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Recommended Diet Journal Articles

Harvard article on Fructose and rancid fats causing NAFLD

How fructose is the gateway to diabetes, obesity, and Non-Alcoholic Fatty Liver Disease (NAFLD) 

At the bottom is this article is my addition on what has been left out.  If you wish to understand the essentials of the obesity and diabetes epidemics then read this commentary.  It explains why eating the current high amount of sugar alone won’t cause fatty liver--except for a few who are genetically susceptible.  The other main causal part for fatty liver is eating a large amount of carbohydrates with a high insulin response, namely foods such as rice, white potatoes, and highly processed grains.  These foods in quantity will cause a high insulin response by the pancreas to lower the high blood glucose level—click on link for tables on glucose levels and insulin response.  The consequences of the two take years to become clinically significant.   Such diet overloads the body’s systems for clearing the liver of excess fat. 

For the sake of completeness I include an article (bottom of page) on how trans-fat and polyunsaturated fats are another major causal factor for NAFLD.  Polyunsaturated fats are subject to rancidification and make their role equivalent to trans-fats in the production of NAFLD and associated comorbidities.  For more on this click on these two links.

One last comment, the cat has gotten out of the bag as to the health consequences of a high-sugar diet.  For example, England, Canada, and Australia have done documentaries on this problem—see video page for links.  But the powerful food manufactures operating though the developed-world governments has got them to support the high carb diet such as through farm-subsides and to oppose efforts to warn the public repeatedly of the role of foods with a high insulin/glycemic index.   

The article below, an important statement of the how fructose causes fatty liver disease, this article is based mainly upon a 2009 article-- http://www.jci.org/articles/view/37385.  A edited version is at the bottom of the page. 



Abundance of fructose not good for the liver, heart

Harvard Heart Letter  Harvard Medical school    September 1, 2011

 Another reason to avoid foods made with a lot of sugar.

The human body handles glucose and fructose — the most abundant sugars in our diet — in different ways. Virtually every cell in the body can break down glucose for energy. About the only ones that can handle fructose are liver cells. What the liver does with fructose, especially when there is too much in the diet, has potentially dangerous consequences for the liver, the arteries, and the heart.

Fructose, also called fruit sugar, was once a minor part of our diet. In the early 1900s, the average American took in about 15 grams of fructose a day (about half an ounce), most of it from eating fruits and vegetables. Today we average four or five times that amount, almost all of it from the refined sugars used to make breakfast cereals, pastries, sodas, fruit drinks, and other sweet foods and beverages.  Refined sugar, called sucrose, is half glucose and half fructose. High-fructose corn syrup is about 55% fructose and 45% glucose [42% glucose & 3% other sugars].

From fructose to fat

The entry of fructose into the liver kicks off a series of complex chemical transformations. (You can see a diagram of these at health.harvard.edu/172.) One remarkable change is that the liver uses fructose, a carbohydrate, to create fat. This process is called lipogenesis. Give the liver enough fructose, and tiny fat droplets begin to accumulate in liver cells (see figure). This buildup is called nonalcoholic fatty liver disease, because it looks just like what happens in the livers of people who drink too much alcohol.

Virtually unknown before 1980, nonalcoholic fatty liver disease now affects up to 30% of adults in the United States and other developed countries, and between 70% and 90% of those who are obese or who have diabetes.

Early on, nonalcoholic fatty liver disease is reversible. At some point, though, the liver can become inflamed. This can cause the low-grade damage known as nonalcoholic steatohepatitis (steato meaning fat and hepatitis meaning liver inflammation). If the inflammation becomes severe, it can lead to cirrhosis — an accumulation of scar tissue and the subsequent degeneration of liver function.

Liver comparison  [the fat expands the

hepatocytes up to 70%.  The normal 3 lb.

liver weighs 5 lb.]     

illustration comparing normal liver and liver with fatty deposits

Beyond the liver

The breakdown of fructose in the liver does more than lead to the buildup of fat. It also:

  • elevates triglycerides

  • increases harmful LDL (so-called bad cholesterol)

  • promotes the buildup of fat around organs (visceral fat)

  • increases blood pressure

  • makes tissues insulin-resistant, a precursor to diabetes

  • increases the production of free radicals, energetic compounds that can damage DNA and cells.

