A highly recommended documentary which exposes the low fat scam.
Foie gras is a French gourmet delicacy. It is delicious and extremely fatty. Foie gras" translates to "fatty liver" in English and in order to make it, geese or ducks are forced-fed large amounts of a wet mash of corn. Their livers balloon up to about 6-10 times their normal size and are packed full of fat. This serves as a clear picture of the fattening effects of carbs and how it promotes a fatty deposition in the liver. It also explains the epidemic proportions of nonalcoholic fatty liver disease (fatty liver for short) that we are seeing nowadays.

For the most part mainstream doctors ignore how to treat or deal with this condition and a lot of folks are left in the dark as to the real reasons behind fatty liver. So I decided to approach the subject for a clinical session with peer reviewed journal articles as a back up. I was amazed to discover how much information is out there! How on Earth it doesn't reach every single individual in this world is beyond me.

Background

Nonalcoholic fatty liver disease (NAFLD) or fatty liver for short, is an accumulation of fat in the liver in individuals who do not consume significant amounts of alcohol (<20 g ethanol/d) and in whom other known causes of steatosis ("fatty change"), such as certain drugs, viruses, and toxins, have been excluded.[1] The spectrum of this condition includes steatosis (type 1), steatosis plus inflammation (type 2), steatosis plus liver cell (hepatocyte) injury or ballooning degeneration (type 3), and steatosis plus sinusoidal fibrosis and/or Mallory bodies (type 4). Nonalcoholic steatohepatitis (NASH) is considered to be the most severe form of fatty liver (types 3 and 4) and is associated with several clinical outcomes, including cirrhosis, liver cancer (hepatocellular carcinoma), and advanced liver disease, which leads to liver-related death. NASH is now recognized as the underlying cause of most cases of cryptogenic cirrhosis, that is, severe liver disease where no other reason for severe liver damage is found.

Foie Gras = Fatty Liver. Ducks are forced-fed corn and their livers grow 6-10 times their size.
The highest prevalence of fatty liver currently is in the age group of 40 to 60 years. Approximately half of the patients with NASH develop liver fibrosis, 15% develop cirrhosis, and 3% may progress to liver failure or liver transplantation. Those who have undergone liver transplantation for end-stage liver disease secondary to NASH have frequent recurrence of steatosis and NASH even after transplantation.

Fatty liver is basically the most common cause of chronic liver disease in the developed world. It affects 70 million adults in the U.S. (30% of the population) and it is expected to reach epidemic status by the year 2030 where 50% of the U.S. population will have it.[2]

Nonalcoholic fatty liver disease is the most common cause of abnormal liver enzyme test results among adults in the United States. Fatty liver has been documented in up to 10% to 15% of normal-weight individuals and 70% to 80% of obese individuals. Correspondingly, about 3% of normal-weight individuals and 15% to 20% of morbidly obese subjects (body mass index
>35 kg/m2) have steatohepatitis, the most severe form of fatty liver.

A higher prevalence of hepatic steatosis is found in Hispanics (45%) compared with Caucasians (33%) or African Americans (24%).

The Insulin and Metabolic Syndrome Connection

Elevated sugar levels stimulate the pancreas to produce insulin which is a hormone responsible for nutrient storage. A diet high in carbohydrates leading to chronically elevated levels of blood sugar and insulin is at the main root of fatty liver. That is, insulin resistance is the key mechanism in fatty liver. Insulin resistance is directly proportional to severity of steatosis. Fatty liver represents a liver manifestation of the metabolic syndrome which features insulin resistance at its core and which includes central obesity, high blood sugar, low good cholesterol (HDL), high blood pressure, and hypertriglyceridemia. People on a low carb diet have better liver function compared to those on a high carb diet for weight loss, despite when both groups may equally lose weight.

In most case series of fatty liver, diabetes is present in 30% to 50% of patients. High blood cholesterol also is associated commonly with fatty liver, found in up to 92% of patients who have fatty liver.

Obesity itself represents a chronic, inflammatory condition where there is an expansion of central/visceral fat which is infiltrated by inflammatory cells, which then leads to fatty liver and a state of heightened insulin resistance and increased oxidative damage.[3] Fatty liver is an independent predictor of cardiovascular disease - a stronger predictor than peripheral or visceral fat mass. [4].

Moreover, in study involving 11,091 individuals, it was shown that fatty liver, as diagnosed by ultrasound, strongly predicts the development of type 2 diabetes regardless of insulin concentration. That is, in a large population of relatively healthy individuals, identifying fatty liver by ultrasound predicts the development of type 2 diabetes in five years.[5]

The role of fructose and sucrose (which is 50% fructose) in metabolic disorders has been reviewed extensively. Dietary fructose consumption in industrialized countries has increased in parallel with the increase in fatty liver, obesity, and diabetes and there is a direct association. The increased consumption of high fructose corn syrup, primarily in the form of soft drinks, is linked with complications of the metabolic syndrome and an increase in liver enzymes. Unlike glucose, fructose stimulates de novo fatty acid synthesis directly and promotes weight gain.

Fructose is also different from glucose in its ability to induce features of metabolic syndrome (insulin resistance, fatty liver, dyslipidemia, and intra-abdominal fat accumulation) both in humans and laboratory animals. The mechanism whereby fructose induces fatty liver appears to be independent of total energy intake.[6]

Data from prospective and intervention studies clearly point to high fructose consumption, mainly in the form of sweetened beverages, as a risk factor for several metabolic diseases. In a short (2 wk) dietary intervention study in fatty liver subjects, it was showed that carbohydrate restriction (<20 g/d) was significantly more effective in reducing liver fatty content than the restriction of calories to 1200-1500 kcal/d (55% vs 28%, respectively), despite the fact that both interventions similarly reduced body weight (by about 4.3%)[7].

