrence 3 Chemical properties 3.1 Basicity 3.2 Structure of fluoride salts 3.3 Inorganic chemistry 3.4 Naked fluoride 3.5 Biochemistry 4 Applications 4.1 Cavity prevention 4.2 Biochemical reagent 4.3 Fluoride-ion Battery 5 Dietary recommendations 6 Estimated daily intake 7 Safety 7.1 Ingestion 7.1.1 Hazard maps for fluoride in groundwater 7.2 Topical 8 Other derivatives 9 See also 10 References 11 External links Nomenclature Fluorides include compounds that contain both ionic fluoride and those where fluoride does not dissociate. The nomenclature does not distinguish these situations. For example, sulfur hexafluoride and carbon tetrafluoride are not sources of fluoride ions under ordinary conditions. The systematic name fluoride, the valid IUPAC name, is determined according to the additive nomenclature. However, the name fluoride is also used in compositional IUPAC nomenclature which does not take the nature of bonding involved into account. Fluoride is also used non-systematically, to describe compounds which release fluoride upon dissolving. Hydrogen fluoride is itself an example of a non-systematic name of this nature. However, it is also a trivial name, and the preferred IUPAC name for fluorane.[citation needed] Occurrence Fluorite crystals Fluorine is estimated to be the 13th-most abundant element in the earth's crust and is widely dispersed in nature, almost entirely in the form of fluorides. Many minerals are known, but of paramount commercial importance is fluorite (CaF2), which is roughly 49% fluoride by mass.[4] The soft, colorful mineral is found worldwide. In water Fluoride is naturally present at low concentration in most fresh and saltwater sources. In addition, it can be found in rain water that washes fluoride-containing particulates from the atmosphere.[5] Seawater fluoride levels are usually in the range of 0.86 to 1.4 mg/L, and average 1.1 mg/L[6] (milligrams per litre). For comparison, chloride concentration in seawater is about 19 g/L. The low concentration of fluoride reflects the insolubility of the alkaline earth fluorides, e.g., CaF2. Concentrations in fresh water vary more significantly. Surface water such as rivers or lakes generally contains between 0.01–0.3 ppm.[7] Groundwater (well water) concentrations vary even more, depending on the presence of local fluoride-containing minerals. For example, natural levels of under 0.05 mg/L have been detected in parts of Canada but up to 8 mg/L in parts of China; in general levels rarely exceed 10 mg/litre[8] In some locations, such as Tanzania, the drinking water contains dangerously high levels of fluoride, leading to serious health problems. Worldwide, 50 million people receive water from water supplies that naturally have close to the "optimal level".[9] In other locations the level of fluoride is very low, sometimes leading to fluoridation of public water supplies to bring the level to around 0.7–1.2 ppm. Fluoride can be present in rain, with its concentration increasing significantly upon exposure to volcanic activity or atmospheric pollution derived from burning fossil fuels or other sorts of industry.[10][11] In plants All vegetation contains some fluoride, which is absorbed from soil and water.[8] Some plants concentrate fluoride from their environment more than others. All tea leaves contain fluoride; however, mature leaves contain as much as 10 to 20 times the fluoride levels of young leaves from the same plant.[12][13][14] Chemical properties Basicity Fluoride can act as a base. It can combine with a proton ( H+): F− +  H+ → HF (1) This neutralization reaction forms hydrogen fluoride (HF), the conjugate acid of fluoride. In aqueous solution, fluoride has a pKb value of 10.8. It is therefore a weak base, and tends to remain as the fluoride ion rather than generating a substantial amount of hydrogen fluoride. That is, the following equilibrium favours the left-hand side in water: F− + H 2O {\displaystyle {\ce {<<=>}}} {\displaystyle {\ce {<<=>}}} HF + HO− (2) However, upon prolonged contact with moisture, soluble fluoride salts will decompose to their respective hydroxides or oxides, as the hydrogen fluoride escapes. Fluoride is distinct in this regard among the halides. The identity of the solvent can have a dramatic effect on the equilibrium shifting it to the right-hand side, greatly increasing the rate of decomposition. Structure of fluoride salts Salts containing fluoride are numerous and adopt myriad structures. Typically the fluoride anion is surrounded by four or six cations, as is typical for other halides. Sodium fluoride and sodium chloride adopt the same structure. For compounds containing more than one fluoride per cation, the structures often deviate from those of the chlorides, as illustrated by the main fluoride mineral fluorite (CaF2) where the Ca2+ ions are surrounded by eight F− centers. In CaCl2, each Ca2+ ion is surrounded by six Cl− centers. The difluorides of the transition metals often adopt the rutile structure whereas the dichlorides have cadmium chloride structures. Inorganic chemistry Upon treatment with a standard acid, fluoride salts convert to hydrogen fluoride and metal salts. With strong acids, it can be doubly protonated to give H 2F+ . Oxidation of fluoride gives fluorine. Solutions of inorganic fluorides in water contain F− and bifluoride HF− 2.[15] Few inorganic fluorides are soluble in water without undergoing significant hydrolysis. In terms of its reactivity, fluoride differs significantly from chloride and other halides, and is more strongly solvated in protic solvents due to its smaller radius/charge ratio. Its closest chemical relative is hydroxide, since both have similar geometries. Naked fluoride When relatively unsolvated, for example in nonprotic solvents, fluoride anions are called "naked". Naked fluoride is a very strong Lewis base,[16] it is easily reacted with Lewis acids, forming strong adducts. Naked fluoride salts have been prepared as tetramethylammonium fluoride, tetramethylphosphonium fluoride, and tetrabutylammonium fluoride.[17] Many so-called naked fluoride sources are in fact bifluoride salts. In late 2016 a new type of imidazolium fluoride was synthesized that is thermodynamically stable example of a "naked" fluoride source in acetonitrile[18] and its reactivity shows significant potential.[19][20] Biochemistry At physiological pHs, hydrogen fluoride is usually fully ionised to fluoride. In biochemistry, fluoride and hydrogen fluoride are equivalent. Fluorine, in the form of fluoride, is considered to be a micronutrient for human health, necessary to prevent dental cavities, and to promote healthy bone growth.[21] The tea plant (Camellia sinensis L.) is a known accumulator of fluorine compounds, released upon forming infusions such as the common beverage. The fluorine compounds decompose into products including fluoride ions. Fluoride is the most bioavailable form of fluorine, and as such, tea is potentially a vehicle for fluoride dosing.[22] Approximately, 50% of absorbed fluoride is excreted renally with a twenty-four-hour period. The remainder can be retained in the oral cavity, and lower digestive tract. Fasting dramatically increases the rate of fluoride absorption to near 100%, from a 60% to 80% when taken with food.[22] Per a 2013 study, it was found that consumption of one litre of tea a day, can potentially supply the daily recommended intake of 4 mg per day. Some lower quality brands can supply up to a 120% of this amount. Fasting can increase this to 150%. The study indicates that tea drinking communities are at an increased risk of dental and skeletal fluorosis, in the case where water fluoridation is in effect.[22] Fluoride ion in low doses in the mouth reduces tooth decay.