Fast Five Quiz: Are You Prepared to Face the Obesity Epidemic?

Fast Five Quiz: Are You Prepared to Face the Obesity Epidemic?

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Romesh Khardori, MD, PhD

March 06, 2020

Obesity has become a global public health crisis, with the prevalence increasing rapidly in numerous industrialized and developing nations. Latest reports from the World Health Organization (WHO) estimate that there were 1.9 billion overweight adults and 650 million obese adults in 2016. These statistics represent an obesity prevalence that has tripled since 1975. Given rising rates of obesity worldwide and the potential for serious comorbidities, do you know best practices to prevent and treat obesity? Test yourself with our quick quiz.

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Any views expressed above are the author’s own and do not necessarily reflect the views of WebMD or Medscape.

Cite this: Romesh Khardori. Fast Five Quiz: Are You Prepared to Face the Obesity Epidemic? – Medscape – Mar 06, 2020.

Professor of Endocrinology; Director of Training Program, Division of Endocrinology, Diabetes and Metabolism, Strelitz Diabetes and Endocrine Disorders Institute, Department of Internal Medicine, Eastern Virginia Medical School, Norfolk, Virginia

Disclosure: Romesh Khardori, MD, PhD, has disclosed no relevant financial relationships.

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Fast Five Quiz: Are You Prepared to Face the Obesity Epidemic?

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Trending Clinical Topic: Weight Loss

Trending Clinical Topic: Weight Loss

Trending Clinical Topic: Weight Loss

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Ryan Syrek

January 24, 2020

Each week, we identify one top search term, speculate about what caused its popularity, and provide an infographic on a related condition. If you have thoughts about what’s trending and why, feel free to share them with us on Twitter or Facebook.

The increased interest in this week’s top trending clinical topic is linked to new data about the obesity epidemic, recommendations about diet, and a warning from the US Food and Drug Administration (FDA). A study that was recently published in the New England Journal of Medicine found that nearly half of all Americans will have obesity by 2030. The obesity rate is predicted to rise above 50% in 29 states, with no state having a prevalence below 35%. A separate review, published in Current Treatment Options in Gastroenterology , suggests that the obesity epidemic and the rise of related chronic conditions correspond with the increased intake of ultra-processed food. The authors stress that clinicians can play a role by using key strategies.

In regard to healthy eating strategies, the Mediterranean diet was again named the best overall in the U.S. News & World Report annual rankings. Last year it shared the title with the DASH (Dietary Approaches to Stop Hypertension) diet, which placed second this year along with the Flexitarian diet. WW, formerly Weight Watchers, was named the best diet for weight loss, with volumetrics and a vegan diet tying for second place. A new study suggests that another dietary strategy to prevent obesity may involve milk. Research published in the American Journal of Clinical Nutrition found that the odds of being overweight were substantially lower in children who drank whole milk compared with those who drank reduced-fat milk. However, critics suggest that confounding factors were not properly considered and that reverse causality is just as plausible as any other explanation for the findings.

In more encouraging news about weight loss, a new study in the Journal of the National Cancer Institute found that women in their 50s who experience sustained weight loss over 10 years are at reduced risk for breast cancer compared with women whose weight remains stable. Women who lost 10 lb (4.5 kg) had a 13% lower risk for breast cancer, those who 20 lb (9 kg) had a 16% reduced risk, and those who lost more than 20 lb (> 9 kg) had a 26% reduced risk.

Finally, the FDA has issued a safety alert regarding the weight-management drug lorcaserin. Results from a clinical trial showed a possible increased risk for cancer. Although the cause is uncertain and lorcaserin has not been conclusively shown to contribute to this risk, patients and providers were advised to consider the potential danger.

In addition to being a popular New Year’s resolution, a surge in news about weight loss helped to make it this week’s top trending clinical topic.



Read more about obesity.

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Cite this: Ryan Syrek. Trending Clinical Topic: Weight Loss – Medscape – Jan 24, 2020.

Senior Editor, Medical Students, Medscape Drugs & Diseases

Disclosure: Ryan Syrek has disclosed no relevant financial relationships.

