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5 mg rosuvastatin calcium

บทความที่เกี่ยวข้อง 5 mg rosuvastatin calcium

Owner Review : ถ้าเทียบกับ Sylphy และAltis ผมถูกใจ All New MG 5 2021มากกว่า

**บทความนี้เป็นประสบการณ์ส่วนตัวของเจ้าของรถ 2021 MG5 (MG Pilot) และมาจากเว็บไซต์ประเทศจีน ไม่ได้เป็นความเห็นของ

2021 MG5 ความหวังใหม่ MG ไทย คาดเปิดตัวปลายปีนี้ ด้วยราคาไม่เกิน 7 แสน

ช่วงนี้หลาย ๆ คนตามโซเชี่ยล อาจได้ยินข่าวกันหนาหู ว่า MG5 (เอ็มจี5) ใหม่อาจจะเข้ามาในไทย หรือที่ฮือฮากันใน

รู้ข้อดีข้อด้อยก่อนซื้อ MG HS ตัวท็อป

MG HS (เอ็มจี เอชเอส) ถือเป็นรถอเนกประสงค์อีกรุ่นที่ได้รับความนิยมไม่แพ้ MG ZS ของค่ายเอ็มจีเลย ด้วยความโดดเด่นในด้านเทคโนโลยี

ทำงี้ได้ไง MG HS โปรใหม่ไม่มีฝาท้ายไฟฟ้า มีแต่เครื่องฟอกอากาศแทน

ในงาน BIG Motor Sale 2020 ค่ายรถยนต์ MG ได้จัดโปรโมชั่นน่าสนใจให้กับรถ SUV ZS และ HS มาแล้ว ล่าสุด MG

เสียงวิจารณ์โลกโซเชียลไม่ระคาย ทำไม MG ทำยอดขายผงาดผู้นำ

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

ไทยเอาบ้างไหม MG อังกฤษช่วยลูกค้าจ่ายค่ารถไฟฟ้า 3.3 หมื่นบาทกระตุ้นยอดขาย

ความพยายามในการเดินหน้าตลาดรถยนต์ไฟฟ้าในหลายประเทศยังดำเนินการไปอย่างเข้มข้น หนึ่งในนั้นคือเจ้าพ่อรถยนต์ไฟฟ้าอย่าง MG

MG คว้ารางวัลแบรนด์รถยนต์คุ้มค่ายอดเยี่ยม – MG ZS EV รับรางวัลรถใหม่คุ้มค่าสูงสุด

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

2020 MG HS PHEV เทียบ MG HS 1.5X เจาะออพชั่นต่างกันทุกด้าน เพิ่มเงินแค่ 240,000 บาท

เอ็มจี เอชเอส ปลั๊กอินไฮบริด เปิดตัวในราคา 1,359,000 บาท2020 MG HS PHEV (เอ็มจี เอชเอส ปลั๊กอินไฮบริด

รู้ข้อดีข้อเสีย MG V80 ก่อนเป็นเจ้าของ

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

แบงค์บอกต่อ รวมแคมเปญรถดีน่าใช้ปี 2021 MG ZS, MG EP หรือจะ Honda ก็ยังมีนะ

แบงค์บอกต่อ เรามาดูโปรโมชั่นรถยนต์น่าสนใจหลายขนาดจากทางฝั่ง MG (เอ็มจี) ที่มีทั้ง 2021 MG ZS (เอ็มจี

ดูเพิ่มเติม

ส่อง 5 จุดเด่น MG HS ก่อนซื้อ

ค่ายรถยนต์ MG สัญชาติจีนเริ่มต้นบุกเบิกตลาดรถเอสยูวีมาได้สักระยะ ล่าสุดก็เปิดตัว Compact SUV รุ่นล่าสุดอย่าง

MG เปิดบริการรถไฟฟ้าเหมาจ่ายเดือนละ 250 บาท ทำไมเมืองไทยไม่มีแบบนี้บ้าง!!!

MG Motor (เอ็มจี มอเตอร์) แห่งสหราชอาณาจักร เปิดตัวบริการรูปแบบใหม่เพื่อเอาใจลูกค้าผู้ใช้รถยนต์ไฟฟ้าในสหราชอาณาจักร

รีวิว 2020 MG ZS สมาร์ทเอสยูวีที่กวาดยอดขายระดับผู้นำเซกเมนท์

บริษัท เอ็มจี เซลส์ (ประเทศไทย) จํากัด เปิดตัว 2020 เอ็มจี แซดเอส (2020 MG ZS) ออกทำตลาดประเทศไทยทั้งหมด

2020 MG ZS ผ่าน 5 ดาวเต็มความปลอดภัย แต่ยังตามหลัง Toyota Corolla Cross

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

Owner Review : แค่เห็น MG 5ครั้งแรก ก็แทบไม่คิดแล้วว่าจะต้องหารุ่นอื่นมาเปรียบเทียบกัน

**บทความนี้เป็นประสบการณ์ส่วนตัวของเจ้าของรถ 2021 MG5 (MG Pilot) และมาจากเว็บไซต์ประเทศจีน ไม่ได้เป็นความเห็นของ

รวม 5 จุดเด่น MG HS PHEV ที่ทำให้คุณต้องซื้อในราคา 1,359,000 บาท

2020 MG HS PHEV (เอ็มจี เอชเอส พีเอชอีวี) เปิดตัวอย่างเป็นทางการแล้ว เคาะราคาที่ 1,359,000 บาท โดยจะเป็นรถปลั้กอินไฮบริดรุ่นแรกของ

MG เตรียมเปิดตัวรถยนต์ไฟฟ้าใหม่ปลายปี 2021 ในทรงแฮทช์แบ็ค ลือคล้าย MG3

MG (เอ็มจี) ในปี 2021 วางแผนที่จะทำการเปิดตัวรถยนต์ไฟฟ้ารุ่นใหม่ปลายปีนี้ ในตัวถังแฮทช์แบ็ค 5 ประตู อาจคล้ายกับ

ไขข้อสงสัยข้อดีข้อเสียก่อนซื้อ MG HS

หลังจาก MG HS รถสไตล์รถครอบครัวจากแบรนด์จีนเปิดตัวก็ได้รับความสนใจล้นหลาม และก็กลายเป็น Compact SUV ที่มียอดขายดีในกลุ่มได้อย่างรวดเร็วด้วยชื่อ

MG ประกาศขึ้นแท่นผู้นำตลาดเอสยูวีในครึ่งปีแรกของปี 2563

MG (เอ็มจี) แบรนด์รถยนต์น้องใหม่ประเทศไทย ประกาศขึ้นแท่นผู้นำตลาดเอสยูวีในครึ่งแรกของปี 2563 ด้วยยอดจำหน่ายรวม

อ่านก่อนซื้อ! MG EXTENDER มีข้อดีกับข้อเสียอย่างไร

และต้องบอกเลยว่า MG กล้าหาญชาญชัยมากที่นำรถกระบะ MG EXTENDER (เอ็มจี เอกซ์เทนเดอร์) เข้ามาขายในประเทศไทย

MG เผยคอนเซปท์สปอร์ตไฟฟ้าคันใหม่ MG Cyberster วิ่งไกล 800 กม.