[23] For this reason, it is used in toothpaste and water fluoridation. At much higher doses and frequent exposure, fluoride causes health complications and can be toxic. Applications See also: Fluorochemical industry, Biological aspects of fluorine, and Fluorine Fluoride salts and hydrofluoric acid are the main fluorides of industrial value. Compounds with C-F bonds fall into the realm of organofluorine chemistry. The main uses of fluoride, in terms of volume, are in the production of cryolite, Na3AlF6. It is used in aluminium smelting. Formerly, it was mined, but now it is derived from hydrogen fluoride. Fluorite is used on a large scale to separate slag in steel-making. Mined fluorite (CaF2) is a commodity chemical used in steel-making. Hydrofluoric acid and its anhydrous form, hydrogen fluoride, is also used in the production of fluorocarbons. Hydrofluoric acid has a variety of specialized applications, including its ability to dissolve glass.[4] Cavity prevention Main articles: Fluoride therapy and Water fluoridation Fluoride is sold in tablets for cavity prevention. Fluoride-containing compounds, such as sodium fluoride or sodium monofluorophosphate are used in topical and systemic fluoride therapy for preventing tooth decay. They are used for water fluoridation and in many products associated with oral hygiene.[24] Originally, sodium fluoride was used to fluoridate water; hexafluorosilicic acid (H2SiF6) and its salt sodium hexafluorosilicate (Na2SiF6) are more commonly used additives, especially in the United States. The fluoridation of water is known to prevent tooth decay[25][26] and is considered by the U.S. Centers for Disease Control and Prevention as "one of 10 great public health achievements of the 20th century".[27][28] In some countries where large, centralized water systems are uncommon, fluoride is delivered to the populace by fluoridating table salt. For the method of action for cavity prevention, see Fluoride therapy. Fluoridation of water has its critics (see Water fluoridation controversy).[29] Fluoridated toothpaste is in common use, but is only effective at concentrations above 1,000 ppm, as is common in North America and Europe.[30] Biochemical reagent Fluoride salts are commonly used in biological assay processing to inhibit the activity of phosphatases, such as serine/threonine phosphatases.[31] Fluoride mimics the nucleophilic hydroxide ion in these enzymes' active sites.[32] Beryllium fluoride and aluminium fluoride are also used as phosphatase inhibitors, since these compounds are structural mimics of the phosphate group and can act as analogues of the transition state of the reaction.[33][34] Fluoride-ion Battery A large team of researchers, including Simon C. Jones of California Institute of Technology and Christopher J. Brooks of the Honda Research Institute, have come up with a liquid electrolyte that shuttles fluoride ions to and fro and demonstrated its use in a room-temperature, rechargeable FIB (Science 2018, DOI: 10.1126/science.aat7070).[35][36] Dietary recommendations The U.S. Institute of Medicine (IOM) updated Estimated Average Requirements (EARs) and Recommended Dietary Allowances (RDAs) for some minerals in 1997. Where there was not sufficient information to establish EARs and RDAs, an estimate designated Adequate Intake (AI) was used instead. AIs are typically matched to actual average consumption, with the assumption that there appears to be a need, and that need is met by what people consume. The current AI for women 19 years and older is 3.0 mg/day (includes pregnancy and lactation). The AI for men is 4.0 mg/day. The AI for children ages 1–18 increases from 0.7 to 3.0 mg/day. The major known risk of fluoride deficiency appears to be an increased risk of bacteria-caused tooth cavities. As for safety, the IOM sets tolerable upper intake levels (ULs) for vitamins and minerals when evidence is sufficient. In the case of fluoride the UL is 10 mg/day. Collectively the EARs, RDAs, AIs and ULs are referred to as Dietary Reference Intakes (DRIs).[37] The European Food Safety Authority (EFSA) refers to the collective set of information as Dietary Reference Values, with Population Reference Intake (PRI) instead of RDA, and Average Requirement instead of EAR. AI and UL defined the same as in United States. For women ages 18 and older the AI is set at 2.9 mg/day (includes pregnancy and lactation). For men the value is 3.4 mg/day. For children ages 1–17 years the AIs increase with age from 0.6 to 3.2 mg/day. These AIs are comparable to the U.S. AIs.[38] The EFSA reviewed safety evidence and set an adult UL at 7.0 mg/day (lower for children).[39] For U.S. food and dietary supplement labeling purposes the amount of a vitamin or mineral in a serving is expressed as a percent of Daily Value (%DV). Although there is information to set Adequate Intake, fluoride does not have a Daily Value and is not required to be shown on food labels.[40] Estimated daily intake Daily intakes of fluoride can vary significantly according to the various sources of exposure. Values ranging from 0.46 to 3.6–5.4 mg/day have been reported in several studies (IPCS, 1984).[21] In areas where water is fluoridated this can be expected to be a significant source of fluoride, however fluoride is also naturally present in virtually all foods and beverages at a wide range of concentrations.[41] The maximum safe daily consumption of fluoride is 10 mg/day for an adult (U.S.) or 7 mg/day (European Union).[37][39] The upper limit of fluoride intake from all sources (fluoridated water, food, beverages, fluoride dental products and dietary fluoride supplements) is set at 0.10 mg/kg/day for infants, toddlers, and children through to 8 years old. For older children and adults, who are no longer at risk for dental fluorosis, the upper limit of fluoride is set at 10 mg/day regardless of weight.[42] Examples of fluoride content Food/Drink Fluoride (mg per 1000g/ppm) Portion Fluoride (mg per portion) Black tea (brewed) 3.73 1 cup, 240 g (8 fl oz) 0.884 Raisins, seedless 2.34 small box, 43 g (1.5 oz) 0.101 Table wine 1.53 Bottle, 750 ml (26.4 fl oz) 1.150 Municipal tap-water, (Fluoridated) 0.81 Recommended daily intake, 3 litres (0.79 US gal) 2.433 Baked potatoes, Russet 0.45 Medium potato, 140 g (0.3 lb) 0.078 Lamb 0.32 Chop, 170 g (6 oz) 0.054 Carrots 0.03 1 large carrot, 72 g (2.5 oz) 0.002 Source: Data taken from United States Department of Agriculture, National Nutrient Database[43] Safety Main article: Fluoride toxicity Ingestion According to the U.S. Department of Agriculture, the Dietary Reference Intakes, which is the "highest level of daily nutrient intake that is likely to pose no risk of adverse health effects" specify 10 mg/day for most people, corresponding to 10 L of fluoridated water with no risk. For infants and young children the values are smaller, ranging from 0.7 mg/d for infants to 2.2 mg/d.[44] Water and food sources of fluoride include community water fluoridation, seafood, tea, and gelatin.[45] Soluble fluoride salts, of which sodium fluoride is the most common, are toxic, and have resulted in both accidental and self-inflicted deaths from acute poisoning.[4] The lethal dose for most adult humans is estimated at 5 to 10 g (which is equivalent to 32 to 64 mg/kg elemental fluoride/kg body weight).[46][47][48] A case of a fatal poisoning of an adult with 4 grams of sodium fluoride is documented,[49] and a dose of 120 g sodium fluoride has been survived.[50] For sodium fluorosilicate (Na2SiF6), the median lethal dose (LD50) orally in rats is 0.125 g/kg, corresponding to 12.5 g for a 100 kg adult.[51] Treatment may involve oral administration of dilute calcium hydroxide or calcium chloride to prevent further absorption, and injection of calcium gluconate to increase the calcium levels in the blood.