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Fast Five Quiz: Confronting Obesity

Fast Five Quiz: Confronting Obesity

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Romesh Khardori, MD, PhD

September 20, 2019

A Medscape poll found that more than one third of healthcare providers (HCPs) do not consider obesity to be a disease state. Only 6% of respondents indicated that obese patients receiving interventions often or always succeed at long-term weight management; however, less than a quarter answered that they routinely offer counseling, and only about 6% recommend surgery for weight loss. Worldwide, obesity has nearly tripled since 1975, with more than 650 million individuals now considered obese.

Given the vast number of obese persons and the persistent challenges, misconceptions, and frustrations experienced by both patients and HCPs, an understanding of best practices for confronting obesity is crucial. Are you familiar with the latest guidelines and advice on how to manage the care of patients who are obese? Test yourself with this short quiz.

Medscape © 2019 WebMD, LLC

Any views expressed above are the author’s own and do not necessarily reflect the views of WebMD or Medscape.

Cite this: Romesh Khardori. Fast Five Quiz: Confronting Obesity – Medscape – Sep 20, 2019.

Professor of Endocrinology; Director, Training Program, Division of Endocrinology, Diabetes and Metabolism, Strelitz Diabetes Center(Endocrine and Metabolic Disorders) , Department of Internal Medicine, Eastern Virginia Medical School, Norfolk, Virginia

Disclosure: Romesh Khardori, MD, PhD, has disclosed no relevant financial relationships.

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Obesity, FTO, and Type 2 Diabetes

Obesity, FTO, and Type 2 Diabetes

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The first report linking the FTO (fat mass and obesity-associated) gene (synonyms KIAA1752, MGC5149, ALKBH9) and obesity came from a genomewide association study linking FTO variants with type 2 diabetes in a European population. [1] The connection between FTO and diabetes was lost after correcting for body-mass index, suggesting that FTO -mediated susceptibility to type 2 diabetes was driven through a relationship between FTO and obesity.

Numerous studies have since confirmed the association of FTO with obesity in European populations. [2, 3, 4, 5] Although the strength of this association in other ethnic populations is not as striking, ample evidence suggests that FTO variants are related to obesity in nonwhite populations as well. [6, 7, 8, 9, 10]

In white populations, people who are homozygous for the at-risk allele of rs9939609 have an approximately 1.7-fold increased risk of obesity and are about 3kg heavier than average. Although the average weight difference attributable to common FTO variants is relatively modest, FTO is among the strongest known common genetic risk factors for obesity.

When FTO was first associated with obesity, its function was unknown; its mechanistic relationship with obesity still remains to be discovered. Bioinformatic analysis indicates that FTO is part of a family of enzymes involved in deoxyribonucleic acid (DNA) repair, fatty acid metabolism, and posttranslational modifications, and functional studies suggest that FTO is involved in nucleic acid demethylation. [11] However, it is unclear if and how nucleic acid demethylation is related to obesity.

Animal studies have demonstrated strong FTO expression in the hypothalamus, especially in the arcuate, paraventricular, dorsomedial, and ventromedial nuclei, all of which are key brain regions for the control of appetite. [11, 12] FTO -deficient mice display postnatal growth retardation, significant reduction in adipose tissue, and increased energy expenditure. [13] Conversely, mice who over-express FTO display increased adiposity and increased food intake, with no change in energy expenditure. [14]

In several human studies, individuals with at least 1 of the FTO obesity risk alleles reported increased food intake, especially of high-energy foods, as well as impaired satiety, [15, 16, 17, 18, 19, 20, 21] but changes in energy expenditure appear to be driven by changes in body mass. [22] Thus, while the exact biologic process linking FTO and obesity is unknown, it is clear that FTO variants mediate obesity by increasing energy input.

Before any clinical applications for genetic testing for FTO variants can be considered, the mechanistic link between FTO and obesity needs to be further clarified. One study showed that a loss-of-function FTO mutation in humans led to postnatal growth retardation, microcephaly, severe psychomotor delay, functional brain deficits, facial dysmorphism, and early lethality, [23] indicating that pharmacologic inhibition of FTO in an attempt to combat a predisposition to obesity could yield multiple adverse reactions.

Moreover, a clear link between FTO demethylase activity and obesity has yet to be made. It is possible that FTO plays a specialized role in the hypothalamus, perhaps as a transcriptional regulator, and mediates obesity in a manner independent of its catalytic activity, in which case pharmacologic inhibition would not be useful. On the other hand, it is also possible that the true in vivo effect of FTO has yet to be described.