  • [Has 7.5 times the rate of glycation compared to fructose, and its clearance from the blood is slower

  • Fructose accumulates in the liver where it is metabolized]

None of these changes are good for the arteries and the heart.

Researchers have begun looking at connections between fructose, fatty liver disease, and cardiovascular disease. The early results are in line with changes listed above due to the metabolism of fructose.

An article published in 2010 in The New England Journal of Medicine [NEJM][1] indicated that people with nonalcoholic fatty liver disease are more likely than those without it to have buildups of cholesterol-filled plaque in their arteries. They are also more likely to develop cardiovascular disease or die from it. In fact, people with nonalcoholic fatty liver disease are far more likely to die of cardiovascular disease than liver disease.

A report from the Framingham Heart Study has linked nonalcoholic fatty liver disease with metabolic syndrome, a constellation of changes that is strongly associated with cardiovascular disease. Other studies have linked fructose intake with high blood pressure.

Limit added sugars

Experts still have a long way to go to connect the dots between fructose and nonalcoholic fatty liver disease, obesity, diabetes, and heart disease. Higher intakes of fructose are associated with these conditions, but clinical trials have yet to show that it causes them.

Still, it’s worth cutting back on fructose. But don’t do it by giving up fruit. Fruit is good for you and is a minor source of fructose for most people. The big sources are refined sugar and high-fructose corn syrup [and fruit juices—one glass of apple juice requires five apples, but without the fiber].

The American Heart Association [AHA] recommends limiting the amount of sugar you get from sugar-sweetened drinks, pastries, desserts, breakfast cereals, and more, mainly to avoid gaining weight. The same strategy could also protect your liver and your arteries. [the World Health Organization in 2014 recommendation is 9 teaspoon a day for men, and 6 for woman,  which was then adopted by the AHA.]


The main cause of the inflammatory process which causes cardiovascular disease:  Though it is beyond dispute and accepted in medical text books that atherosclerosis results from an immune response, tobacco science ignores the role of pathogens within the artery walls and blames oxidized LDL.  Though the role of pathogens has been established nearly 100-years ago through the examination of atheroma from those who died of heart attacks, this and other definitive evidence has been ignored due to the rule of pharma upon the information systems and research.  A review of the evidence for pathogens is found at these two links. With the development of metabolic dysfunction from a fatty liver the rate of formation of plaque is accelerated.

Major industries can effectively manipulate the information concerning their products for financial gain.  To prevent atherosclerosis would entail preventing its comorbidities of hypertension, myocardial infarction, and most cases of arrhythmia.  It would also entail conceding that treatment of hypercholesterolemia lacks benefits.  The role of diet in causing fatty liver could be easily be prevented with a healthful diet which would be low in fructose and polyunsaturated vegetable oils—see second article.  This would reduce their sales of drugs for diabetes.  Thus pharma wants us to chase symptoms rather than causes of cardiovascular disease.  Prevention is not on their financial horizon.

[1] Approximately 20 to 30% of adults in the general population in Western countries have nonalcoholic fatty liver disease, and its prevalence increase to 70 to 90% among persons who are obese or have diabetes;… a strong association between nonalcoholic fatty liver disease and the risk of cardiovascular disease…. Strongly associated with increased carotid-artery intimal medial thickness and an increase prevalence of carotid atherosclerosis plaques…. 2006 study.     

http://www.biomedcentral.com/content/pdf/1743-7075-8-65.pdf   COMPLETE  Dhibi et al.   Nutrition & Metabolism 2011, 8:65 http://www.nutritionandmetabolism.com/content/8/1/65 Complete html version

The intake of high fat diet with different trans fatty acid levels differentially induces oxidative stress and non-alcoholic fatty liver disease (NAFLD) in rats


Background: Trans-fatty acids (TFA) are known as a risk factor for coronary artery diseases, insulin resistance and obesity accompanied by systemic inflammation, the features of metabolic syndrome. Little is known about the effects on the liver induced by lipids and also few studies are focused on the effect of foods rich in TFAs on hepatic functions and oxidative stress. This study investigates whether high-fat diets with different TFA levels induce oxidative stress and liver dysfunction in rats.