[49] Hydrogen fluoride is more dangerous than salts such as NaF because it is corrosive and volatile, and can result in fatal exposure through inhalation or upon contact with the skin; calcium gluconate gel is the usual antidote.[52] In the higher doses used to treat osteoporosis, sodium fluoride can cause pain in the legs and incomplete stress fractures when the doses are too high; it also irritates the stomach, sometimes so severely as to cause ulcers. Slow-release and enteric-coated versions of sodium fluoride do not have gastric side effects in any significant way, and have milder and less frequent complications in the bones.[53] In the lower doses used for water fluoridation, the only clear adverse effect is dental fluorosis, which can alter the appearance of children's teeth during tooth development; this is mostly mild and is unlikely to represent any real effect on aesthetic appearance or on public health.[54] Fluoride was known to enhance the measurement of bone mineral density at the lumbar spine, but it was not effective for vertebral fractures and provoked more non vertebral fractures.[55] A popular urban myth claims that the Nazis used fluoride in concentration camps, but there is no historical evidence to prove this claim.[56] In areas that have naturally occurring high levels of fluoride in groundwater which is used for drinking water, both dental and skeletal fluorosis can be prevalent and severe.[57] Hazard maps for fluoride in groundwater Around one-third of the human population drinks water from groundwater resources. Of this, about 10%, approximately three hundred million people, obtains water from groundwater resources that are heavily contaminated with arsenic or fluoride.[58] These trace elements derive mainly from minerals.[59] Maps are available of locations of potential problematic wells.[60] Topical Concentrated fluoride solutions are corrosive.[61] Gloves made of nitrile rubber are worn when handling fluoride compounds. The hazards of solutions of fluoride salts depend on the concentration. In the presence of strong acids, fluoride salts release hydrogen fluoride, which is corrosive, especially toward glass.[4] Other derivatives Organic and inorganic anions are produced from fluoride, including: Bifluoride, used as an etchant for glass[62] Tetrafluoroberyllate Hexafluoroplatinate Tetrafluoroborate used in organometallic synthesis Hexafluorophosphate used as an electrolyte in commercial secondary batteries. Trifluoromethanesulfonate See also icon Dentistry portal Fluorine-19 nuclear magnetic resonance spectroscopy Fluoride deficiency Fluoride selective electrode Fluoride therapy Sodium monofluorophosphate References "Fluorides – PubChem Public Chemical Database". The PubChem Project. USA: National Center for Biotechnology Information. Identification. Chase, M. W. (1998). "Fluorine anion". NIST: 1–1951. Retrieved July 4, 2012. Wells, J.C. (2008). Longman pronunciation dictionary (3rd ed.). Harlow, England: Pearson Education Limited/Longman. p. 313. ISBN 9781405881180.. According to this source, /ˈfluːəraɪd/ is a possible pronunciation in British English. Aigueperse, Jean; Mollard, Paul; Devilliers, Didier; Chemla, Marius; Faron, Robert; Romano, René; Cuer, Jean Pierre (2000). "Fluorine Compounds, Inorganic". Ullmann's Encyclopedia of Industrial Chemistry. doi:10.1002/14356007.a11_307. ISBN 978-3527306732. "Public Health Statement for Fluorides, Hydrogen Fluoride, and Fluorine". ATSDR. September 2003. "Ambient Water Quality Criteria for Fluoride". Government of British Columbia. Retrieved 8 October 2014. Liteplo, Dr R.; Gomes, R.; Howe, P.; Malcolm, Heath (2002). FLUORIDES - Environmental Health Criteria 227 : 1st draft. Geneva: World Health Organization. ISBN 978-9241572279. Fawell, J.K.; et al. "Fluoride in Drinking-water Background document for development of WHO Guidelines for Drinking-water Quality" (PDF). World Health Organization. Retrieved 6 May 2016. Tiemann, Mary (April 5, 2013). "Fluoride in Drinking Water: A Review of Fluoridation and Regulation Issues" (PDF). Congressional Research Service. p. 3. Retrieved 6 May 2016. Smith, Frank A.; Hodge, Harold C.; Dinman, B. D. (9 January 2009). "Airborne fluorides and man: Part I". C R C Critical Reviews in Environmental Control. 8 (1–4): 293–371. doi:10.1080/10643387709381665. Smith, Frank A.; Hodge, Harold C.; Dinman, B. D. (9 January 2009). "Airborne fluorides and man: Part II". C R C Critical Reviews in Environmental Control. 9 (1): 1–25. doi:10.1080/10643387909381666. Wong MH, Fung KF, Carr HP (2003). "Aluminium and fluoride contents of tea, with emphasis on brick tea and their health implications". Toxicology Letters. 137 (1–2): 111–20. doi:10.1016/S0378-4274(02)00385-5. PMID 12505437. Malinowska E, Inkielewicz I, Czarnowski W, Szefer P (2008). "Assessment of fluoride concentration and daily intake by human from tea and herbal infusions". Food Chem. Toxicol. 46 (3): 1055–61. doi:10.1016/j.fct.2007.10.039. PMID 18078704. Gardner EJ, Ruxton CH, Leeds AR (2007). "Black tea--helpful or harmful? A review of the evidence". European Journal of Clinical Nutrition. 61 (1): 3–18. doi:10.1038/sj.ejcn.1602489. PMID 16855537. Wiberg; Holleman, A.F. (2001). Inorganic chemistry (1st English ed., [edited] by Nils Wiberg. ed.). San Diego, Calif. : Berlin: Academic Press, W. de Gruyter. ISBN 978-0-12-352651-9. Schwesinger, Reinhard; Link, Reinhard; Wenzl, Peter; Kossek, Sebastian (2005). "Anhydrous Phosphazenium Fluorides as Sources for Extremely Reactive Fluoride Ions in Solution". Chemistry. 12 (2): 438–45. doi:10.1002/chem.200500838. PMID 16196062. Haoran Sun & Stephen G. DiMagno (2005). "Anhydrous Tetrabutylammonium Fluoride". Journal of the American Chemical Society. 127 (7): 2050–1. doi:10.1021/ja0440497. PMID 15713075. B. Alič, G. Tavčar, Reaction of N-heterocyclic carbene (NHC) with different HF sources and ratios – A free fluoride reagent based on imidazolium fluoride, J. Fluorine Chem. 192 (2016), 141-146, doi: Redirecting . B. Alič, M. Tramšek, A. Kokalj, G. Tavčar, Discrete GeF5– Anion Structurally Characterized with a Readily Synthesized Imidazolium Based Naked Fluoride Reagent, Inorg. Chem., 56(16) (2017), 10070-10077, doi: 10.1021/acs.inorgchem.7b01606. Ž. Zupanek, M. Tramšek, A. Kokalj, G. Tavčar, Reactivity of VOF3 with N-Heterocyclic Carbene and Imidazolium Fluoride: Analysis of Ligand–VOF3 Bonding with Evidence of a Minute π Back-Donation of Fluoride, Inorg. Chem., 57(21) (2018), 13866-13879, doi: 10.1021/acs.inorgchem.8b02377. Fawell, J. "Fluoride in Drinking-water" (PDF). World Health Organization. Retrieved 10 March 2016. Chan, Laura; Mehra, Aradhana; Saikat, Sohel; Lynch, Paul (May 2013). "Human exposure assessment of fluoride from tea (Camellia sinensis L.): A UK based issue?". Food Research International. 51 (2): 564–570. doi:10.1016/j.foodres.2013.01.025. "Fluoride Free Toothpaste – Fluoride (Finally!) Explained". 2016-06-27. McDonagh M. S.; Whiting P. F.; Wilson P. M.; Sutton A. J.; Chestnutt I.; Cooper J.; Misso K.; Bradley M.; Treasure E.; Kleijnen J. (2000). "Systematic review of water fluoridation". British Medical Journal. 321 (7265): 855–859. doi:10.1136/bmj.321.7265.855. PMC 27492. PMID 11021861. Griffin SO, Regnier E, Griffin PM, Huntley V (2007). "Effectiveness of fluoride in preventing caries in adults". J. Dent. Res. 86 (5): 410–5. doi:10.1177/154405910708600504. hdl:10945/60693. PMID 17452559. Winston A. E.; Bhaskar S. N. (1 November 1998). "Caries prevention in the 21st century". J. Am. Dent. Assoc. 