MG (เอ็มจี) ลอนดอน ได้ทำการเปิดคอนเซปท์รถสปอร์ตคันใหม่ในนาม MG Cyberster แบบเปิดประทุน ก่อนที่จะมีรายละเอียดออกมาในงาน

MG เล็งไทยเป็นฮับอาเซียน ผลิต MG ZS พวงมาลัยซ้าย ส่งออกอินโดนีเซีย-เวียดนาม-มาเลเซีย

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

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

5 สิ่งดี ๆ ในรถยนต์ไฟฟ้า 2021 MG ZS EV ที่อยากให้คุณได้ลองก่อนได้รุ่นผลิตไทย

2021 MG ZS EV (เอ็มจี แซดเอส อีวี) รถอเนกประสงค์พลังงานไฟฟ้าล้วนจาก MG (เอ็มจี) ที่ออกแบบเพื่อตอบโจทย์การใช้ชีวิตสไตล์คนเมือง

2020 MG HS PHEV กับคำถามที่พบบ่อยของระบบปลั้กอินไฮบริด อ่านก่อนคิดจะซื้อ

ดีกว่ารถทั่วไปอย่างไรข้อดีหลัก ๆ คือ สมรรถนะที่แรงขึ้น จากการทำงานของมอเตอร์ไฟฟ้า ที่เสริมแรงให้กับเครื่องยนต์ MG

หลุดภาพ All-New 2021 MG 5 เจนเนอเรชั่นใหม่ สวยสปอร์ตด้วยเอกลักษณ์ดีไซน์ใหม่ล่าสุด

2021 MG 5 (2021 เอ็มจี 5) เจนเนอเรชั่นใหม่เตรียมเปิดตัวออกจำหน่ายในเร็ว ๆ นี้ หลังมีภาพหลุดจากกระทรวงอุตสาหกรรมของประเทศจีนออกมาให้แฟน

แบงค์บอกต่อ ซินเจียยู่อี่ซินนี้ฮวดใช้ ซื้อรถแถมทองรับเทศกาลตรุษจีนกับ MG และ BMW

แต่ละบ้านคงออกจะมาทำการไหว้เจ้าและบรรพบุรุษ หลาย ๆ บ้านก็เป็นวันจ่าย และสำหรับบ้านไหนกำลังมองหารถยนต์สักคันจะใช้ เรามีโปรดี ๆ จาก MG

ไฟเขียว! MG เตรียมเปิดตัวรถสปอร์ตพลังไฟฟ้าปลายปีนี้ รอลุ้นราคาจำหน่าย

รถต้นแบบ MG E-Motionรถสปอร์ตพลังงานไฟฟ้ารุ่นแรกของ MG (เอ็มจี) ยุคใหม่เตรียมเปิดตัวครั้งแรกในโลกภายในช่วงปลายปีนี้

ฟันธง! 2021 Haval H6 ในไทยค่าตัวอาจถูกกว่า MG HS เห็นราคาแล้วต้องอึ้ง

2021 Haval H6 และ 2020 MG HS2021 Haval H6 (2021 ฮาวาล เอช6) จะเผยโฉมอย่างเป็นทางการในประเทศไทยในช่วงปลายเดือนมีนาคมนี้

7 เรื่องควรรู้ก่อนซื้อ MG HS 2019

MG HS C ราคา 919,000 บาท, MG HS D ราคา 1.019 ล้านบาท และรุ่นตัวทํอป MG HS X ราคา 1.119 ล้านบาท2.MG HS

รูปภาพที่เกี่ยวข้อง 5 mg rosuvastatin calcium

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รีวิวโพสต์ 5 mg rosuvastatin calcium

Sir , the following are the prescriptions and medicines for both 1.T. Depakote 250 mg: 902.T. Quetipin 25 mg: 453.T. Glycomet SR 500 mg: 454.T. Urimax 0.4 mg: 455.Rosuvastatin Calcium Clopodogrel (RDL-C 5 mg): 456.Clopilet 75 mg: 457.Storvas 10: 45

Generic #Crestor available - #rosuvastatin calcium tablets in 5,10,20 and 40 mg strengths from Sandoz #cholesterol

I’ve been fortunate and haven’t had any noticeable side effects with it; my mom takes it as well and is super sensitive to where it knocks her out hard.I hear you on side effects. My Bisoprolol gives me a lot of issues when I stand, and my other medications have some as well.

I feel like a zombie from the three blood pressure medications I'm prescribed. 100 mg Metoprolol Succ ER twice a day, 5 mg Amlodipine Besylate, 100 mg Losartan Potassium once a day. And my 5 mg Rosuvastatin Calcium. I am always exhausted.

Pls share contact details & prescription

A quien pueda interesar: tengo 6 cajas de CRESTOR rosuvastatin calcium de 5 mg

Biocon Ltd announced today that it has received European approvals for its Rosuvastatin Calcium 5 mg

*प्रधानमंत्री भारतीय जन औषधि केंद्र"कुछ दवाओं का साधारण बाज़ार मूल्य और जन औषधि मूल*1) Rosuvastatin 20 mg**साधारण बाज़ार मूल्य Rs. 289.00**जनऔषधि मूल्य Rs 27.002) Ramipril 5 mgबाज़ार मुल्य: Rs. 78**जन औषधि मुल्य4) Calcium and calcitrol tablet*Rs.80.00*Rs.14.0

For example: /CRESTOR® (rosuvastatin calcium) Dosage | 5 mg, 10 mg, 20 mg, 40 mg. Every time the dosage is increased twice as much. It's very good for fine tuning.