Methods: Male Wistar rats were divided randomly into four groups (n = 12/group): C receiving standard-chow; Experimental groups that were fed high-fat diet included 20% fresh soybean oil diet (FSO), 20% oxidized soybean  oil diet (OSO) and 20% margarine diet (MG). Each group was kept on the treatment for 4 weeks. 

Results: A liver damage was observed in rats fed with high-fat diet via increase of liver lipid peroxidation and decreased hepatic antioxidant enzyme activities (superoxide dismutase, catalase and glutathione peroxidase). The intake of oxidized oil led to higher levels of lipid peroxidation and a lower concentration of plasma antioxidants in comparison to rats fed with FSO. The higher inflammatory response in the liver was induced by MG diet. Liver histopathology from OSO and MG groups showed respectively moderate to severe cytoplasm vacuolation, hypatocyte hypertrophy, hepatocyte ballooning, and necroinflammation.  [Polyunsaturated fats readily undergo oxidation in cooking, on the shelf in foods, and in the body, and once oxidized creates the inflammatory response and worse.]

Conclusion: It seems that a strong relationship exists between the consumption of TFA in the oxidized oils and lipid peroxidation and non-alcoholic fatty liver disease (NAFLD). The extent of the peroxidative events in liver was also different depending on the fat source suggesting that feeding margarine with higher TFA levels may represent a direct source of oxidative stress for the organism. The present study provides evidence for a direct effect of TFA on NAFLD. 

Keywords: trans fatty acids, oxidative stress, non alcoholic fatty liver disease, rats.


Various food processing techniques have been found to leave deleterious effects on the processed foods and fats and oils are no exception [1-3]. In the developing nations, the intermittent use of reprocessed thermoxidised oil is widespread.[4] Due to their long self life, [low price, improved flavor retention], their suitability during deep-frying and their semisolidity, partially hydrogenated vegetable oils are used by food industries to enhance the palatability of baked goods and sweets.  In the process of hydrogenation unsaturated vegetable oils undergo the introduction of hydrogen gas under certain conditions of pressure and temperature using a catalyst metal (nickel, palladium, platinum, and ruthenium).  The hydrogenation process involves the transformation of certain unsaturated fatty acids from cis to trans configurations [preferred because of its lower energy state]…. Recent studies suggest multiple possible mechanisms that might mediate association of TFAs with CVD [12].  For example TFAs influence prostaglandins balance, which in turn promotes thrombogenesis [13] and inhibit the conversion of linoleic acid to arachidonic acid and to other n-6 PUFA, perturbing essential fatty acid metabolism and causing changes in the phospholipid fatty acid composition in the aorta [14].  TFAs have been associated with the activation of systemic inflammatory responses, including substantially increased levels of IL-6, and TNF-alpha, TNF receptors and monocytes chemo-attract protein-1 [15]. Furthermore, TFAs have been associated with increased levels of several markers of endothelial activation, including soluble intercellular adhesion molecule 1, soluble vascular-cell adhesion molecule 1, and E-selectin [10].  TFAs are postulated to be involved in promoting vascular dysfunction, as reflected by a reduction in brachial artery flow [16].  These observations suggest that TFAs are linked to development of CVD, probably via a vascular pro-inflammatory response [17].  Oxidative damage is a major contributor to the development of CVD.  Nevertheless, little is known about the effects on the liver induced lipids [6] and few studies are focused on the effect of foods rich in TFAs on hepatic functions and oxidative stress.  Oxidative stress results from an imbalance between oxidant production and antioxidant defenses [18].  Oxidative stress induced by free radicals has been linked to the development of several diseases such as cardiovascular, cancer, and neurodegenerative diseases [19].   When cellular antioxidant mechanisms are overwhelmed, a long-term decline in their antioxidant capacity causes oxidative stress [20, 21].  Oxidative stress is now believed to be an important factor in the development of non alcoholic fatty liver disease (NAFLD) [20, 22].  NAFLD is the most common liver disorder in the world, and in obesity, type-2 diabetes and related metabolic diseases, it incidence reaches 70-90% [23].   The disease is characterized by the accumulation of triacylglycerols inside liver cells, and the condition can progress into more serious liver disease, such as non alcoholic steatohepatitis, liver fibrosis, cirrhosis, and more rarely, liver carcinoma [23]. Previous works have shown that feeding rats a high fat diet (57% of energy from fat) induces hepatic steatosis and liver damage, which are characteristic of NAFLD and thus provides a suitable model for the early stages of the disease[24,25]. But, in these studies TFAs in the fat diet were not investigated and neglected. Therefore, it is necessary to examine the relationship between the liver functions and TFAs consumption in dietary lipids…. Other section click on link at top of article.