129 (11): 1579–87. doi:10.14219/jada.archive.1998.0104. PMID 9818575. Archived from the original on 15 July 2012. "Community Water Fluoridation". Centers for Disease Control and Prevention. Retrieved 10 March 2016. "Ten Great Public Health Achievements in the 20th Century". Centers for Disease Control and Prevention. Archived from the original on 2016-03-13. Retrieved 10 March 2016. Newbrun E (1996). "The fluoridation war: a scientific dispute or a religious argument?". J. Public Health Dent. 56 (5 Spec No): 246–52. doi:10.1111/j.1752-7325.1996.tb02447.x. PMID 9034969. Walsh, Tanya; Worthington, Helen V.; Glenny, Anne-Marie; Appelbe, Priscilla; Marinho, Valeria C. C.; Shi, Xin (2010-01-20). "Fluoride toothpastes of different concentrations for preventing dental caries in children and adolescents". Cochrane Database of Systematic Reviews (1): CD007868. doi:10.1002/14651858.cd007868.pub2. PMID 20091655. Nakai C, Thomas JA (1974). "Properties of a phosphoprotein phosphatase from bovine heart with activity on glycogen synthase, phosphorylase, and histone". J. Biol. Chem. 249 (20): 6459–67. PMID 4370977. Schenk G, Elliott TW, Leung E, et al. (2008). "Crystal structures of a purple acid phosphatase, representing different steps of this enzyme's catalytic cycle". BMC Struct. Biol. 8: 6. doi:10.1186/1472-6807-8-6. PMC 2267794. PMID 18234116. Wang W, Cho HS, Kim R, et al. (2002). "Structural characterization of the reaction pathway in phosphoserine phosphatase: crystallographic "snapshots" of intermediate states". J. Mol. Biol. 319 (2): 421–31. doi:10.1016/S0022-2836(02)00324-8. PMID 12051918. Cho H, Wang W, Kim R, et al. (2001). "BeF(3)(-) acts as a phosphate analog in proteins phosphorylated on aspartate: structure of a BeF(3)(-) complex with phosphoserine phosphatase". Proc. Natl. Acad. Sci. U.S.A. 98 (15): 8525–30. Bibcode:2001PNAS...98.8525C. doi:10.1073/pnas.131213698. PMC 37469. PMID 11438683. Jones, Simon C.; Grubbs, Robert H.; Miller, Thomas F.; Brooks, Christopher J.; Ahmed, Musahid; Rosenberg, Daniel; Hightower, Adrian; Nair, Nanditha G.; Darolles, Isabelle M. (2018-12-07). "Room-temperature cycling of metal fluoride electrodes: Liquid electrolytes for high-energy fluoride ion cells". Science. 362 (6419): 1144–1148. doi:10.1126/science.aat7070. ISSN 0036-8075. PMID 30523107. "Fluoride-ion battery runs at room temperature". Chemical & Engineering News. Retrieved 2019-02-08. Institute of Medicine (1997). "Fluoride". Dietary Reference Intakes for Calcium, Phosphorus, Magnesium, Vitamin D and Fluoride. Washington, DC: The National Academies Press. pp. 288–313. "Overview on Dietary Reference Values for the EU population as derived by the EFSA Panel on Dietetic Products, Nutrition and Allergies" (PDF). 2017. Tolerable Upper Intake Levels For Vitamins And Minerals (PDF), European Food Safety Authority, 2006 "Federal Register May 27, 2016 Food Labeling: Revision of the Nutrition and Supplement Facts Labels. FR page 33982" (PDF). "Nutrient Lists". Agricultural Research Service United States Department of Agriculture. Retrieved 25 May 2014. Levy N. Total fluoride intake and implications for dietary fluoride supplementation. - PubMed - NCBI "Food Composition Databases: Food Search: Fluoride". Agricultural Research Service, United States Department of Agriculture. Retrieved 5 December 2018. "Dietary Reference Intakes: EAR, RDA, AI, Acceptable Macronutrient Distribution Ranges, and UL". United States Department of Agriculture. Retrieved 9 September 2017. "Fluoride in diet". U.S. National Library of Medicine. Retrieved 10 March 2016. Gosselin, RE; Smith RP; Hodge HC (1984). Clinical toxicology of commercial products. Baltimore (MD): Williams & Wilkins. pp. III–185–93. ISBN 978-0-683-03632-9. Baselt, RC (2008). Disposition of toxic drugs and chemicals in man. Foster City (CA): Biomedical Publications. pp. 636–40. ISBN 978-0-9626523-7-0. IPCS (2002). Environmental health criteria 227 (Fluoride). Geneva: International Programme on Chemical Safety, World Health Organization. p. 100. ISBN 978-92-4-157227-9. Rabinowitch, IM (1945). "Acute Fluoride Poisoning". Canadian Medical Association Journal. 52 (4): 345–9. PMC 1581810. PMID 20323400. Abukurah AR, Moser AM Jr, Baird CL, Randall RE Jr, Setter JG, Blanke RV (1972). "Acute sodium fluoride poisoning". JAMA. 222 (7): 816–7. doi:10.1001/jama.1972.03210070046014. PMID 4677934. The Merck Index, 12th edition, Merck & Co., Inc., 1996 Muriale L, Lee E, Genovese J, Trend S (1996). "Fatality due to acute fluoride poisoning following dermal contact with hydrofluoric acid in a palynology laboratory". Ann. Occup. Hyg. 40 (6): 705–710. doi:10.1016/S0003-4878(96)00010-5. PMID 8958774. Murray TM, Ste-Marie LG (1996). "Prevention and management of osteoporosis: consensus statements from the Scientific Advisory Board of the Osteoporosis Society of Canada. 7. Fluoride therapy for osteoporosis". CMAJ. 155 (7): 949–54. PMC 1335460. PMID 8837545. National Health and Medical Research Council (Australia) (2007). A systematic review of the efficacy and safety of fluoridation (PDF). ISBN 978-1-86496-415-8. Summary: Yeung CA (2008). "A systematic review of the efficacy and safety of fluoridation". Evid. Based Dent. 9 (2): 39–43. doi:10.1038/sj.ebd.6400578. PMID 18584000. Lay summary (PDF) – NHMRC (2007). Haguenauer, D; Welch, V; Shea, B; Tugwell, P; Adachi, JD; Wells, G (2000). "Fluoride for the treatment of postmenopausal osteoporotic fractures: a meta-analysis". Osteoporosis International. 11 (9): 727–38. doi:10.1007/s001980070051. PMID 11148800. Bowers, Becky (6 October 2011). "Truth about fluoride doesn't include Nazi myth". Fact-checking U.S. politics | PolitiFact . Tampa Bay Times. Retrieved 26 March 2015. World Health Organization (2004). "Fluoride in drinking-water" (PDF). Archived from the original (PDF) on 2016-03-04. Retrieved 2014-02-13. Eawag (2015) Geogenic Contamination Handbook – Addressing Arsenic and Fluoride in Drinking Water. C.A. Johnson, A. Bretzler (Eds.), Swiss Federal Institute of Aquatic Science and Technology (Eawag), Duebendorf, Switzerland. (download: Geogenic Contamination Handbook ) Rodríguez-Lado, L.; Sun, G.; Berg, M.; Zhang, Q.; Xue, H.; Zheng, Q.; Johnson, C.A. (2013) Groundwater arsenic contamination throughout China. Science, 341(6148), 866-868, doi:10.1126/science.1237484 Groundwater Assessment Platform Nakagawa M, Matsuya S, Shiraishi T, Ohta M (1999). "Effect of fluoride concentration and pH on corrosion behavior of titanium for dental use". Journal of Dental Research. 78 (9): 1568–72. doi:10.1177/00220345990780091201. PMID 10512392. Ammonium bifluoride in the glass industry - Chimex LTD

What could be causing sudden spikes in blood pressure in a fairly healthy 40 year old male? How would you advise them going forward if their doctor only gave them pills with no life advice?

