Western Diet and Refined Sweeteners Impair Liver Function
Research has now confirmed what many nutritionists and doctors have observed among some of their patients: That the Western diet and refined sugars impair liver function and increase the risk of liver failure.
The new research, led by Dr. François Jornayvaz of Switzerland’s Geneva University Hospital system, looked into the causes and progression of nonalcoholic fatty liver disease – also called steatohepatitis – but unrelated to alcohol and drug intake.
Nonalcoholic fatty liver disease is difficult to diagnose, and often sneaks up on patients and their doctors. One of the most prevalent symptoms is general fatigue.
Fatty liver disease can also produce abdominal pain in the upper right region just below the ribs.
Fatty liver – also called steatosis – may or may not become serious, depending upon the diet and general health of the person. Research has indicated that fatty liver is quite common, especially among the obese and those who eat a Western diet.
But when inflammation occurs with fatty liver, liver tissues can become scarred. This is called fibrosis. Should the fibrosis scarring worsen, cirrhosis may develop. During cirrhosis the liver begins to shut down – often termed liver failure.
While alcohol and prescription medications are commonly involved in the majority of fibrosis and cirrhosis cases, those not involving alcohol or medications have been traced to dietary choices that lead to fatty liver. This can be exasperated by the intake of toxins, including preservatives and other chemicals within foods, as well as many OTC medications such as acetaminophen and others that have proved harmful to the liver.
Comparing diets with liver enzymes
In recent years, the impact of diet upon the liver has been studied by comparing diets with levels of liver enzymes such as ALT (alanine aminotransferase), AST (aspartate transaminase) and GGT (gamma-glutamyl transpeptidase).
Elevated levels of these typically indicate a diseased liver, especially in the case of ALT.
GGT measures the ability of the liver to process glutathione – one of the liver’s key actions to help clear the body of toxins. As such GGT is dramatically increased with alcohol consumption and medication intake, indicating stress on the liver.
In addition to measuring these liver enzymes, fatty deposits within the liver is also being measured among these studies. Glutathione levels and antioxidant levels also indicate liver function as well.
As patients with fatty liver have been followed with regard to their diet, and measured for these parameters, it has becom¬e increasingly evident that certain types of foods worsen these indicators, and increase the progression of cirrhosis.
Liver disease and fatty acids
The type of fats consumed is a critical element of fatty liver for obvious reasons. Clinicians have tracked the type of fatty acids most consumed among patients with liver disease compared with the diets of healthy control subjects.
For example, a team of Japanese doctors and dieticians followed 28 patients with non-alcoholic fatty liver disease. They compared their diets to matched Japanese healthy adults, and measured the progression of their disease with respect to diet. The research found that the Western diet pattern of high saturated fat intake and reduced long-chain polyunsaturated fat intake was lower among the liver disease patients.
This connection was confirmed by researchers from Portugal’s Institute of Molecular Medicine, who studied 43 patients with non-alcoholic liver disease together with 33 healthy subjects. This study found that consuming more saturated fats and less healthy carbohydrates was linked to greater incidence of fatty liver disease progression.
This study also found that reduced incidence of liver disease was associated with greater consumption of fiber, monounsaturated fatty acids, polyunsaturated fatty acids (specifically omega-3s such as ALA), as well as vitamin E, vitamin C, folate and selenium.
These nutrients are all prevalent among primarily plant-based diets such as the Mediterranean diet. Saturated fats are highest among red meats, lard and whole-fat dairy foods such as butter.
The type and ratio of saturated fats among plant-based foods such as coconuts, palm, nuts and others are not to be confused with these. Plant-based oils and even nuts such as cashews contain little saturated fat as a percentage of total fat.
For example, one of the fattiest nuts are cashews. An ounce of cashews will contain 2.2 grams of saturated fat, but will also contain 2.2 grams of polyunsaturated fat and 7 grams of monounsaturated fat. Meanwhile, an while an ounce (28 grams) of butter – about two tablespoons – will contain 14 grams of saturated fat. Meanwhile, butter will contain less than a gram of polyunsaturated fat and 6 grams of monounsaturated fat, and one gram of trans fat.
While butter can be a healthy food if eaten in moderation, we can see how consuming too much can spike saturated fat levels as a ratio of other fats. This element was discussed in an extensive report and review of research by scientists at the World Health Organization, where they stated:
“The evidence shows that intake of saturated fatty acids is directly related to cardiovascular risk. The traditional target is to restrict the intake of saturated fatty acids to less than 10%, of daily energy intake and less than 7% for high-risk groups.”