The association of FTO variants with obesity certainly hints at a novel pathway to obesity and suggests ways in which genetic testing for FTO variants might play a role in potential clinical interventions down the road.

In the meantime, since diet and lifestyle changes seem to blunt the effects of a genetic predisposition toward obesity due to the presence of an FTO risk allele, [24] there may be a more immediate role for genetic testing in the clinic; such testing may provide a means of encouraging allele carriers to implement diet and lifestyle changes that discourage obesity and improve their overall health.

Frayling TM, Timpson NJ, Weedon MN, Zeggini E, Freathy RM, Lindgren CM, et al. A common variant in the FTO gene is associated with body mass index and predisposes to childhood and adult obesity. Science. 2007 May 11. 316(5826):889-94. [Medline]. [Full Text].

Dina C, Meyre D, Gallina S, Durand E, Körner A, Jacobson P, et al. Variation in FTO contributes to childhood obesity and severe adult obesity. Nat Genet. 2007 Jun. 39(6):724-6. [Medline].

Scuteri A, Sanna S, Chen WM, Uda M, Albai G, Strait J, et al. Genome-wide association scan shows genetic variants in the FTO gene are associated with obesity-related traits. PLoS Genet. 2007 Jul. 3(7):e115. [Medline]. [Full Text].

Hinney A, Nguyen TT, Scherag A, Friedel S, Brönner G, Müller TD, et al. Genome wide association (GWA) study for early onset extreme obesity supports the role of fat mass and obesity associated gene (FTO) variants. PLoS One. 2007 Dec 26. 2(12):e1361. [Medline]. [Full Text].

Hertel JK, Johansson S, Sonestedt E, Jonsson A, Lie RT, Platou CG, et al. FTO, type 2 diabetes, and weight gain throughout adult life: a meta-analysis of 41,504 subjects from the Scandinavian HUNT, MDC, and MPP studies. Diabetes. 2011 May. 60 (5):1637-44. [Medline].

Hassanein MT, Lyon HN, Nguyen TT, Akylbekova EL, Waters K, Lettre G, et al. Fine mapping of the association with obesity at the FTO locus in African-derived populations. Hum Mol Genet. 2010 Jul 15. 19(14):2907-16. [Medline]. [Full Text].

Villalobos-Comparán M, Teresa Flores-Dorantes M, Teresa Villarreal-Molina M, Rodríguez-Cruz M, García-Ulloa AC, Robles L, et al. The FTO gene is associated with adulthood obesity in the Mexican population. Obesity (Silver Spring). 2008 Oct. 16(10):2296-301. [Medline].

Liu Y, Liu Z, Song Y, Zhou D, Zhang D, Zhao T, et al. Meta-analysis added power to identify variants in FTO associated with type 2 diabetes and obesity in the Asian population. Obesity (Silver Spring). 2010 Aug. 18(8):1619-24. [Medline].

Vasan SK, Karpe F, Gu HF, Brismar K, Fall CH, Ingelsson E, et al. FTO genetic variants and risk of obesity and type 2 diabetes: a meta-analysis of 28,394 Indians. Obesity (Silver Spring). 2014 Mar. 22 (3):964-70. [Medline].

Fawwad A, Siddiqui IA, Basit A, Zeeshan NF, Shahid SM, Nawab SN, et al. Common variant within the FTO gene, rs9939609, obesity and type 2 diabetes in population of Karachi, Pakistan. Diabetes Metab Syndr. 2015 Feb 24. [Medline].

Gerken T, Girard CA, Tung YC, Webby CJ, Saudek V, Hewitson KS, et al. The obesity-associated FTO gene encodes a 2-oxoglutarate-dependent nucleic acid demethylase. Science. 2007 Nov 30. 318(5855):1469-72. [Medline]. [Full Text].

Stratigopoulos G, Padilla SL, LeDuc CA, Watson E, Hattersley AT, McCarthy MI, et al. Regulation of Fto/Ftm gene expression in mice and humans. Am J Physiol Regul Integr Comp Physiol. 2008 Apr. 294(4):R1185-96. [Medline]. [Full Text].

Fischer J, Koch L, Emmerling C, Vierkotten J, Peters T, Brüning JC, et al. Inactivation of the Fto gene protects from obesity. Nature. 2009 Apr 16. 458(7240):894-8. [Medline].