Not a doctor. I do understand yours opted only for meds, which is not unusual. If I were looking at what you described (40 year old male with no known serious health issues) I would probably ask the doctor if he’d considered some things which my reading of the issue indicates are pertinent: Do we know the status of your kidney function? How old was the kidney function testing because maybe it’s time revisit that. Ditto thyroid PANEL, not just a TSH. MOST MDs are going to roll their eyes over the fullness of what I think makes sense for a baseline panel (there are a LOT of thyroid issues out there. One of the people I am turning to for this list of tests is neurologist Dale Bredesen, MD, who I think is doing critical and inspiring work on cognitive function. In his book, The End of Alzheimer’s—and yes I know you’re NOT asking about that—he suggests testing for things like endocrine issues which DO affect cognitive function. They also affect the entire body and cardiovascular and endocrine most certainly are linked.) I will put what HE wants the values to be because he is not sold on just the reference range: TSH < 2.0 microIU/ml Free T3 3.2-4.2 pg/ml Reverse T3 < 20 ng/dL Free T3 x 100 reverse T3 > 20 Free T4 1.3 – 1.8 ng/dL That data comes from pp. 127–129 of the Alzheimer’s book I noted. He admits this IS controversial (and frankly not just for cognition but a LOT of MDs think that panel is overkill and ALL you need is TSH, esp. as you are not complaining of typical “thyroid issues.”) I understand what they are saying but to me when we are having things such as BP SPIKES I am interested in the WHY and I suspect that you may have some other CORRECTABLE (not merely treatable with meds) issues going on. A comprehensive panel would indicate if there is merit in that or not. There is NO medical controversy over thyroid and BP linkage. It’s the quantity of testing that will not sit well with many—and then Bredesen’s values will bother some as well. I am assuming you don’t smoke or use “drugs.” If you drink, not more than 2 a day; after that, it certainly factors into a lot of issues. Your caffeine use could be pertinent. How you handle STRESS and how much you experience could be the causes of the spikes. I don’t know if you are on medications. Even something that is OTC, over the counter, like NSAIDs (Tylenol and such), can be an issue. It’s logical to work with the idea that there IS a cardiovascular issue to consider. Typically the Mediterranean diet has produced excellent results for those issues (as well as others). Personally I think people are better off if they are ALSO gluten-free, cow dairy free, off all table sugar and fake ones as well. (A LITTLE coconut sugar, date sugar, blackstrap molasses, real maple syrup, honey can be reasonable alternatives when used VERY sparingly. If I have to use a “fake” sugar: xylitol (keep away from dogs!), stevia, or monk fruit are probably least objectionable). Avoid fruit JUICES (high levels of fructose). You need proper sleep for many reasons; hopefully you are getting 7–9 hours of quality unbroken refreshing sleep. If not, that is absolutely worth working on. Proper hydration (don’t wait to get thirsty) and some daily appropriate exercise (at the very least a brisk walk of 20–30 minutes is good; some resistance exercise as well, even better!). Also most folks are magnesium deficient. You won’t easily be able to overdo that, so would suggest going for a 400 mg magnesium supplement. If you have constipation issues, citrate form is great; otherwise choices like glycinate, threonate (may well be super helpful form for brain), malate (esp. good if you have muscle aches) are worth considering. You can also use a magnesium oil product ON you and it should absorb well. Mg IS a factor in blood pressure control without question. I think a lot of folks are low on selenium and that ties in. THAT can become toxic, so you want to be cautious with that one. Most likely you are safe to use 200 mcg a day of that. I do like lab tests instead of guessing. An RBC Selenium would be wonderful as that mineral is involved in a LOT of health issues that many experience. RBC (Red Blood Cell) over the typical serum draw. A third commonly low or flat out deficient nutrient is Vitamin D, esp. in the winter. The reference range is too low to many. From my readings, closer to 80 on the 50–80 ng/ml is far better. There is a test for that as well: 25-hydroxycholecalciferol). Many supplement at 5,000 IU (yes higher than the RDA by far) if deficient. ALSO use some Vitamin K2 and some calcium as well would be good. Personally I use Decalcify for the K2 & calcium. (Some will get excited about calcium being in it saying it’s clogging arteries. Again, research I’ve read doesn’t really support that that APPROPRIATE level of supplementation is an issue and with the magnesium on board, all should be well.) Those are things I’d consider and not saying that is everything worth doing, but that is a good start. I would not expect a huge change for probably around a month because I think the diet is crucial in this and to be honest most folks will have some issues going full on and it’s not like taking a pill. IF you are really magnesium deficient, however, that may produce a change that occurs quickly. Without being able to examine someone, review appropriate tests, ask a lot of questions, these are suggestions playing the ODDS so your doc may be on board with these or not. Many WOULD be open to this but don’t bring it up for many reasons, including a lot of patients will NOT be compliant because those are a lot of things to do and many will say they are NOT going to change their diet; can’t afford that much time to walk; and they can’t spend that much time sleeping. It is a real struggle for many to DO these things. Docs know the prescription will tend to keep the BP lower and taking a pill is something most folks WILL do. Good luck with getting the problem under control. Do remember that if you’re monitoring your BP that some spikes are TOO high and do need to be treated urgently; if you have SOME other issues such as blurred vision, shortness of breath, headache, confusion, fatigue, restlessness, anxiety, chest pain, nausea, vomiting, coughing, numbness in hands, feet, legs, or arms, that you need to go to the ER for proper evaluation. Not saying that is the full list either because remember: NOT a doctor.

What causes an immune response that will destroy the pancreas' ability to produce insulin as in Type 1 diabetes?

Q: “What causes an immune response that will destroy the pancreas’ ability to produce insulin as in Type 1 diabetes?” Come up with the definitive answer to that, and there’s a Nobel Peace Prize in Medicine in your future. That said… we’ve some pretty good ideas. In short… T1 is a genetic condition, but MUST be “triggered” (by one of several known - or as yet unknown - environmental factors), and it MUST be at a susceptible time - when the gut microbiome is in a weakened state, or simply not “in prime condition”. BUT FIRST… it is ABSOLUTELY NECESSARY to carry the genetic markers that bestow susceptibility; without those, you WILL NOT develop T1 - whether exposed to a “trigger” or not. AND… even in identical twins, T1 is NOT consistent; having a T1 relative - even an identical twin - does NOT mean you will get the disease; as a matter of fact, in more than 50% of those that develop T1 that have an identical twin, the identical twin never develops the disease. It is important to understand that there is NO single gene that causes susceptibility to T1; it is a combination of certain genetic alleles that bestows the risk upon an individual, and that alone is NOT enough to cause the disease. AND… there are several causative combinations of alleles, though some confer more risk than others. On “triggers” that initiate the disease development… Many viruses have been linked to T1; the most common ones are the family of enteroviruses. This “family” is the largest family of viruses that plague humans, though most of them are relatively harmless, causing little more than mild cold symptoms, and readily overcome. Except, of course, in those cases where they trigger the T1 autoimmune response. A few other common viruses that have been identified as triggers of T1 are mumps, rubella, rotavirus, cytomegalovirus, and ljunganvirus. AND… several bacteria are suspected triggers of T1. The gut microbiome is a key component of the immune system - and issues therein can make a carrier of the genetic risk factors more susceptible to development of the disease. SO… not only do you have to carry the genetic risk factors, AND be exposed to an environmental trigger, but ALSO that exposure must happen at a susceptible time vis-a-vis the gut microbiome. AND… several dietary habits are suspected sources of “triggers” for T1. AND a few other environmental factors. In short - this is a very complex issue, and