Be it High BP or High cholesterol or High LP(A) or High arterial Plaques determining optimum treatment is allways a challenge . Without further damaging our body or organs it is important to know target ,we are trying to achieve & technique to monitor it

รีวิว Q&A 5 mg rosuvastatin calcium

Are there any side effects of Crestor 5mg?

Yes : Read this Crestor (rosuvastatin calcium) is a statin drug, that works by slowing the production of cholesterol by the body, used to lower cholesterol and fats (triglycerides ) in the blood and is used to reduce the chances of developing problems like heart disease and strokes that can be caused, in part, by high cholesterol levels. It is often recommended to use Crestor in conjunction with a diet low in fats and cholesterol, and exercise (about 30 min. per day). Crestor is available in generic form. Side effects of Crestor include headache , depression , muscle aches or pains, joint pain , sleep problems (insomnia or nightmares ), constipation , nausea , stomach pain, indigestion , or diarrhea . Infrequent but serious side effects of Crestor include rhabdomyolysis (muscle damage or destruction) that can lead to acute renal failure and liver damage. Crestor is available in tablets of 5, 10, 20 and 40 mg strengths. Usual dose ranges from 5 to 20 mg per day. Crestor should be taken with water once a day at the same time of day, with or without food. Dosage may be adjusted depending on what medicines the patient is already taking. Crestor may interact with birth control pills, cimetidine, blood thinners, spironolactone, niacin, or other "statin" medications. Tell your doctor all medications and supplements you use. Crestor should not be taken during pregnancy or during breastfeeding because of potential birth defects. Our Crestor Side Effects Drug Center provides a comprehensive view of available drug information on the potential side effects when taking this medication. This is not a complete list of side effects and others may occur. Call your doctor for medical advice about side effects. You may report side effects to FDA at 1-800-FDA-1088. Crestor Consumer Information Get emergency medical help if you have any of these signs of an allergic reaction: hives; difficulty breathing; swelling of your face, lips, tongue, or throat. Stop taking rosuvastatin and call your doctor at once if you have any of these serious side effects: unexplained muscle pain, tenderness, or weakness; confusion, memory problems; fever, unusual tiredness, and dark colored urine; swelling, weight gain, urinating less than usual or not at all; increased thirst, increased urination, hunger, dry mouth, fruity breath odor, drowsiness, dry skin, blurred vision, weight loss; or nausea, upper stomach pain, itching, loss of appetite, dark urine, clay-colored stools, jaundice (yellowing of the skin or eyes). Less serious side effects may include: headache, depressed mood; mild muscle pain; joint pain; sleep problems (insomnia), nightmares; constipation; mild nausea; or stomach pain or indigestion. This is not a complete list of side effects and others may occur. Call your doctor for medical advice about side effects. You may report side effects to FDA at 1-800-FDA-1088. Read the entire detailed patient monograph for Crestor ( Rosuvastatin Calcium ) Learn More » Crestor Professional Information SIDE EFFECTS The following serious adverse reactions are discussed in greater detail in other sections of the label: Rhabdomyolysis with myoglobinuria and acute renal failure and myopathy (including myositis ) [see WARNINGS AND PRECAUTIONS ] Liver enzyme abnormalities [see WARNINGS AND PRECAUTIONS ] Clinical Studies Experience Because clinical studies are conducted under widely varying conditions, adverse reaction rates observed in the clinical studies of a drug cannot be directly compared to rates in the clinical studies of another drug and may not reflect the rates observed in clinical practice. In the CRESTOR controlled clinical trials database (placebo or active-controlled) of 5394 patients with a mean treatment duration of 15 weeks, 1.4% of patients discontinued due to adverse reactions. The most common adverse reactions that led to treatment discontinuation were: myalgia abdominal pain nausea The most commonly reported adverse reactions (incidence ≥ 2%) in the CRESTOR controlled clinical trial database of 5394 patients were: headache myalgia abdominal pain asthenia nausea Adverse reactions reported in ≥ 2% of patients in placebo-controlled clinical studies and at a rate greater than placebo are shown in Table 1. These studies had a treatment duration of up to 12 weeks. Other adverse reactions reported in clinical studies were abdominal pain, dizziness, hypersensitivity (including rash, pruritus , urticaria , and angioedema ) and pancreatitis . The following laboratory abnormalities have also been reported: dipstick-positive proteinuria and microscopic hematuria [seeWARNINGS AND PRECAUTIONS ]; elevated creatine phosphokinase, transaminases, glucose, glutamyl transpeptidase, alkaline phosphatase, and bilirubin; and thyroid function abnormalities. In the METEOR study, involving 981 participants treated with rosuvastatin 40 mg (n=700) or placebo (n=281) with a mean treatment duration of 1.7 years, 5.6% of subjects treated with CRESTOR versus 2.8% of placebo-treated subjects discontinued due to adverse reactions. The most common adverse reactions that led to treatment discontinuation were: myalgia, hepatic enzyme increased, headache, and nausea [see Clinical Studies ]. Adverse reactions reported in ≥ 2% of patients and at a rate greater than placebo are shown in Table 2. In the JUPITER study, 17,802 participants were treated with rosuvastatin 20 mg (n=8901) or placebo (n=8901) for a mean duration of 2 years. A higher percentage of rosuvastatin-treated patients versus placebo-treated patients, 6.6% and 6.2%, respectively, discontinued study medication due to an adverse event, irrespective of treatment causality. Myalgia was the most common adverse reaction that led to treatment discontinuation. In JUPITER, there was a significantly higher frequency of diabetes mellitus reported in patients taking rosuvastatin (2.8%) versus patients taking placebo (2.3%). Mean HbA1c was significantly increased by 0.1% in rosuvastatin-treated patients compared to placebo-treated patients. The number of patients with a HbA1c > 6.5% at the end of the trial was significantly higher in rosuvastatin-treated versus placebotreated patients [see WARNINGS AND PRECAUTIONS and Clinical Studies ]. Adverse reactions reported in ≥ 2% of patients and at a rate greater than placebo are shown in Table 3. Pediatric Patients With Heterozygous Familial Hypercholesterolemia In a 12-week controlled study in boys and postmenarcheal girls 10 to 17 years of age with heterozygous familial hypercholesterolemia with CRESTOR 5 to 20 mg daily [see Use in Specific Populations and Clinical Studies ], elevations in serum creatine phosphokinase (CK) > 10 x ULN were observed more frequently in rosuvastatin compared with placebo-treated children. Four of 130 (3%) children treated with rosuvastatin (2 treated with 10 mg and 2 treated with 20 mg) had increased CK > 10 x ULN, compared to 0 of 46 children on placebo. Postmarketing Experience The following adverse reactions have been identified during postapproval use of CRESTOR: arthralgia , fatal and non-fatal hepatic failure, hepatitis , jaundice , thrombocytopenia , depression, sleep disorders (including insomnia and nightmares), peripheral neuropathy and gynecomastia . Because these reactions are reported voluntarily from a population of uncertain size, it is not always possible to reliably estimate their frequency or establish a causal relationship to drug exposure. There have been rare reports of immune-mediated necrotizing myopathy associated with statin use [see WARNINGS AND PRECAUTIONS ]. There have been rare postmarketing reports of cognitive impairment (e.g., memory loss, forgetfulness, amnesia , memory impairment, confusion) associated with statin use. These cognitive issues have been reported for all statins . The reports are generally nonserious, and reversible upon statin discontinuation, with variable times to symptom onset (1 day to years) and symptom resolution (median of 3 weeks)