Yes, but not all saturated fats are the same
At the same time, we know that saturated fats are not equal. Their effects in the body are governed by their fatty acid content. The five principle fatty acids that are saturated (all the carbon bonds are single not double) include stearic acid, palmitic acid, myristic acid, lauric acid and butyric acid.
Among the saturated fatty acids, palmitic acid and myristic acid are the fatty acids most found to product higher levels of low-density lipoprotein – a cholesterol carrier that oxidizes easily and damages blood vessels. Palmitic acid contains 16 carbons, while myristic acid contains 14 carbons.
This relationship between different fatty acids among saturated fats was discussed specifically in the World Health Report mentioned above, regarding saturated fats:
“If populations are consuming less than 10%, they should not increase that level of intake. Within these limits, intake of foods rich in myristic and palmitic acids should be replaced by fats with a lower content of these particular fatty acids.”
In their review of research, they isolated that the connection between myristic and palmitic fatty acids and artery damage/cardiovascular disease was “convincing.” At the same time, they found the evidence connecting stearic acid with cardiovascular disease as “probable.”
As we examine the foods that have a predominant dietary sources of these three fatty acids, we find butter, cheese, red meats and eggs are greatest sources. These foods all have more than 40% of their fats from myristic acid, palmitic acid and stearic acid – with a predominance of palmitic acid. In comparison, only 18% of the fat in cashews are myristic acid, palmitic acid and stearic acid – and this ratio goes down even further among the other nuts.
Coconut oil lies within a completely different category of saturated fat. Nearly half of the fat in coconut oil is composed of a type of middle-length carbon chain fatty acid called lauric acid. Lauric acid contains 12 carbons.
Lauric acid and coconut oil in particular has been connected to reduced low-density lipoprotein, meaning a reduction in artery damage. Over 6% of breast milk’s fat is also lauric acid, and dairy will contain 3-5% lauric acid, depending upon the type of dairy. However, red meats contain no lauric acid. Lauric acid has been connected with cognition as we’ve reported in Realnatural.
What about polyunsaturated fats and liver damage?
The diets of most of these studies related to high-saturated fat diets relating to the Western diet. They were not relating to coconut oil. In fact, diets rich in coconut oil are related to traditional diets among tropical cultures.
In addition to the The Western diet also contains higher levels of fried foods. Fried foods – even those fried using polyunsaturated fats will produce higher low-density lipoproteins within the body. This is because heating a saturated or polyunsaturated fat at high degrees will oxidize and degrade the fatty acids in the oil.
As many polyunsaturated fats and saturated are heated to high temperatures, the heat will break apart the linkages between the carbons – or in the case of saturates – the triglycerides. This will produce what are called free fatty acids. These fatty acid types are unstable, becoming neutralized by stealing elements from elsewhere.
These unstable fatty acids become candidates for lipid peroxidation within the body. This will damage intestinal tissues, liver tissues and arteries due to the toxic nature of the free radicals released.
Frying fats also produces trans-fats, as the orientation of the fatty acids are switched from cis- configuration to trans- configuration. These also become unstable within the body.
Certainly, lightly frying foods that are antioxidant can neutralize the oxidation produced by the oil. But this does not take place in foods such as French fries and other fried foods where the oil is reused over and over at high heat – degrading the oil further with each fry.
So a person might be thinking that because they consume low levels of saturated fats, they are off the hook when it comes to fats. But an excessive amount of foods fried in polyunsaturated fats has been shown to move the body’s dial towards greater inflammation.
Actually, both elements – high consumption of fats with higher content of myristic and palmitic acids along with an abundance of fried foods fried in either saturated or polyunsaturated fats – are common among the Western diet, and thus are linked here with liver damage.
What does liver damage have to do with LDL?
We should know by now that low-density lipoprotein is linked with cardiovascular disease. This is one of the most accepted associations in medicine. Why? Because LDL oxidizes more easily than HDL. As it oxidizes, it will steal electrons from artery tissues – thereby damaging those arteries, producing plaque.
But what about the liver? Does LDL also hurt the liver? The evidence says yes. Research from the University of Texas studied 824 patients and measured their liver enzymes together with the LDL-to-HDL-c levels.
They found that LDL and large VLDL (most easily oxidized of all LDL) was associated with greater levels of ALT liver enzymes. This of course links LDL to liver damage.
Multiple studies have also linked non-alcoholic liver disease to the consumption of refined sugars such as refined sucrose and high-fructose corn syrup.