involves a LOT of factors. It is likely that many more years of study will be required to even begin to identify who’s “really” at risk for the disease, and then, many more years of research to identify the actual diseases progression “steps” in order to intervene effectively. For a more in-depth understanding of these issues… here’s a short reading list: Åkerblom HK, Vaarala O, Hyöty H, Ilonen J, Knip M 2002. Environmental factors in the etiology of type 1 diabetes. Am J Med Genet 115: 18–29 [PubMed ] [Google Scholar ] Atarashi K, Tanoue T, Shima T, Imaoka A, Kuwahara T, Momose Y, Cheng G, Yamasaki S, Saito T, Ohba Y, et al. 2011. Induction of colonic regulatory T cells by indigenous Clostridium species. Science 331: 337–341 [PMC free article ] [PubMed ] [Google Scholar ] Barnett AH, Eff C, Leslie RDG, Pyke DA 1981. Diabetes in identical twins. A study of 200 pairs. Diabetologia 20: 87–93 [PubMed ] [Google Scholar ] Blomquist M, Juhela S, Erkkilä S, Korhonen S, Simell T, Kupila A, Vaarala O, Simell O, Knip M, Ilonen J 2002. Rotavirus infections and development of diabetes-associated autoantibodies during the first 2 years of life. Clin Exp Immunol 128: 511–515 [PMC free article ] [PubMed ] [Google Scholar ] Brown CT, Davis-Richardson AG, Giongo A, Gano KA, Crabb DB, Mukherjee N, Casella G, Drew JC, Ilonen J, Knip M, et al. 2011. Gut microbiome metagenomics analysis suggests a functional model for the development of autoimmunity for type 1 diabetes. PLoS ONE 6: e25792. [PMC free article ] [PubMed ] [Google Scholar ] Chase HP, Lescheck R, Rafkin-Mervis L, Krause-Steinrauf H, Chritton S, Asare S, Adams S, Skyler JS, Clare-Salzier M, Type 1 Diabetes Trialnet NIP Study Group 2009. Nutritional intervention to prevent (NIP) type 1 diabetes: A pilot trial. Infant Child Adolesc Nutr 1: 99–107 [Google Scholar ] Dahlquist GG, Blom L, Persson LÅ, Sandström AI, Wall SG 1990. Dietary factors and the risk of developing insulin dependent diabetes in childhood. Br Med J 300: 1302–1306 [PMC free article ] [PubMed ] [Google Scholar ] Fuchtenbusch M, Irnstetter A, Jager G, Ziegler AG 2001. No evidence for an association of coxsackie virus infections during pregnancy and early childhood with development of islet autoantibodies in offspring of mothers or fathers with type 1 diabetes. J Autoimmun 17: 333–340 [PubMed ] [Google Scholar ] Gillespie KM, Bain SC, Barnett AH, Bingley PJ, Christie MR, Gill GV, Gale EA 2004. The rising incidence of childhood type 1 diabetes and reduced contribution of high-risk HLA haplotypes. Lancet 364: 1699–1700 [PubMed ] [Google Scholar ] Giongo A, Mukherjee N, Gano KA, Crabb DB, Casella G, Drew JC, Ilonen J, Knip M, Hyöty H, Veijola R, et al. 2011. Toward defining the autoimmune microbiome for type 1 diabetes. ISME J 5: 82–91 [PMC free article ] [PubMed ] [Google Scholar ] Graves PM, Rotbart HA, Nix WA, Pallansch MA, Erlich HA, Norris JM, Hoffman M, Eisenbarth GS, Rewers M 2003. Prospective study of enteroviral infections and development of β-cell autoimmunity. Diabetes autoimmunity study in the young (DAISY). Diabetes Res Clin Pract 59: 51–61 [PubMed ] [Google Scholar ] Hermann R, Knip M, Veijola R, Simell O, Laine AP, Åkerblom HK, Groop PH, Forsblom C, Petterson-Fernholm K, Ilonen J, et al. 2003. Temporal changes in the frequencies of HLA genotypes in patients with type 1 diabetes—indication of an increased environmental pressure? Diabetologia 46: 420–425 [PubMed ] [Google Scholar ] Hindmarsh PC, Matthews DR, Di Silvio L, Kurz AB, Brook CG 1988. Relation between height velocity and fasting insulin concentrations. Arch Dis Child 63: 665–666 [PMC free article ] [PubMed ] [Google Scholar ] Holmberg H, Wahlberg J, Vaarala O, Ludvigsson J, the ABIS studygroup 2007. Short duration of breast-feeding as a risk factor for β-cell autoantibodies in 5-year-old children from the general population. Br J Nutr 97: 111–116 [PubMed ] [Google Scholar ] Honeyman MC, Stone NL, Harrison LC 1998. T-cell epitopes in type 1 diabetes autoantigen tyrosine phosphatase IA-2: Potential for mimicry with rotavirus and other environmental agents. Mol Med 4: 231–239 [PMC free article ] [PubMed ] [Google Scholar ] Honeyman MC, Coulson BS, Stone NL, Gellert SA, Goldwater PN, Steele CE, Couper JJ, Tait BD, Colman PG, Harrison LC 1999. Association between rotavirus infection and pancreatic islet autoimmunity in children at risk of developing type 1 diabetes. Diabetes 49: 1319–1324 [PubMed ] [Google Scholar ] Honeyman MC, Stone NL, Falk BA, Nepom G, Harrison LC 2010. Evidence for molecular mimicry between human T cell epitopes in rotavirus and pancreatic islet autoantigens. J Immunol 184: 2204–2210 [PubMed ] [Google Scholar ] Hummel M, Bonifacio E, Naserke HE, Ziegler AG 2002. Elimination of dietary gluten does not reduce titers of type 1 diabetes-associated autoantibodies in high-risk subjects. Diabetes Care 25: 1111–1116 [PubMed ] [Google Scholar ] Hummel S, Pflüger M, Hummel M, Bonifacio E, Ziegler AG 2011. Primary dietary intervention study to reduce the risk of islet autoimmunity in children at increased risk for type 1 diabetes: The BABYDIET study. Diabetes Care 34: 1301–1305 [PMC free article ] [PubMed ] [Google Scholar ] Hyöty H, Taylor KW 2002. The role of viruses in human diabetes. Diabetologia 45: 1353–1361 [PubMed ] [Google Scholar ] Hyppönen E, Kenward MG, Virtanen SM, Piitulainen A, Virta-Autio P, Knip M, Åkerblom HK, the Childhood Diabetes in Finland Study Group 1999. Infant feeding, early weight gain and risk of type 1 diabetes. Diabetes Care 22: 1961–1965 [PubMed ] [Google Scholar ] Hyppönen E, Virtanen SM, Kenward MG, Knip M, Åkerblom HK, the Childhood Diabetes in Finland Study Group 2000. Obesity, increased linear growth and risk of type 1 diabetes mellitus in children. Diabetes Care 23: 1755–1760 [PubMed ] [Google Scholar ] Hyppönen E, Läärä E, Järvelin MR, Virtanen SM 2001. Intake of vitamin D and risk of type 1 diabetes: A birth cohort study. Lancet 358: 1500–1504 [PubMed ] [Google Scholar ] Kaprio J, Tuomilehto J, Koskenvuo M, Romanov K, Reunanen A, Eriksson J, Stengård J, Kesäniemi YA 1992. Concordance for Type 1 (insulin-dependent) and Type 2 (non-insulin-dependent) diabetes mellitus in a population-based cohort of twins in Finland. Diabetologia 35: 1060–1067 [PubMed ] [Google Scholar ] Kim CY, Quarsten H, Bergseng E, Khosla C, Sollid LM 2004. Structural basis for HLA-DQ2-mediated presentation of gluten epitopes in celiac disease. Proc Natl Acad Sci 101: 4175–4179 [PMC free article ] [PubMed ] [Google Scholar ] Kimpimäki T, Kupila A, Hämäläinen A-M, Kukko M, Kulmala P, Savola K, Simell T, Muona P, Ilonen J, Simell O, et al. 2001a. The first signs of ß-cell autoimmunity appear in infancy in genetically susceptible children from the general population: The Finnish Type 1 Diabetes Prediction and Prevention Study. J Clin Endocrinol Metab 86: 4782–4788 [PubMed ] [Google Scholar ] Kimpimäki T, Erkkola M, Korhonen S, Kupila A, Virtanen SM, Ilonen J, Simell O, Knip M 2001b. Short exclusive breast-feeding predisposes young children with increased genetic risk of type 1 diabetes to progressive β-cell autoimmunity. Diabetologia 44: 63–69 [PubMed ] [Google Scholar ] Knip M 2011. Pathogenesis of type 1 diabetes: Implications for incidence trends. Horm Res 76: 57–64 [PubMed ] [Google Scholar ] Knip M, Hyöty H 2008. Environmental determinants: The role of viruses and standard of hygiene. In Epidemiology of Pediatric and Adolescent Diabetes (ed. Dabelea D, Klingensmith GJ), pp. 63–64 Informa Healthcare, New York [Google Scholar ] Knip M, Siljander H 2008. Autoimmune mechanisms in type 1 diabetes. Autoimmun Rev 7: 550–557 [PubMed ] [Google Scholar ] Knip M, Veijola R, Virtanen SM, Hyöty H, Vaarala O, Åkerblom HK 2005. Environmental triggers and determinants of