My mother and my stepmother are very sick. My mother has Alzheimer’s and my stepmother has ALS. Can CBD oil help cure them?

What a miserable situation for you and your loved ones. I'm so sorry. I apologize for taking so long to get back to you, but I wanted to be sure I had the latest information that's available. I’ve read many dozens of papers. The information is summarized below. I’m including links to a few of the most recent papers that are readily available, in case you want to get into more of the details. I can always provide more references, if you’d like. (Note: Always read the full paper — never rely on just the abstract. It’s amazing how misleading an abstract can be.) Sadly, there is no cure for either disease. However, there is a lot of research into treatments for both diseases, and you might wish to see if there are any clinical trials near you. Since I don't know where you live, I just pulled up everything for each disease. You can filter by location. Amyotrophic lateral sclerosis: Search of: Recruiting, Not yet recruiting Studies | Amyotrophic Lateral Sclerosis - List Results - ClinicalTrials.gov Alzheimer's: Search of: Recruiting, Not yet recruiting Studies | Alzheimer Disease - List Results - ClinicalTrials.gov If you need help navigating the clinical trials website, figuring out how to pull up trials near you or of a particular kind of treatment and/or phase, interpreting its listings, etc., let us know. Back to your question: I would be very hesitant to try CBD oil for either of your loved ones, even to treat some of their symptoms. Their brains are very fragile, you have no way of knowing how they'll react or what harm might be done ... and you'll have no way of knowing what, exactly, you're giving them. There are currently dozens, if not hundreds, of producers and sellers of CBD oils active in the market, and their number is increasing rapidly. They vary from individuals who prepare oils on a small scale for family and (Facebook) friends to compounding pharmacies, pharmaceutical companies, and licensed cannabis producers. CBD products are rarely manufactured under good manufacturing practices (GMP) and are not subject to regulations governing labeling, purity, and reliability. In other words, currently, there is no guarantee of consistency between products, or even between different lots produced by the same manufacturer. Note, especially, that studies have identified the intentional addition of contaminants, such as pesticides, metal particles, and synthetic cannabinoids, to increase the yield of a product, and the unintentional presence of other contaminants that entered the plant, such as molds, bacteria, or aflatoxins. CBD Oil: All the Rage, But Is It Safe & Effective? CBD Oil: All the Rage, But Is It Safe & Effective? WebMD 2018. The Trouble with CBD Oil Hazekamp A. The trouble with CBD oil. Medical cannabis and cannabinoids. 2018;1(1):65-72. Cannabis sativa L. is an ancient medicinal plant from which over 100 cannabinoids are extracted. Among them, the most studied are Δ9–tetrahydrocannabinol (Δ9–THC), a psychoactive compound that causes the marijuana "high," and cannabidiol (CBD), a non-psychotropic phytocannabinoid. Most cannabinoids -- both endogenous and plant-derived -- exert their action by interacting with G protein-coupled cannabinoid receptors type 1 (CB1), which is widely expressed in the nervous system, and type 2 (CB2), which is mainly expressed in immune cells. However, current evidence suggests that CBD does not directly interact with the cannabinoid receptors except in vitro at supraphysiological concentrations; but it can indirectly act as agonist or antagonist of the CB1 receptor, antagonizing the pharmacological effects of CB1 agonists such as Δ9-THC and AEA. In fact, depending on the dosage and the clinical condition, potential CBD activity over CB1 (agonism or antagonism) results in different outcomes -- either therapeutic or harmful. CBD directly affects the activity of other receptors such as serotonin receptors [5-HT], opioid receptors, and non-endocannabinoid G protein-coupled receptors (GPCRs), as well as classical ion channels, transporters, and enzymes. This makes CBD's effects on the human body and brain highly unpredictable. Both the general population, as well as much of the healthcare community, apparently assume cannabis and cannabis-derived substances such as CBD are safe, due to marijuana's long history of recreational use. For CBD specifically, safety is further assumed because CBD is currently broadly available and lacks the euphoric, psychoactive properties of Δ9–THC. In point of fact, however, there is very limited information available about CBD, including its adverse effects on the body and brain, even when carefully prepared and characterized products are used. Only epilepsy, cancer-related pain, and multiple sclerosis are recognized by any international federal agencies as indications for CBD. Products include Sativex® (nabiximols), an oromucosal spray containing CBD plus THC, and Epidiolex®, an oral solution containing a plant-derived, pharmaceutical-grade isolated CBD. Sativex® is not yet approved in the United States but is available in some other countries for the treatment of spasticity related to multiple sclerosis. Epidiolex® recently received FDA approval for treating the rare, treatment-resistant seizure disorders, Lennox-Gastaut and Dravet syndromes. The FDA has very stringent requirements for proving that a product is safe and effective for use in treating a given disorder, or even a given symptom in patients with a disorder. Other than Epidiolex for treatment-resistant seizure disorders, the FDA has not approved any other CBD products for the diagnosis, cure, mitigation, treatment, or prevention of any other disease. Even when CBD therapy is approved for a given disorder, it does not always work for all patients. Some studies have used CBD-enriched cannabis extracts, which contain Δ9-THC that may have played a role. Even controlled clinical trials investigating pure CBD involved mostly short treatment periods and short follow-up periods, which will not reveal the possible long-term effects of CBD and possible developmental adverse effects. Hence, more clinical trials, with larger population sizes and longer chronic pure CBD administration, are warranted in order to clarify under which conditions it is worthwhile and safe to use. In addition, it is still unknown how CBD acts on hormones, hepatic enzymes, and drug transporters, along with its interactions with other drugs (see below.) CBD-based consumer products have entered the U.S. market spurred in part by the 2018 "Farm Bill", which effectively legalized hemp (which is any cannabis plant that has <0.3% THC) for agricultural purposes. CBD-infused products are becoming available in many consumer settings including gas stations, health spas, retail pharmacies, bakeries, and coffee shops. FDA has clearly