Differentiating Nutrition Science From Media Essay 9
Differentiating Nutrition Science From Media Essay 9
More people are becoming interested in detox diets and organ health. As a health educator, one of your roles is differentiating evidence versus popular media and marketing. In this discussion, we will explore evidence that supports the role of nutrition in liver health to add to your ability to differentiate nutrition science from media.
Initial post:
Start by reading the article titled, Impact of nutritional changes on nonalcoholic fatty liver disease.
Focus on the general concepts, as opposed to understanding every word. After completing the reading, answer the following question for your initial post: “What evidence-based general nutrition recommendations would you share with patients interested in liver health?”
Use the assigned article, with appropriate APA citations, to support your position with at least 5-6 sentences to support your case.
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Non-alcoholic fatty liver disease (NAFLD) results from hepatic fat accumulation (>5% of liver weight), which is not due to excess alcohol consumption, autoimmune, infectious or other established liver diseases [1,2]. NAFLD can exist as pure steatosis, steatosis with mild lobular inflammation, non-alcoholic steatohepatitis (NASH) and hepatocellular carcinoma. In addition to the degree of fibrosis, in the liver biopsy NASH is classified as mild fibrosis (F0–F1), significant fibrosis (≥F2), advanced fibrosis (≥F3, bridging) and cirrhosis (F4). No accurate data exist on the incidence of NAFLD [3]. The worldwide prevalence of NAFLD ranges between 8–45%. In North America and Europe, it is estimated to range from 25–34% and, in Asia, between 15–20%. The highest prevalence is described in the Middle East and South America. However, in certain subpopulations (i.e., obesity, type 2 diabetes [T2D]) the estimated prevalence of NAFLD is significantly higher, ranging from 43–92%. When compared to the general population, patients with NAFLD have higher mortality from both liver and non-liver-related causes. They are at increased risk for cardiovascular diseases [4], T2D and chronic kidney disease [2]. NAFLD is currently ranked as the second most common cause of liver transplantation and is predicted to become the first in Western countries [3]. Additionally, NAFLD is the second most common cause of hepatocellular carcinoma. Therefore, NAFLD is a major global health threat; its prevention and treatment represent a mounting challenge in health services. Therapeutic approaches focus on lifestyle modification [5]. Diet and exercise interventions remain as the first line of therapy, aiming mainly at controlling body weight and cardio-metabolic risk factors related to metabolic syndrome. In the early stages of NAFLD, a healthy diet and weight loss of at least 7% might be sufficient [4]. In more advanced stages, high genetic risk or, in the presence of diabetes, intensified lifestyle intervention reinforced by pharmacological treatment might be necessary, though there is still no registered drug for the treatment of NAFLD. This review assesses the evidence available for dietary recommendations against NAFLD.
We searched for original articles and reviews published between 1 January 2000 and 31 December 2018, focusing on NAFLD dietary treatment in PubMed and MEDLINE using the following search terms (or combination of terms): “NAFLD”, “NASH”, “fatty liver”, “macronutrient”, “dietary”, “recommendations”, “composition”, “life-style intervention”, “Mediterranean diet”. Only full-text articles written in English were included. More weight was given to studies with a high level of evidence from either randomized controlled trials, prospective case-control studies, meta-analyses or systematic reviews. Articles in journals with explicit policies governing conflicts of interest and stringent peer-review processes were favored. Data from larger replicated studies with longer periods of observation when possible were systematically chosen to be presented. Reference lists of retrieved articles were used to obtain additional references. Differentiating Nutrition Science From Media Essay 9
2. Pathophysiology
The major established risk factors for NAFLD include obesity, insulin resistance and dyslipidemia [5]. Genetic modifiers are associated with the increased progression to NASH and cirrhosis, however, some of them are associated with apparent protection from cardiovascular diseases [4]. The best-characterized genetic association is with PNPLA3 [6] encoding I148M (regulator of the mobilization of triglycerides from lipid droplets) and with TM6SF2 [1,3,4] encoding E167K (regulator of very low-density lipoprotein (VLDL) secretion).
Dietary lipids (15%), lipolysis of adipose tissue (60–80%) and de novo lipogenesis (5%) contribute to the pool of lipids stored in the liver [7]. Adipose tissue lipolysis is regulated by the actions of insulin on adipocytes [2,8]. De novo lipogenesis is the process in which hepatocytes convert excess carbohydrates, especially fructose, into fatty acids [2], it is strictly regulated by nuclear receptor and cytoplasmic transcription factors including the liver X receptor (intervening in hepatic fatty acid synthesis), the farnesoid X receptor (interfering in VLDL assembly) and the peroxisome proliferator-activated receptors [PPARs] family [7]. PPAR-α regulates free fatty acids oxidation, PPAR-γ has an anti-inflammatory function, and PPAR-δ suppresses hepatic lipogenesis and reduces the hepatic expression of pro-inflammatory genes.
Lipid removal is mediated by both mitochondrial fatty acid β-oxidation and re-esterification to form triglyceride [7]. Triglycerides can be exported into the blood as VLDL or may be stored in lipid droplets. Lipid droplet triglycerides may undergo lipolysis to release fatty acids back into the hepatocyte free fatty acid pool. In order to understand the different nutritional advice for the treatment of NAFLD, it is necessary to comprehend that insulin resistance in adipose tissue contributes to fat accumulation and NASH through dysregulated lipolysis, resulting in the excessive delivery of fatty acids to the liver.
A ‘two-hit’ hypothesis to explain NAFLD development has been proposed. The ‘first hit’ is steatosis, the accumulation of fat in hepatocytes because of excessive triglycerides due to an imbalance in the lipid metabolism [7,9]. Steatosis is a consequence of insulin resistance [5,10,11]. Insulin resistance leads to hepatic triglyceride accumulation due to the increase of lipolysis in the peripheral adipose tissue resulting in higher levels of circulating non-esterified fatty acids, which are taken up by the liver and esterified into triglycerides. Impaired insulin signaling results in compensatory hyperinsulinemia [5]. Hyperinsulinemia decreases glycogen synthesis, which increases the hepatic fatty acid uptake, alters triglycerides transportation, and inhibits liver β-oxidation. In addition, glucose can be taken up by the liver through an insulin-independent transporter and be converted to pyruvate (a precursor of acetyl-CoA and malonyl-CoA) which can be transformed into fatty acids through de novo lipogenesis [5,10]. All of these alterations increase the pro-inflammatory cytokine activity leading to oxidative stress-mediated lipotoxicity, impaired hepatocyte apoptosis, inflammasome activation and mitochondrial dysfunction, contributing to fatty acid accumulation, hepatocellular injury, inflammation and the progressive accumulation of excess extracellular matrix [2]. Oxidative stress, triggered by pro-inflammatory cytokines (such as tumor necrosis factor-alpha [TNF-α], interleukin-6 and interleukin-8) or the reduction of anti-inflammatory cytokines (adiponectin), is considered the ‘second hit’ of NAFLD’s pathogenesis [11]. This may further exacerbate insulin resistance and hepatocyte injury induced by genetic or environmental susceptibilities. Differentiating Nutrition Science From Media Essay 9