β-cell autoimmunity and type 1 diabetes. Diabetes 54: S125–S136 [PubMed ] [Google Scholar ] Knip M, Korhonen S, Kulmala P, Veijola R, Reunanen A, Raitakari OT, Viikari J, Åkerblom HK 2010a. Prediction of type 1 diabetes in the general population. Diabetes Care 33: 1206–1212 [PMC free article ] [PubMed ] [Google Scholar ] Knip M, Virtanen SM, Åkerblom HK 2010b. Infant feeding and risk of type 1 diabetes. Am J Clin Nutr 91: 1506S–1513S [PMC free article ] [PubMed ] [Google Scholar ] Knip M, Virtanen SM, Seppä K, Ilonen J, Savilahti E, Vaarala O, Reunanen A, Teramo K, Hämäläinen AM, Paronen J, et al. 2010c. Dietary intervention in infancy and later signs of β-cell autoimmunity. N Engl J Med 363: 1900–1908 [PMC free article ] [PubMed ] [Google Scholar ] Kondrashova A, Reunanen A, Romanov A, Karvonen A, Viskari H, Vesikari T, Ilonen J, Knip M, Hyöty H 2005. A sixfold gradient in the incidence of type 1 diabetes at the eastern border of Finland. Ann Med 37: 67–72 [PubMed ] [Google Scholar ] Kostraba JN, Cruickshanks KJ, Lawler-Heavner J, Jobim LF, Rewers MJ, Gay EC, Chase HP, Klingensmith G, Hamman RF 1993. Early exposure to cow's milk and solid foods in infancy, genetic predisposition, and risk of IDDM. Diabetes 42: 288–295 [PubMed ] [Google Scholar ] Kukko M, Virtanen SM, Toivonen A, Erkkilä S, Korhonen S, Ilonen J, Simell O, Knip M 2004. Geographic variation in risk HLA-DQB1 genotypes for type 1 diabetes and signs of β-cell autoimmunity within a high incidence country. Diabetes Care 27: 676–681 [PubMed ] [Google Scholar ] Kukko M, Kimpimäki T, Korhonen S, Kupila A, Simell S, Veijola R, Simell T, Ilonen J, Simell O, Knip M 2005. Dynamics of diabetes-associated autoantibodies in young children with HLA-conferred risk of type 1 diabetes recruited from the general population. J Clin Endocrinol Metab 90: 2712–2717 [PubMed ] [Google Scholar ] Lamb MM, Yin X, Barriga K, Hoffman MR, Barón AE, Eisenbarth GS, Rewers M, Norris JM 2008. Dietary glycemic index, development of islet autoimmunity, and subsequent progression to type 1 diabetes in young children. J Clin Endocrinol Metab 93: 3936–3942 [PMC free article ] [PubMed ] [Google Scholar ] Lamb MM, Yin X, Zerbe GO, Klingensmith GJ, Dabelea D, Fingerlin TE, Rewers M, Norris JM 2009. Height growth velocity, islet autoimmunity and type 1 diabetes development: The Diabetes Autoimmunity Study in the Young. Diabetologia 52: 2064–2071 [PMC free article ] [PubMed ] [Google Scholar ] Lempainen J, Vaarala O, Mäkelä M, Veijola R, Simell O, Knip M, Hermann R, Ilonen J 2009. Interplay between genetic and dietary factors in type 1 diabetes. J Autoimmun 33: 155–163 [PubMed ] [Google Scholar ] Lempainen J, Tauriainen S, Vaarala O, Mäkelä M, Honkanen H, Marttila J, Veijola R, Simell O, Hyöty H, Knip M, et al. 2012. Interaction of enterovirus infection and cow's milk based formula nutrition in type 1 diabetes-associated autoimmunity. Diabetes Metab Res Rev 28: 177–185 [PubMed ] [Google Scholar ] Lipponen K, Gombos Z, Kiviniemi M, Siljander H, Hermann R, Veijola R, Simell O, Knip M, Ilonen J 2010. Effect of HLA class I and class II alleles on progression from autoantibody positivity to overt type 1 diabetes. Diabetes 59: 3253–3256 [PMC free article ] [PubMed ] [Google Scholar ] Lönnrot M, Korpela K, Knip M, Ilonen J, Simell O, Korhonen S, Savola K, Muona P, Simell T, Koskela P, et al. 2000. Enterovirus infection as a risk factor for ß-cell autoimmunity in a prospectively observed birth cohort—The Finnish Diabetes Prediction and Prevention (DIPP) Study. Diabetes 49: 1314–1318 [PubMed ] [Google Scholar ] Mrena S, Savola K, Kulmala P, Åkerblom HK, Knip M, the Childhood Diabetes in Finland Study Group 2003. Natural course of preclinical Type 1 diabetes in siblings of affected children. Acta Paediatr 92: 1403–1410 [PubMed ] [Google Scholar ] Norris JM, Barriga K, Klingensmith G, Hoffman M, Eisenbarth GS, Erlich HA, Rewers M 2003. Timing of initial cereal exposure in infancy and risk of islet autoimmunity. JAMA 290: 1713–1720 [PubMed ] [Google Scholar ] Norris JM, Yin X, Lamb MM, Barriga K, Seifert J, Hoffman M, Orton HD, Barón AE, Clare-Salzler M, Chase HP, et al. 2007. Omega-3 polyunsaturated fatty acid intake and islet autoimmunity in children at increased risk for type 1 diabetes. JAMA 298: 1420–1428 [PubMed ] [Google Scholar ] Oikarinen S, Martiskainen M, Tauriainen S, Huhtala H, Ilonen J, Veijola R, Simell O, Knip M, Hyöty H 2011. Enterovirus RNA in blood is linked to the development of type 1 diabetes. Diabetes 60: 276–279 [PMC free article ] [PubMed ] [Google Scholar ] Orešič M, Simell S, Sysi-Aho M, Nänto-Salonen K, Seppänen-Laakso T, Parikka V, Mattila I, Keskinen P, Katajamaa M, Yetukuri L, et al. 2008. Dysregulation of lipid and amino acid metabolism precedes autoimmunity in children who later progress to type 1 diabetes. J Exp Med 205: 2975–2984 [PMC free article ] [PubMed ] [Google Scholar ] Palmer JP, Helquist S, Spinas GA, Mølvig J, Mandrup-Poulsen T, Andersen HU, Nerup J 1989. Interaction of β-cell activity and IL-1 concentration and exposure time in isolated rat islets of Langerhans. Diabetes 38: 1211–1216 [PubMed ] [Google Scholar ] Parikka V, Näntö-Salonen K, Saarinen M, Simell T, Ilonen J, Hyöty H, Veijola R, Knip M, Simell O 2012. Early seroconversion and rapidly increasing autoantibody concentrations predict prepubertal manifestation of type 1 diabetes in children at genetic risk. Diabetologia 10.1007/s00125-012-2523-3 [PubMed ] [CrossRef ] [Google Scholar ] Pastore MR, Bazzigaluppi E, Belloni C, Arcovio C, Bonifacio E, Bosi E 2003. Six months of gluten-free diet do not influence autoantibody titers, but improve insulin secretion in subjects at high risk for type 1 diabetes. J Clin Endocrinol Metab 88: 162–165 [PubMed ] [Google Scholar ] Peng H, Hagopian W 2006. Environmental factors in the development of Type 1 diabetes. Rev Endocr Metab Disord 7: 149–162 [PubMed ] [Google Scholar ] Pescovitz MD, Greenbaum CJ, Krause-Steinrauf H, Becker DJ, Gitelman SE, Goland R, Gottlieb PA, Marks JB, McGee PF, Moran AM, et al. 2009. Rituximab, B-lymphocyte depletion, and preservation of β-cell function. N Engl J Med 361: 2143–2152 [PMC free article ] [PubMed ] [Google Scholar ] Pflueger M, Seppänen-Laakso T, Suortti T, Hyötyläinen T, Achenbach P, Bonifacio E, Oresic M, Ziegler AG 2011. Age- and islet autoimmunity-associated differences in amino acid and lipid metabolites in children at risk for type 1 diabetes. Diabetes 60: 2740–2747 [PMC free article ] [PubMed ] [Google Scholar ] Pociot F, Akolkar B, Concannon P, Erlich HA, Julier C, Morahan G, Nierras CR, Todd JA, Rich S, Nerup J 2010. Genetics of type 1 diabetes: What's next? Diabetes 59: 1561–1571 [PMC free article ] [PubMed ] [Google Scholar ] Räsänen M, Kronberg-Kippilä C, Ahonen S, Uusitalo L, Kautiainen S, Erkkola M, Veijola R, Knip M, Kaila M, Virtanen SM 2006. Intake of vitamin D by Finnish children aged 3 months to 3 years in relation to sociodemographic factors. Eur J Clin Nutr 60: 1317–1322 [PubMed ] [Google Scholar ] Sabbah E, Savola K, Ebeling T, Kulmala P, Vähäsalo P, Salmela P, Knip M 2000. Genetic, autoimmune, and clinical characteristics of childhood- and adult-onset Type 1 diabetes mellitus. Diabetes Care 23: 1326–1332 [PubMed ] [Google Scholar ] Siljander H, Simell S, Hekkala A, Lähde J, Simell T, Vähäsalo P, Veijola R, Ilonen J, Simell O, Knip M 2009. Predictive value of diabetes-associated autoantibodies among children with HLA-conferred disease susceptibility recruited from the general population. Diabetes 58: 2835–2842 [PMC free article ] [PubMed ] [Google Scholar ] Simonen-Tikka ML, Pflueger M, Klemola P, Savolainen-Kopra C, Smura T, Hummel S, Kaijalainen S, Nuutila K, Natri O, Roivainen M, et al. 2011. Human enterovirus infections in children at