stated that cannabis- or hemp-derived CBD products that are marketed with claims of a therapeutic benefit remain under the purview of the FDA and require approval. FDA further stated that no food products containing CBD can enter inter-state commerce, CBD is not a safe food additive, and that CBD or other cannabis-derived compounds cannot be considered dietary supplements as they are or contain pharmacologically active ingredients. Nevertheless, without clear enforcement, numerous products, primarily containing CBD extracted from industrial hemp, are being sold in concentrations ranging from very low (e.g., 20 mg soft drinks) to potentially super-therapeutic doses that exceed FDA-approved dosing for seizure disorders (e.g., gummies with 1500 mg CBD). There seems to be a great deal of confusion about the differences between regulatory scrutiny for dietary supplements and those for prescription drugs and over-the-counter medications. In the US, carefully designed and conducted studies have to demonstrate safety and efficacy of a prescription drug to the FDA prior to market approval. Before a prescription drug or over-the-counter drug can be sold, there has to be clear evidence of a positive effect, it must be thoroughly tested for safety, and all side effects found must be reported to the FDA. However, the same level of government review and approval are not required for dietary supplements before they are put on the market. There has been no FDA evaluation regarding whether a dietary supplement is safe and effective to treat a particular disease, what the proper dosage is, how it could interact with other drugs or foods, or whether it has dangerous side effects or other safety concerns. If the manufacturer intends to make claims that a given supplement treats diseases such as Alzheimer's when it is put on the market, those claims must be substantiated by competent and reliable scientific evidence before they are made. The substantiation requirement is not generally reviewed by the FDA prior to marketing. The FDA can only take enforcement action against unsubstantiated or false claims once the product is already on the market, and then it is usually done in response to complaints of serious adverse effects (which the layman often does not realize are associated with the product.) It takes time for the FDA to take enforcement action, so snake oil types may get away with selling useless, or even harmful products for a long time before the FDA catches up with them. (I've seen this happen all the time when it comes to products touted as treatments for Alzheimer's, discussed on dementia caregiver discussion forums.) Some CBD products are being marketed with unproven medical claims. Under federal law, it is illegal to market CBD products this way. The FDA has started warning companies selling CBD products they claim are intended to prevent, diagnose, treat, or cure serious diseases, such as cancer, Alzheimer's disease, psychiatric disorders and diabetes, to cease and desist. Other products on the market add CBD to a food or label CBD as a dietary supplement. Under federal law, it is illegal to market CBD this way. See, e.g.: What to Know About Products Containing Cannabis and CBD What You Need to Know (And What We’re Working to Find Out) About Products Containing Cannabis or Cannabis-derived Compounds, Including CBD. US Food & Drug Administration, as of 07/17/2019 Warning Letters and Test Results for Cannabidiol-Related Products Warning Letters and Test Results for Cannabidiol-Related Products. US Food & Drug Administration, as of 10/22/2019 Note, however, that much of the "marketing" is done by word of mouth on social media, without the manufacturer making any claims at all. But!!! you often have no idea who is actually posting those glowing reviews of CBD oil on discussion forums, Facebook, Amazon, etc. There were and are clearly plenty of trolls on the Alzheimer's Association discussion forum claiming wonderful benefits for all sorts of dubious products. Other times, people may be referring to scientific papers that state CBD is "good" for a given disease when, if you actually read the full paper and pay attention to the details, the evidence is usually exclusively derived from preclinical studies -- i.e., studies done in cell and tissue culture, or in animal models of the disease. Those of you who have been in the caregiving trenches for any length of time are painfully aware that none of the drugs that have appeared so very promising in animal models of Alzheimer's have successfully made it through clinical trials in humans. I'm not all that familiar with studies on ALS, but I do know that most of those involving CBD were done in mice, genetically engineered to carry the human gene for mutant SOD1; and while they may provide interesting insights, they cannot possibly be used as proof that CBD will affect a human in the same way. The only evidence you can rely on when it comes to evaluating new treatments for human diseases are studies done in humans using carefully designed and controlled protocols, preferably double-blind, placebo-controlled studies, such as many of the clinical trials listed at http://clinicaltrial.gov . . Now that Epidiolex® is approved, it is likely that off-label prescriptions will increase. It is even more likely that non-prescription CBD products will be assumed to be completely innocuous by the general public. It is essential that physicians and patients understand that CBD, like any other medication, is not appropriate for every individual or every disease and that it has side effects that are not negligible and must be considered prior to use. During its review of the request for approval for Epidiolex®, the FDA identified certain serious safety risks, including the potential for liver injury. These are risks that can be managed when an FDA-approved CBD drug product given for an FDA-approved application is taken under medical supervision, but it is less clear how these risks might be managed when CBD is used far more widely, without medical supervision and not in accordance with FDA-approved labeling. The effects of the cumulative exposure if people access CBD across a broad range of consumer products -- e.g., in lip balms, beverages, edibles, topicals, essential oils, vapors, skin creams, etc, used on the same day, or used daily for weeks or months -- are unknown. Most studies on humans have involved very few patients and durations between two weeks and four months. Only one clinical study lasted longer, i.e., a multicenter, open-label Epidiolex® study, which was conducted for one year in patients with epilepsy. Additional studies are needed to analyze long-term safety effects in humans to establish toxicologic parameters if CBD has an effect on endocrine hormones and immune system biomarkers. In fact, even when Epidiolex® is being considered for FDA-approved applications, a careful case-to-case evaluation on