Church C, Moir L, McMurray F, Girard C, Banks GT, Teboul L, et al. Overexpression of Fto leads to increased food intake and results in obesity. Nat Genet. 2010 Dec. 42(12):1086-92. [Medline]. [Full Text].

Haupt A, Thamer C, Staiger H, Tschritter O, Kirchhoff K, Machicao F, et al. Variation in the FTO gene influences food intake but not energy expenditure. Exp Clin Endocrinol Diabetes. 2009 Apr. 117(4):194-7. [Medline].

Tanofsky-Kraff M, Han JC, Anandalingam K, Shomaker LB, Columbo KM, Wolkoff LE, et al. The FTO gene rs9939609 obesity-risk allele and loss of control over eating. Am J Clin Nutr. 2009 Dec. 90(6):1483-8. [Medline]. [Full Text].

Speakman JR, Rance KA, Johnstone AM. Polymorphisms of the FTO gene are associated with variation in energy intake, but not energy expenditure. Obesity (Silver Spring). 2008 Aug. 16(8):1961-5. [Medline].

Wardle J, Llewellyn C, Sanderson S, Plomin R. The FTO gene and measured food intake in children. Int J Obes (Lond). 2009 Jan. 33(1):42-5. [Medline].

Cecil JE, Tavendale R, Watt P, Hetherington MM, Palmer CN. An obesity-associated FTO gene variant and increased energy intake in children. N Engl J Med. 2008 Dec 11. 359(24):2558-66. [Medline].

Timpson NJ, Emmett PM, Frayling TM, Rogers I, Hattersley AT, McCarthy MI, et al. The fat mass- and obesity-associated locus and dietary intake in children. Am J Clin Nutr. 2008 Oct. 88(4):971-8. [Medline].

Luczyński W, Fendler W, Ramatowska A, Szypowska A, Szadkowska A, Młynarski W, et al. Polymorphism of the FTO Gene Influences Body Weight in Children with Type 1 Diabetes without Severe Obesity. Int J Endocrinol. 2014. 2014:630712. [Medline].

Do R, Bailey SD, Desbiens K, Belisle A, Montpetit A, Bouchard C, et al. Genetic variants of FTO influence adiposity, insulin sensitivity, leptin levels, and resting metabolic rate in the Quebec Family Study. Diabetes. 2008 Apr. 57(4):1147-50. [Medline].

Boissel S, Reish O, Proulx K, Kawagoe-Takaki H, Sedgwick B, Yeo GS, et al. Loss-of-function mutation in the dioxygenase-encoding FTO gene causes severe growth retardation and multiple malformations. Am J Hum Genet. 2009 Jul. 85(1):106-11. [Medline]. [Full Text].

Ahmad T, Lee IM, Paré G, Chasman DI, Rose L, Ridker PM, et al. Lifestyle Interaction With Fat Mass and Obesity-Associated (FTO) Genotype and Risk of Obesity in Apparently Healthy U.S. Women. Diabetes Care. 2011 Mar. 34(3):675-80. [Medline]. [Full Text].

Ali Torkamani, PhD Director of Genome Informatics and Drug Discovery, The Scripps Translational Science Institute; Assistant Professor of Integrative Structural and Computational Biology, The Scripps Research Institute

Disclosure: Nothing to disclose.

Keith K Vaux, MD Professor of Medicine, Clinical Chief and Division Director, Division of Medical Genetics, Department of Medicine, University of California, San Diego, School of Medicine; Director, Rare Disease Program, Rady Children’s Hospital San Diego and UC San Diego

Keith K Vaux, MD is a member of the following medical societies: American Academy of Pediatrics, Western Society for Pediatric Research

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Obesity, FTO, and Type 2 Diabetes

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Obesity is the second biggest preventable cause of cancer after smoking, but how can that actually happen?

You can find more information on the facts about how being overweight causes cancer, the evidence and advice on how to keep a healthy weight at https://www.cancerresearchuk.org/abou…


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What Is Prediabetes?

What Is Prediabetes?

This sneaky health condition has no symptoms. But it’s almost always present before you get type 2 diabetes. It means your blood sugar level is higher than normal, but not yet high enough for you to be diagnosed with the disease. 