increased risk for type 1 diabetes: The Babydiet study. Diabetologia 54: 2995–3002 [PubMed ] [Google Scholar ] Simpson M, Brady H, Yin X, Seifert J, Barriga K, Hoffman M, Bugawan T, Barón AE, Sokol RJ, Eisenbarth G, et al. 2011. No association of vitamin D intake or 25-hydroxyvitamin D levels in childhood with risk of islet autoimmunity and type 1 diabetes: The Diabetes Autoimmunity Study in the Young (DAISY). Diabetologia 54: 2779–2788 [PMC free article ] [PubMed ] [Google Scholar ] Stene LC, Joner G, Norwegian Childhood Diabetes Study Group 2003. Use of cod liver oil during the first year of life is associated with lower risk of childhood-onset type 1 diabetes: A large, population-based, case-control study. Am J Clin Nutr 78: 1128–1134 [PubMed ] [Google Scholar ] Stene LC, Thorsby PM, Berg JP, Rønningen KS, Joner G, Norwegian Childhood Diabetes Study Group 2008. Peroxisome proliferator-activated receptor-γ2 Pro12Ala polymorphism, cod liver oil and risk of type 1 diabetes. Pediatr Diabetes 9: 40–45 [PubMed ] [Google Scholar ] Stene LC, Oikarinen S, Hyöty H, Barriga KJ, Norris JM, Klingensmith G, Hutton JC, Erlich HA, Eisenbarth GS, Rewers M 2010. Enterovirus infection and progression from islet autoimmunity to type 1 diabetes: The Diabetes and Autoimmunity Study in the Young (DAISY). Diabetes 39: 3174–3180 [PMC free article ] [PubMed ] [Google Scholar ] Streng J 1946. Over de beoordeling van de voedingstoestand in de praktijk (in Dutch, summary in English). Maandschrift v Kindergen 14: 67–78 [Google Scholar ] Sysi-Aho M, Ermolov A, Tripathi A, Seppänen-Laakso T, Ruohonen ST, Toukola L, Yetukuri L, Härkönen T, Lindfors E, Nikkilä J, et al. 2011. Metabolic regulation in progression to autoimmune diabetes. PLoS Comput Biol 7: e1002257. [PMC free article ] [PubMed ] [Google Scholar ] Tauriainen S, Oikarinen S, Oikarinen M, Hyöty H 2011. Enteroviruses in the pathogenesis of type 1 diabetes. Semin Immunopathol 33: 45–55 [PubMed ] [Google Scholar ] The EURODIAB ACE Study Group and The EURODIAB ACE Substudy 2 Study Group 1998. Familial risk of Type I diabetes in European children. Diabetologia 41: 1151–1156 [PubMed ] [Google Scholar ] The EURODIAB ACE Study Group 2000. Variation and trends in incidence of childhood diabetes in Europe. Lancet 355: 873–876 [PubMed ] [Google Scholar ] The EURODIAB Substudy 2 Study Group 1999. Vitamin D supplement in early childhood and risk of Type I (insulin-dependent) diabetes mellitus. Diabetologia 42: 51–54 [PubMed ] [Google Scholar ] The EURODIAB Substudy 2 Study Group 2001. Rapid early growth is associated with increased risk of childhood type 1 diabetes in various European populations. Diabetes Care 25: 1755–1760 [PubMed ] [Google Scholar ] The TRIGR Study Group 2011. The Trial to Reduce IDDM in the Genetically at Risk (TRIGR ) study: Recruitment, intervention and follow-up. Diabetologia 54: 627–633 [PMC free article ] [PubMed ] [Google Scholar ] Vaarala O, Knip M, Paronen J, Hämäläinen A-M, Muona P, Väätäinen M, Ilonen J, Simell O, Åkerblom HK 1999. Cow milk formula feeding induces primary immunization to insulin in infants at genetic risk for type 1 diabetes. Diabetes 48: 1389–1394 [PubMed ] [Google Scholar ] Vaarala O, Atkinson MA, Neu J 2008. The “perfect storm” for type 1 diabetes: The complex interplay between intestinal microbiota, gut permeability, and mucosal immunity. Diabetes 57: 2555–2562 [PMC free article ] [PubMed ] [Google Scholar ] Vaarala O, Ilonen J, Ruohtula T, Pesola J, Virtanen SM, Härkönen T, Koski M, Kallioinen H, Tossavainen O, Poussa T, et al. 2012. Removal of bovine insulin from cow's milk formula and early initiation of β-cell autoimmunity. Arch Pediat Adol Med 10.1001/archpediatrics.2011.1559 [PubMed ] [CrossRef ] [Google Scholar ] Verge CF, Howard NJ, Irwig L, Simpson JM, Mackerras D, Silink M 1994. Environmental factors in childhood IDDM: A population-based case-control study. Diabetes Care 17: 1381–1389 [PubMed ] [Google Scholar ] Virtanen SM, Knip M 2003. Nutritional risk predictors of β cell autoimmunity and type 1 diabetes at a young age. Am J Clin Nutr 78: 1053–1067 [PubMed ] [Google Scholar ] Virtanen SM, Räsänen L, Aro A, Lindström J, Sippola H, Lounamaa R, Toivanen L, Tuomilehto J, Akerblom HK 1991. Infant feeding in Finnish children <7 yr of age with newly diagnosed IDDM. Diabetes Care 14: 415–417 [PubMed ] [Google Scholar ] Virtanen SM, Räsänen L, Ylönen K, Aro A, Clayton D, Langholz B, Pitkäniemi J, Savilahti E, Lounamaa R, Tuomilehto J, et al. 1993. Early introduction of dairy products associated with increased risk of IDDM in Finnish children. Diabetes 42: 1786–1790 [PubMed ] [Google Scholar ] Virtanen SM, Hyppönen E, Läärä E, Vähäsalo P, Kulmala P, Savola K, Räsänen L, Knip M, Åkerblom HK, the Childhood Diabetes in Finland Study Group 1998. Cow's milk consumption, disease associated autoantibodies and Type 1 diabetes mellitus: A follow-up study in siblings of diabetic children. Diabetic Med 15: 730–738 [PubMed ] [Google Scholar ] Virtanen SM, Kenward MG, Erkkola M, Kautiainen S, Kronberg-Kippilä C, Hakulinen T, Ahonen S, Uusitalo L, Veijola R, Simell OG, et al. 2006. Age at introduction of new foods and advanced β-cell autoimmunity in young children with HLA-conferred susceptibility to type 1 diabetes. Diabetologia 49: 1512–1521 [PubMed ] [Google Scholar ] Virtanen SM, Nevalainen J, Kronberg-Kippilä C, Ahonen S, Tapanainen H, Uusitalo L, Takkinen HM, Niinistö S, Ovaskainen M-L, Kenward MG, et al. 2012. Food consumption during childhood and advanced β-cell autoimmunity in young children with HLA-conferred susceptibility to type 1 diabetes: A nested case-control study. Am J Clin Nutr 95: 471–478 [PubMed ] [Google Scholar ] Viskari H, Kondrashova A, Koskela P, Knip M, Hyöty H 2006. Circulating vitamin D concentrations in two neighboring populations with markedly different incidence of type 1 diabetes. Diabetes Care 49: 1458–1459 [PubMed ] [Google Scholar ] Wadsworth EJK, Shield JPH, Hunt LP, Baum JD 1997. A case-control study of environmental factors associated with diabetes in the under 5s. Diabet Med 14: 390–396 [PubMed ] [Google Scholar ] Wen L, Ley RE, Volchkov PY, Stranges PB, Avanesyan L, Stonebraker AC, Hu C, Wong FS, Szot GL, Bluestone JA, et al. 2008. Innate immunity and intestinal microbiota in the development of Type 1 diabetes. Nature 455: 1109–1113 [PMC free article ] [PubMed ] [Google Scholar ] Wenzlau JM, Juhl K, Yu L, Moua O, Sarkar SA, Gottlieb P, Rewers M, Eisenbarth GS, Jensen J, Davidson HW, et al. 2007. The cation efflux transporter ZnT8 (Slc30A8) is a major autoantigen in human type 1 diabetes. Proc Natl Acad Sci 104: 17040–17045 [PMC free article ] [PubMed ] [Google Scholar ] Wilkin TJ 2001. The accelerator hypothesis: Weight gain as the missing link between type 1 and type 2 diabetes. Diabetologia 44: 914–922 [PubMed ] [Google Scholar ] Yeung WC, Rawlinson WD, Craig M 2011. Enterovirus infection and type 1 diabetes mellitus: Systematic review and meta-analysis of observational molecular studies. BMJ 342: d35 [PMC free article ] [PubMed ] [Google Scholar ] Ziegler A-G, Hummel M, Schenker M, Bonifacio E 1999. Autoantibody appearance and risk for development of childhood diabetes in offspring of parents with type 1 diabetes: The 2-year analysis of the German BABYDIAB Study. Diabetes 48: 460–468 [PubMed ] [Google Scholar ] Ziegler A-G, Schmid S, Huber D, Hummel M, Bonifacio E 2003. Early infant feeding and risk of developing Type 1 diabetes-associated autoantibodies. JAMA 290: 1721–1728 [PubMed ] [Google Scholar ] Zipitis CS, Akobeng AK 2008. Vitamin D supplementation in early childhood and risk of type 1 diabetes: A systematic review and meta-analysis. Arch Dis Childr 93: 512–517 [PubMed ] [Google Scholar ]

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