the risk/benefit balance must be made. The studies submitted to gain FDA approval showed that many severe adverse effects are possible (see below). However, in the most serious cases of treatment-resistant epilepsy in children, repetitive infantile seizures can cause severe developmental, cognitive, and motor impairment. These may be more detrimental than the adverse effects and possible neurodevelopmental implications of CBD; hence, CBD may be a therapeutic option in these cases. When considering trying CBD for other patients and/or indications, the most important consideration is whether or not there is sufficient scientific data that CBD is efficacious in treating a patient's disease or condition. The field is changing rapidly, but proof of efficacy is currently limited to CBD as an anti-epileptic. Factors that could contribute to CBD efficacy and/or adverse events in patients with other disorders include CBD potency, amount and frequency of use, route of administration (vaporized, transdermal, oral), concurrent use of other drugs (both legal and illicit), drug-drug interactions, and any co-morbidities. Route of administration can have a huge impact on the bioavailability and pharmacokinetics of the active ingredients. The considerable variability in CBD formulations (tablets, oromucosal spray, oral capsules, oral solutions, vaporized cannabis plant material, powder in oil, and CBD-THC products), and the wide CBD dose range (18- 1500 mg) will have unknown effects on CBD efficacy and adverse events. Research is still needed on larger cohorts of patients, and on the impact of long-term exposure to CBD on genotoxicity and cytotoxicity, hormones, and the immune system. The effects of CBD on special populations (e.g., the elderly, those with neurological disorders, children, adolescents, and pregnant and lactating women) are unknown. (Just FYI, some cannabis products are also being marketed as pet food and health products for animals. The FDA has not approved cannabis for any use in animals, and the safety of CBD use in animals, including pets, is unknown.) . Adverse effects Due to the greatly increased interest in CBD oil, scientists have been pulling together reliable information from preclinical and clinical studies. A review by Huestis et al that was published last month (October 2019) says: "CBD is not risk-free. In animals, CBD [adverse events] included developmental toxicity, embryo-fetal mortality, central nervous system inhibition and neurotoxicity, hepatocellular injuries, spermatogenesis reduction, organ weight alterations, male reproductive system alterations, and hypotension, although at doses higher than recommended for human pharmacotherapies. Human CBD studies for epilepsy and psychiatric disorders reported CBD-induced drug-drug interactions, hepatic abnormalities, diarrhea, fatigue, vomiting, and somnolence." The paper includes a table of all adverse effects reported in animal studies and in clinical trials. In the human epilepsy clinical trials (which led to FDA approval, remember), moderate adverse events included somnolence, fatigue, lethargy, sedation, decreased or changes in appetite, diarrhea, transaminases increase, pyrexia, convulsions, gastrointestinal disturbances, irritability, vomiting, ataxia, abnormal behavior, rash, and/or upper respiratory tract infection. Severe adverse effects included liver abnormalities, convulsions, status epilepticus, elevated alanine aminotransferase (ALT) concentrations, elevated aspartate aminotransferase (AST) concentrations, increased γ-glutamyltransferase concentrations, worsening chronic cholecystitis, pyrexia, maculopapular rash, diarrhea, weight loss, thrombocytopenia, hyperammonaemia, constipation, and hepatotoxicity. I'm used to seeing very low percentages of study participants suffering from adverse effects in clinical trials, but the percentages reported for epilepsy were appalling. Long-term (1 year) CBD safety and efficacy were evaluated in children and adults who were taking antiepileptic drugs. Twenty-four percent of 607 patients in the safety dataset withdrew, primarily due to failed efficacy and adverse effects. Adverse events were reported in 88% of all patients, and severe adverse effects such as convulsions and status epilepticus were reported for 33% of patients. For all clinical trials, including short- and long-term epilepsy trials, adverse events were reported in 47% to 94% of all participants. Cannabidiol Adverse Effects and Toxicity Huestis MA, Solimini R, Pichini S, Pacifici R, Carlier J, Busardò FP. Cannabidiol Adverse Effects and Toxicity. Current neuropharmacology. 2019 Oct 1;17(10):974-89. Now, these were very sick patients and I'm guessing side effects might be much milder in other, healthier patient populations. But Alzheimer's and ALS patients are very sick, too, and the adverse effects they might experience are unpredictable. All of the epilepsy patients were on antiepileptic drugs including clobazam, valproic acid, levetiracetam, lamotrigine, stiripentol, rufinamide, topiramate, and felbamate; and CBD-drug interactions have been reported to significantly change the levels of some of these drugs. Alzheimer's and ALS patients are often on a number of drugs -- including antiepileptics for various indications -- and CBD clearly has the potential to interfere with at least some, if not many, of them, in unpredictable ways. And on the other hand, the epilepsy patients in the clinical trials were taking CBD products that were made under strict GMP guidelines and whose properties were well characterized. You are talking about using CBD products that are not manufactured under any sort of government oversight, whose composition is unknown and likely to be highly variable, and which may be intentionally adulterated with pesticides, metal particles, and synthetic cannabinoids or accidentally contaminated with molds, bacteria, or aflatoxins. And, as an aside, I encourage anyone considering trying CBD oil (or medical marijuana) on a child to read: https://kclpure.kcl.ac.uk/portal/files/101688792/Cannabinoid_Based_Therapies_and_SCHONHOFEN_Accepted16July2018_GREEN_AAM.pdf Schonhofen P, Bristot IJ, Crippa JA, Hallak JE, Zuardi AW, Parsons RB, Klamt F. Cannabinoid-based therapies and brain development: potential harmful effect of early modulation of the endocannabinoid system. CNS drugs. 