About 86 million people in the U.S. over age 20 have prediabetes. And doctors see the need to diagnose it more often. Treating it can prevent more serious health problems later on. These range from type 2 diabetes to problems with your heart, blood vessels, eyes, and kidneys

By the time you’re diagnosed with diabetes, many of these problems have already taken hold.

You’re most likely to get this disease if you:

 

 

You should get tested for prediabetes if you meet the criteria above and you:

 

Although most people with prediabetes have no symptoms, you might notice you’re extra thirsty, pee a lot more, or have blurred vision or extreme fatigue.

Your doctor can perform one of three different blood tests — the fasting plasma glucose test, the oral glucose tolerance test, or the hemoglobin A1c  test.

The fasting plasma glucose test measures your blood sugar after an 8-hour fast. If your blood sugar level is higher than normal after the test, you may have prediabetes.

The oral glucose tolerance test records your blood sugar after a fast and then again 2 hours after you have a very sweet drink. If your blood sugar is higher than normal 2 hours after the test, you may have prediabetes.

The hemoglobin A1c test looks at your average blood sugar for the past 2 to 3 months. It can be used to see if your diabetes is under control or to diagnose the disease.

Treatment for prediabetes is simple:

 

 

 

 

 

SOURCES: 

American Diabetes Association: “Standards of Medical Care in Diabetes — 2012.”

American Diabetes Association: “Pre-Diabetes.”

American Diabetes Association: “How to Tell if You Have Pre-Diabetes.”

National Diabetes Clearinghouse: “Insulin Resistance and Pre-Diabetes.”

Shoelson, S. Journal of Clinical Investigation, 2006.

Phillips, L. Diabetes Care, 2006.

Kim, S. Journal of the American College of Cardiology, 2006.

American Diabetes Association: “Diabetes Basics.”

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See how one patient learned to manage her weight and diet.

Are your ‘good’ habits doing harm?

How they help diabetes.

Are you at risk?

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Weight Loss & Obesity

Weight Loss & Obesity

Do you know how to lose them?

Test your knowledge.

10 tips for burning calories.

17 ways to do it.

Being obese means having so much body fat that your health is in danger. Having too much body fat can lead to type 2 diabetes, heart disease, high blood pressure, arthritis, sleep apnea, and stroke.

McDonald’s Says It Will Trim Antibiotics in Beef

The company’s first step is to partner with its supplying beef producers in the top 10 beef sourcing markets to measure and understand the current use of antibiotics in its global supply chains.

Read Full Article

If doctors tell you you’re obese, they’re not trying to make you feel bad. They’re using a specific medical term — obesity — to talk with you about your weight.

The word “obesity” means too much body fat. It’s usually based on your body mass index (BMI), which you can check using a BMI calculator. BMI compares your weight to your height.

Test your knowledge of different types.

What to know before taking them.

Are they closer than you think?

What to expect.

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Weight Loss & Obesity

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Surprising Things That Can Damage Your Liver

Surprising Things That Can Damage Your Liver

Too much sugar isn’t just bad for your teeth. It can harm your liver, too. The organ uses one type of sugar, called fructose, to make fat. Too much refined sugar and high-fructose corn syrup causes a fatty buildup that can lead to liver disease. Some studies show that sugar can be as damaging to the liver as alcohol, even if you’re not overweight. It’s one more reason to limit foods with added sugars, such as soda, pastries, and candy.

Even if the label says “natural,” it may not be OK for you. For instance, some people take an herb called kava kava for menopause symptoms or to help them relax. But studies show that it can keep the liver from working right. That can lead to hepatitis and liver failure. Some countries have banned or restricted the herb, but it’s still available in the U.S. You should always talk to your doctor before you take any herbs to make sure they’re safe.

The extra fat can build up in your liver cells and lead to non-alcoholic fatty liver disease (NAFLD). As a result, your liver may swell. Over time, it can harden and scar liver tissue (doctors call this cirrhosis). You are more likely to get NAFLD if you are overweight or obese, middle-aged, or have diabetes. You may be able to turn things around. Diet and exercise can stop the disease.

Your body needs vitamin A, and it’s fine to get it from plants such as fresh fruits and vegetables, especially those that are red, orange, and yellow. But if you take supplements that have high doses of vitamin A, that can be a problem for your liver. Check with your doctor before you take any extra vitamin A because you probably don’t need it.