For example, researchers from Denmark’s Aarhus University Hospital studied 47 overweight subjects. They tested the subjects’ increase in liver fat along with various metabolic diagnostics. They found that consuming more sugary soft drinks was directly linked to an increase in liver fat by 32-43%.
In another study, gastroenterology researchers from Duke University followed 427 adults for three months with liver biopsy testing. They found that the consumption of sodas and drinks with high fructose corn syrup or sucrose increased liver fibrosis.
Refined sucrose releases fructose together with glucose, allowing them to be quickly absorbed. Fructose contained within whole fruits is trapped within complex polysaccharides that will slow its release and absorption rate.
Any food with little fiber (especially soft drinks) that contain refined sugar or corn syrup can thus be considered harmful to the liver.
Nonalcoholic fatty liver disease is one of the quietest lethal diseases, as it can sneak up on us with few symptoms. We can safely conclude that taking a proactive look at our diet before symptoms occur is prudent. Especially with the toxins now prevalent in our environment and drinking water.
Mohamed Asrih, François R. Jornayvaz. Diets and nonalcoholic fatty liver disease: The good and the bad. Clin nutr. 2013; 11 Nov 2013; DOI: 10.1016/j.clnu.2013.11.003
Toshimitsu K, Matsuura B, Ohkubo I, Niiya T, Furukawa S, Hiasa Y, Kawamura M, Ebihara K, Onji M. Dietary habits and nutrient intake in non-alcoholic steatohepatitis. Nutrition. 2007 Jan;23(1):46-52.
Machado MV, Ravasco P, Jesus L, Marques-Vidal P, Oliveira CR, Proença T, Baldeiras I, Camilo ME, Cortez-Pinto H. Blood oxidative stress markers in non-alcoholic steatohepatitis and how it correlates with diet. Scand J Gastroenterol. 2008 Jan;43(1):95-102.
Musso G, Gambino R, Pacini G, De Michieli F, Cassader M. Prolonged saturated fat-induced, glucose-dependent insulinotropic polypeptide elevation is associated with adipokine imbalance and liver injury in nonalcoholic steatohepatitis: dysregulated enteroadipocyte axis as a novel feature of fatty liver. Am J Clin Nutr. 2009 Feb;89(2):558-67. doi: 10.3945/ajcn.2008.26720.
Choe E, Min DB. Chemistry of deep-fat frying oils. J Food Sci. 2007 Jun;72(5):R77-86.
Goburdhun D, Jhurree B. Effect of deep-fat frying on fat oxidation in soybean oil. Int J Food Sci Nutr. 1995 Nov;46(4):363-71.
Goburdhun D, Jhaumeer-Laulloo SB, Musruck R. Evaluation of soybean oil quality during conventional frying by FTIR and some chemical indexes. Int J Food Sci Nutr. 2001 Jan;52(1):31-42.
Lorenzo C, Hanley AJ, Rewers MJ, Haffner SM. The association of alanine aminotransferase within the normal and mildly elevated range with lipoproteins and apolipoproteins: the Insulin Resistance Atherosclerosis Study. Diabetologia. 2013 Apr;56(4):746-57. doi: 10.1007/s00125-012-2826-4.
Basaranoglu M, Basaranoglu G, Sabuncu T, Sentürk H. Fructose as a key player in the development of fatty liver disease. World J Gastroenterol. 2013 Feb 28;19(8):1166-72. doi: 10.3748/wjg.v19.i8.1166.
Asrih M, Jornayvaz FR. Inflammation as a potential link between nonalcoholic fatty liver disease and insulin resistance. J Endocrinol. 2013 Aug 28;218(3):R25-36. doi: 10.1530/JOE-13-0201.
Maersk M, Belza A, Stødkilde-Jørgensen H, Ringgaard S, Chabanova E, Thomsen H, Pedersen SB, Astrup A, Richelsen B. Sucrose-sweetened beverages increase fat storage in the liver, muscle, and visceral fat depot: a 6-mo randomized intervention study. Am J Clin Nutr. 2012 Feb;95(2):283-9. doi:10.3945/ajcn.111.022533.
Abdelmalek MF, Suzuki A, Guy C, Unalp-Arida A, Colvin R, Johnson RJ, Diehl AM; Nonalcoholic Steatohepatitis Clinical Research Network. Increased fructose consumption is associated with fibrosis severity in patients with nonalcoholic fatty liver disease. Hepatology. 2010 Jun;51(6):1961-71. doi: 10.1002/hep.23535.
Microscope image by Ed Uthman