2018 Aug 1;32(8):697-712. . Drug-drug interactions The human genome carries 57 genes encoding active cytochrome P450 (CYP) enzymes. About 6-8 of these genes encode CYP enzymes active in the metabolism of clinically used drugs. A large majority of these genes are polymorphic and alleles causing defective, diminished, qualitatively altered or increased drug metabolism have been described. This variation is of importance for explaining interindividual differences in drug metabolism, drug efficacy and adverse drug reactions. Because of the major function for metabolism of exogenous compounds in the hepatic detoxifications processes, these polymorphisms do not cause any major alterations in the phenotype of the individual, and so their presence is difficult to detect. In the human liver, CYP2C9, CYP2C19, CYP2D6, CYP1A2, and CYP3A4 are responsible for the oxidative metabolism of most xenobiotic substrates. CYP3A4 is one of the most abundant enzymes in the liver and intestine, and is not only responsible for the metabolism of a large number of drugs, but also of endogenous compounds, such as prostaglandins, steroid hormones, and fatty acids. Because CBD is metabolized in the liver and gut by CYP3A4 and CYP2C19, the potential for CBD interactions with commonly used drugs is high. For example, approximately 60% of clinically prescribed drugs are metabolized via CYP3A4. Oral CBD undergoes extensive first-pass metabolism via CYP3A4, with a bioavailability of 6%. Following single doses in humans, the CBD half-life is about 1 to 2 days. Various drugs such as ketoconazol, itraconazol, ritonavir, and clarithromycin inhibit CYP3A4, which leads to slower CBD degradation and consequently to effectively higher CBD doses that are pharmaceutically active for longer periods. In contrast, phenobarbital, rifampicin, carbamazepine, and phenytoin induce CYP3A4, causing reduced CBD bioavailability. Metabolic drug-drug interactions are possible between CBD and enzyme substrates, inhibitors, or inducers such as immunosuppressants, chemotherapeutics, antidepressants, antipsychotics, opioids, benzodiazepines, z-hypnotics, statins, calcium channel blockers, protease inhibitors, cimetidine, phenytoin, carbamazepine, topiramate, phenobarbital, rifampicin, efavirenz, pioglitazone, antidepressants, antiepileptics, proton pump inhibitors, clopidogrel, propranolol, carisoprodol, cyclophosphamide, warfarin, fluvoxamine, fluoxetine, fluconazole, rifampin, St. John's Wort, celecoxib, sulfonylureas, losartan, naproxen, rosuvastatin, valsartan, omeprazole, diclofenac, and risperidone, among others. Drug–drug interactions are also possible between CBD and drugs that bind to secondary metabolism or drug transport proteins (e.g., p-glycoprotein), such as acetaminophen, propofol, mycophenolate, valproic acid, haloperidol, ezetimibe, lovastatin, simvastatin, valproate, imatinib, methotrexate, mitoxantrone, nitrofurantoin, prazosin, dipyridamole, paclitaxel, digoxin, telmisartan, glyburide, ketoconazole, and rosiglitazone, among others. A very recent review, by Brown and Winterstein (July 2019), focused on drug-drug interactions. Anyone who is using or considering using CBD oil should download this paper, and check all of the drugs you're taking (including OTC medicines such as acetaminophen and ibuprofen) against the tables of drug-drug interactions in the paper. Potential Adverse Drug Events and Drug–Drug Interactions with Medical and Consumer Cannabidiol (CBD) Use Brown JD, Winterstein AG. Potential Adverse Drug Events and Drug–Drug Interactions with Medical and Consumer Cannabidiol (CBD) Use. Journal of clinical medicine. 2019 Jul;8(7):989. Also note: Drug-drug interactions may lead some patients to believe that CBD is effective for a given application when, in fact, an improvement may be due to another medicine that the patient has been taking. For example, a randomized, placebo-controlled, clinical trial of pure CBD reported a significant reduction in total seizures of all types. This sounds impressive. However, the report on this clinical trial did not evaluate possible drug–drug interactions between CBD and clobazam, which 65% of patients enrolled on the study were taking. CBD can increase plasma clobazam concentrations; hence, the beneficial effects of CBD may have arisen indirectly due to the increased pharmacological effects of clobazam, and not as a direct pharmacological effect of CBD itself. Ergo, patients not taking clobazam may see far less benefit from CBD. . CYP enzymes in the brain New evidence has shown that CYP enzymes in the brain are responsible for the oxidative metabolism of exogenous substrates (e.g., xenobiotics, dietary components, and pollutants) and endogenous substrates (e.g., steroids, cholesterol, and bile acids), potentially affecting the drug response independently from hepatic mechanisms. This aspect was rarely mentioned in the papers I read, but the impact can be profound. Drug response is not only linked to brain CYP enzymes, but also indirectly influenced by factors that independently or synergistically affect CYP enzymatic activity: (i) endogenous factors or regulators (e.g., hormones, neurotransmitters, biological clock, or cerebral blood flow); (ii) exogenous factors (e.g., xenobiotics, dietary constituents, substances of abuse, or pesticides); (iii) demographics (e.g., genetics, age, gender, ethnicity or race); and (iv) disease-specific factors (e.g., cancer, epilepsy, psychiatric diseases, neurodegenerative disease, or stroke). Although the hepatic and brain CYP isoforms are broadly identical, functional differences can occur. In contrast to peripheral organs of metabolic competence, the brain is not 'homogeneous' because each region differs in cellular composition, cell density, and function. As a result, the expression of CYP isoforms vary from location to location within the brain. Findings from various studies support the hypothesis that drug-metabolizing enzymes are located at blood–brain interfaces, where they form an 'enzymatic and metabolic barrier'. Predicting the pharmacokinetic properties of a drug might become more complex when co-administering drugs that inhibit P-glycoprotein, including clarithromycin, erythromycin, ritonavir, or verapamil, as well as P-glycoprotein inducers, such as rifampicin and St. John's Wort. In addition, P-glycoprotein substrates overlap with those of CYP3A4 and most P-glycoprotein inhibitors are also inhibitors of CYP3A4 -- as is the case for CBD. As a result, drug interactions could result from the influence on transporter and metabolic mechanisms in the liver or brain. This indicates that CNS drugs should be selected with more caution while considering the brain CYPs. CYP isoforms are now thought to play various roles in psychiatric and neurodegenerative diseases, in addition to their roles in drug metabolism. For example, the polymorphic CYP2D6 is one of the major brain CYP isoforms and has been implicated in neurodegeneration, psychosis, schizophrenia, and personality traits. Neuroimaging studies have recently shown an effect of CYP2D6 polymorphism on brain functions and vulnerability to mental disorder, as well as influencing extrapyramidal adverse effects of neuroleptics and antidepressants. Neuropsychiatric differences have been reported among individuals with genetic variations in CYP2D6, which metabolizes the endocannabinoid anandamide and influences brain function. Another study suggested that the abundant presence of CYPs in selective cell populations has a role in