In conclusion, oxidized edible oils fed to rats for four weeks induced lipid peroxidation in liver compared with the same non-oxidized oils. It seems that a strong relationship exists between the consumption of TFAs in the oxidized oils and lipid peroxidation. [Trans-fats are made from partially hydrogenated polyunsaturated fats, and is mainly these polyunsaturated fats—to a lesser extent monounsaturated fats—that are oxidized; viz. become rancid.  To jump from oxidized to trans is an unwarranted given the hundreds of articles on rancid fats.] The extent of the peroxidative events in liver was also different depending on the fat source suggesting that feeding margarine with higher TFA level may represent a direct source of oxidative stress for the organism. The present study provides evidence for a direct effect of TFAs on liver dysfunction causing the disturbances in liver lipid metabolism that result in NAFLD which is a key component of the cardiometabolic syndrome. This suggests that TFAs may influence risk factors for CVD.


JK:   While the author writes about the effects of TFAs, the same must be stated for OSO (oxidized soy oil) based on his findings.  Oxidation naturally occurs in the body due to the presence of reactive chemical mainly in the mitochondria where soy oil is metabolized.  Thus by extension all polyunsaturated fats—not just soy oil—are subject to oxidation.  Oxidation also readily occurs to polyunsaturated fats while cooking due to heat of activation.  Given that in the Western diet polyunsaturated fats are several fold greater than transfats, their role in developing NAFLD is major.  A second major cause, as per first article above, is fructose.   

This is another example of how KOLs manipulate the abstract and conclusion in a way that favors industry and is contrary to the contents of the research.  Over and over again I find that the devil is in the details (as Prof. Ben Goldacre states).



Diabetic Medicine Volume 22, Issue 9, pages 1129–1133, September 2005

Recent concepts in non-alcoholic fatty liver disease


Non-alcoholic fatty liver disease (NAFLD) is present in up to one-third of the general population and in the majority of patients with metabolic risk factors such as obesity and diabetes. Insulin resistance is a key pathogenic factor resulting in hepatic fat accumulation. Recent evidence demonstrates NAFLD in turn exacerbates hepatic insulin resistance and often precedes glucose intolerance. Once hepatic steatosis is established, other factors, including oxidative stress, mitochondrial dysfunction, gut-derived lipopolysaccharide and adipocytokines, may promote hepatocellular damage, inflammation and progressive liver disease. Confirmation of the diagnosis of NAFLD can usually be achieved by imaging studies, however, staging the disease requires a liver biopsy. NAFLD is associated with an increased risk of all-cause death, probably because of complications of insulin resistance such as vascular disease, as well as cirrhosis and hepatocellular carcinoma, which occur in a minority of patients. NAFLD is also now recognized to account for a substantial proportion of patients previously diagnosed with ‘cryptogenic cirrhosis’. Diabetes, obesity and the necroinflammatory form of NAFLD known as non-alcoholic steatohepatitis, are risk factors for progressive liver disease. Current treatment relies on weight loss and exercise, although various insulin-sensitizing medications appear promising. Further research is needed to identify which patients will achieve the most benefit from therapy.

This is another example of how KOLs manipulate the content to ignore the proven fix, in this case that of an Atkins type diet which is fat burning (ketogenic), a diet which also cures diabetes.  But what we have is corporate medicine.    

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