Research shows that people who drink a lot of soft drinks are more likely to have non-alcoholic fatty liver disease (NAFLD). Studies don’t prove that the drinks were the cause. But if you down a lot of sodas and have been meaning to cut back, this could be a good reason to switch what you sip.

You’ve got a sore back, or a headache, or a cold, and you reach for a pain reliever. Be sure to take the right amount! If you accidentally take too much of anything that has acetaminophen — for instance, a pill for your headache and something else for your cold, and both have acetaminophen in it — it can harm your liver. Check the dose and how much is OK to take in one day. Stick to those limits, and you should be fine.

Trans fats are a man-made fat in some packaged foods and baked goods. (You’ll see them listed as “partially hydrogenated” ingredients). A diet high in trans fats makes you more likely to gain weight. That’s not good for your liver. Check the ingredients list. Even if it says “0” grams of trans fat, it may still have a small amount, and that adds up.

A doctor or nurse gets nicked by a needle they’ve used on a patient. Or people injecting illegal drugs share a needle. The needle isn’t the problem. It’s what’s on it. Hepatitis C can spread through blood. Even if it only happened once, or you’re at high risk for other reasons (like if you have HIV or your mom had hepatitis C while pregnant with you), you should get tested. So should everyone born from 1945 through 1965.

You probably already know that drinking too much is bad for your liver. But you might not realize that “too much” can happen without you being an alcoholic or addicted to alcohol. It’s easy to drink more than you think. Many glasses can hold a lot more than one standard serving, which is 5 ounces of wine (that’s a little more than half a cup), 12 ounces of regular beer, or 1.5 ounces of liquor. If you drink, be sure to keep it moderate — that’s one drink a day for women and up to 2 per day for men.

Sources
|

Medically Reviewed on 01/11/2018

Reviewed by Jennifer

Robinson, MD on January 11, 2018

IMAGES PROVIDED BY:

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(9)    Thinkstock 

 

SOURCES:

Kavanaugh, K. The American Journal of Clinical Nutrition, June 19, 2013.

Nature.com: “The Toxic Truth About Sugar.”

Harvard Medical School: “Abundance of Fructose Not Good for the Liver, Heart.”

Nakanishi, Y. Journal of Autoimmunology, Feb-March 2008.

Parthasarathy, S. Journal of Medicinal Food, 17 (5) 2014.

FDA: “Questions and Answers about Monosodium Glutamate.”

Collison, K. The Journal of Lipid Research, August 2009.

University of Maryland Medical Center: “Comfrey,” “Vitamin A.”

Clayton, N. Experimental and Toxicologic Pathology, January 2007.

FDA: “Kava.”

Fu, S. World Journal of Gastroenterology, Feb. 23, 2008.

News release, Wiley Publishers.

National Institute of Diabetes and Digestive and Kidney Diseases: LiverTox: “Kava Kava (Piper  Methysticum.”)

National Institute of Diabetes and Digestive and Kidney Disease/Weight-control Information Network: “Do You Know Some of the Health Risks of Being Overweight?”

American Liver Foundation: “NAFLD.”

U.S. National Library of Medicine: “LiverTox: Vitamin A.”

Harvard School of Public Health: “The Nutrition Source: Vitamin A,” “Shining the Spotlight on Trans Fats.”

CDC: “Hepatitis FAQs for the Public.”

Assy, N. Canadian Journal of Gastroenterology, October 2008.

Whitehouse, C. American Association of Occupational Health Nurses, June 2008.

Abhilash, M. Food and Chemical Toxicology, June 2011.

Cosmin, S. The American Journal of Psychiatry, April 2014.

DeSanty, K. Annals of Pharmacotherapy, July-August 2007.

News release, Cincinnati Children’s Hospital Medical Center.

News Release, Saint Louis University.

Reviewed by Jennifer

Robinson, MD on January 11, 2018

This tool does not provide medical advice. See additional information.

THIS TOOL DOES NOT PROVIDE MEDICAL ADVICE. It is intended for general informational purposes only and does not address individual circumstances. It is not a substitute for professional medical advice, diagnosis or treatment and should not be relied on to make decisions about your health. Never ignore professional medical advice in seeking treatment because of something you have read on the WebMD Site. If you think you may have a medical emergency, immediately call your doctor or dial 911.

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