maintaining brain function in psychiatric disorders. Parkinson's is a progressive neurodegenerative disease characterized by loss of dopamine neurons in the substantia nigra. Decreased levels of the CYP2D6 gene translates into a higher risk of developing Parkinson's. In rat models, brain CYP2D catalyzes the conversion of tyramine into dopamine. Therefore, the loss of dopamine due to decreased CYP2D6-activated gene expression in the brain could be a potential factor in the onset of Parkinson's. There is evidence that carrying high-risk alleles or mutation in both CYP17 and CYP19 genes was associated with a fourfold increased risk for Alzheimer's in subjects with Down syndrome. Another study reported that the APP23 mouse model of Alzheimer's presented an abundance of amyloid-β peptides following inhibition of CYP46A1 expression, which resulted in brain cholesterol accumulation and neuronal death, suggesting a neuroprotective role of brain CYP. Pathophysiological implications of neurovascular P450 in brain disorders Ghosh C, Hossain M, Solanki J, et al. Pathophysiological implications of neurovascular P450 in brain disorders. Drug Discov Today. 2016;21:1609–1619. . Is there any information that would lead us to believe that CBD oil might be beneficial to patients with Alzheimer's or ALS? Given public interest in CBD oil, there have been many recent clinical studies on its potential therapeutic effects. However, reviews published as recently as April 2019 concluded that clinical studies conducted to date do not support the popular uses of CBD oil for Parkinson disease, schizophrenia, cancer palliation and treatment, chronic pain and spasticity, depression, anxiety disorder, insomnia, or inflammation. The Trouble with CBD Oil Hazekamp A. The trouble with CBD oil. Medical cannabis and cannabinoids. 2018;1(1):65-72. https://www.researchgate.net/publication/332166483_Cannabidiol_The_Need_for_More_Information_About_Its_Potential_Benefits_and_Side_Effects Hande K. Cannabidiol: The Need for More Information About Its Potential Benefits and Side Effects. Clinical journal of oncology nursing. 2019 Apr;23(2):131-4. There is no evidence that CBD oil will be safe when given to an Alzheimer's patient, let alone helpful in stopping the progression of Alzheimer's. Home - ClinicalTrials.gov does not list any clinical trials on the use of cannabidiol in Alzheimer's patients. AlzForum pulls up 30 hits on cannabidiol and Alzheimer's. I've plowed through the first ten papers, going back some 10 years or so. All discussions on the potential use of this compound are hypothetical, based on studies in cell culture (what happens in cell culture may have nothing whatsoever to do with what happens in the human body) and in animal models, primarily mice (which do not develop Alzheimer's, whether or not they are genetically engineered), with the odd study in rats or zebrafish. See, e.g.: In vivo Evidence for Therapeutic Properties of Cannabidiol (CBD) for Alzheimer's Disease Watt G, Karl T. In vivo evidence for therapeutic properties of cannabidiol (CBD) for Alzheimer's disease. Frontiers in pharmacology. 2017 Feb 3;8:20 The therapeutic potential of the phytocannabinoid cannabidiol for Alzheimer’s disease Karl T, Garner B, Cheng D. The therapeutic potential of the phytocannabinoid cannabidiol for Alzheimer's disease. Behavioural pharmacology. 2017 Apr 1;28(2):142-60. Cannabinoids and Dementia: A Review of Clinical and Preclinical Data Walther S, Halpern M. Cannabinoids and dementia: a review of clinical and preclinical data. Pharmaceuticals. 2010 Aug 17;3(8):2689-708. There is even less evidence for the use of CBD oil with amyotrophic lateral sclerosis (ALS). The only thing I found was a single case report, Nahler (2017), in which the patient -- himself a doctor, in his early 60's -- decided to try CBD oil, along with his riluzole. (It is not clear to me whether his motor neuron disease was properly diagnosed -- I don't know enough about differential diagnosis of this disease.) Some symptoms temporarily improved, but then progression became obvious again. "Eighteen months after onset, speech is almost completely lost, and dysphagia also progressed. However, symptoms of the limbs (weakness, fasciculation, atrophy) worsened much less. It is concluded, that co-medication with CBD may be able to slow down the progression of some but not all symptoms of motor neuron disease." https://pdfs.semanticscholar.org/1a0b/e7c311c19544b76b0ae951403c20dd3839ca.pdf Nahler G. Co-medication with cannabidiol may slow down the progression of motor neuron disease: a case report. J Gen Pract (Los Angel) 2017; 5:4. There are no completed trials on using CBD oil in ALS patients listed on Home - ClinicalTrials.gov (There are two trials recruiting overseas, but their listings don't provide the background that inspired the researchers to do the study.) AlzForum pulls up only 4 hits on cannabidiol and ALS, none of which contain information on studies in humans. PubMed pulls up 12 hits for CBD oil, total, no matter what disorder you're interested in, or what type of study has been done. These do, however, raise some issues of which you need to be aware. Most importantly, cannabis products are widely used by cancer patients, but a survey revealed that very few of them notify their doctors that they do. That is extremely foolish -- the doctors are flying blind. If you do decide to try CBD oil for either/both of your loved ones, notify their doctors when you start them on a product, when you change the dosage, when you change your source, and when you discontinue it. Make any changes in medications, whether prescription or OTC, one at a time. If you make multiple changes simultaneously and your loved one's symptoms change, you won't have any idea which treatment was responsible for the change. Keep a journal of all symptoms and all factors that might affect the symptoms of your loved ones -- injuries, infections, stresses of all sorts, even weather extremes -- and also keep track of all treatments, whether prescription, OTC, or nutritional supplements, as well as CBD oil. This is invaluable in helping you figure out if a given treatment is having any effect, positive or negative. You think you'll remember, but trust me, you won't! And remember, adverse effects can be chronic as well as acute. Your loved one may gradually develop an adverse reaction to the CBD weeks or even months after you start her on it.

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    ลำโพงด้านหน้าของMG 5มีอะไรบ้าง

    Chatchai Srikham

    มีลำโพงด้านหน้าและรุ่นย่อยของMG 5 ได้แก่

    อ่านเพิ่มเติม
  • Q

    กล้องส่องภาพด้านหลังของMG 5มีอะไรบ้าง

    มีให้เธอเสมอ

    มีกล้องส่องภาพด้านหลังและรุ่นย่อยของMG 5 ได้แก่

    อ่านเพิ่มเติม
  • Q

    กระจกไฟฟ้าด้านหน้าของMG 5มีอะไรบ้าง

    Tee Rayong

    มีกระจกไฟฟ้าด้านหน้าและรุ่นย่อยของMG 5 ได้แก่

    อ่านเพิ่มเติม

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