Dr. Robert H. Lustig from the University of California had the following comment published in the prestigious journal Nature[8]:
Last September, the United Nations declared that, for the first time in human history, chronic non-communicable diseases such as heart disease, cancer and diabetes pose a greater health burden worldwide than do infectious diseases, contributing to 35 million deaths annually. This is not just a problem of the developed world. Every country that has adopted the Western diet - one dominated by low-cost, highly processed food - has witnessed rising rates of obesity and related diseases. There are now 30% more people who are obese than who are undernourished.[...]

Over the past 50 years, consumption of sugar has tripled worldwide. In the United States, there is fierce controversy over the pervasive use of one particular added sugar - high-fructose corn syrup (HFCS). It is manufactured from corn syrup (glucose), processed to yield a roughly equal mixture of glucose and fructose. Most other developed countries eschew HFCS, relying on naturally occurring sucrose as an added sugar, which also consists of equal parts glucose and fructose.

Authorities consider sugar as 'empty calories' - but there is nothing empty about these calories. A growing body of scientific evidence shows that fructose can trigger processes that lead to liver toxicity and a host of other chronic diseases. A little is not a problem, but a lot kills - slowly (see 'Deadly effect'). If international bodies are truly concerned about public health, they must consider limiting fructose - and its main delivery vehicles, the added sugars HFCS and sucrose - which pose dangers to individuals and to society as a whole.

NO ORDINARY COMMODITY

In 2003, social psychologist Thomas Babor and his colleagues published a landmark book called Alcohol: No Ordinary Commodity, in which they established four criteria, now largely accepted by the public-health community, that justify the regulation of alcohol - unavoidability (or pervasiveness throughout society), toxicity, potential for abuse and negative impact on society. Sugar meets the same criteria, and we believe that it similarly warrants some form of societal intervention.[...]

Now, let's consider toxicity. A growing body of epidemiological and mechanistic evidence argues that excessive sugar consumption affects human health beyond simply adding calories. Importantly, sugar induces all of the diseases associated with metabolic syndrome. This includes: hypertension (fructose increases uric acid, which raises blood pressure); high triglycerides and insulin resistance through synthesis of fat in the liver; diabetes from increased liver glucose production combined with insulin resistance; and the ageing process, caused by damage to lipids, proteins and DNA through nonenzymatic binding of fructose to these molecules. It can also be argued that fructose exerts toxic effects on the liver similar to those of alcohol. This is no surprise, because alcohol is derived from the fermentation of sugar. Some early studies have also linked sugar consumption to human cancer and cognitive decline.[...]

Specifically, sugar dampens the suppression of the hormone ghrelin, which signals hunger to the brain. It also interferes with the normal transport and signalling of the hormone leptin, which helps to produce the feeling of satiety. And it reduces dopamine signalling in the brain's reward centre, thereby decreasing the pleasure derived from food and compelling the individual to consume more.[...]


Lustig, R.H. Fructose: Metabolic, Hedonic, and Societal Parallels with Ethanol J. Am. Diet. Assoc. 110, 1307-1321 (2010).
The long-term economic, health-care and human costs of metabolic syndrome place sugar overconsumption in the same category. The United States spends $65 billion in lost productivity and $150 billion on health-care resources annually for co-morbidities associated with metabolic syndrome. Seventy-five per cent of all US health-care dollars are now spent on treating these diseases and resultant disabilities. Because 75% of military applicants are now rejected for obesity-related reasons, the past three US surgeons general and the chairman of the US Joint Chiefs of Staff have declared obesity a "threat to national security".[...]
But the problem doesn't end with sugar. While a diet high in carbohydrates leading to chronically elevated levels of blood sugar and insulin is at the main root of fatty liver, there are other culprits, such as trans fats.

Trans fats typically found in animal products do not have adverse effects on cholesterol profiles. On the other hand, trans fats from hydrogenated oils such as margarine, induces endothelial dysfunction and unfavorably alter cholesterol levels by increasing the bad: good cholesterol ratio and the total cholesterol: good cholesterol ratio. (LDL:HDL, TC: HDL).[9] Excess insulin triggered by a high carbohydrate diet strongly influences a pro-inflammatory response in the body, especially when coupled with excess omega-6s fatty acids from vegetable oil and hydrogenated oils.

People who get at least 25% of their daily calories from added sugars of any kind -fructose or other sugar sweeteners used by the food industry and consumers as ingredients in processed or prepared foods - are 3.1 times more likely to have low levels of so-called good cholesterol in their bloodstream than people who get less than 5% of their calories from added sweeteners. Additionally, those who consume more than 17.5% of their calories from the sugars - be it ordinary table sugar derived from sugar cane or sugar beets, high fructose corn syrup or any other caloric sweetener - are 20% to 30% more likely to have high levels of blood fats called triglycerides than people with the low-sugar diets.[10] The American Heart Association suggests no more than 5 percent of calories come from sugar. On a 2,000 calorie diet, that's 24 grams, or the equivalent of six teaspoons. A can of Coke has 39 grams of sugar; a regular size frozen yogurt has 40 grams...

Dracula in Charge of the Blood Blank

In the BBC documentary "The Men Who Made Us Fat" (available here), Jacques Peretti refers to America as the home of the most profitable food industry in the world. He goes there to find out about the low fat scam, since if there is a way to get us to buy more food is probably being tried in America first. He interviews Pierre Chandon, visiting professor at Harvard Business School who has studied "The Paradox of Low Fat Food and High Fat People". Chandon noticed how people basically tried so hard to lose weight while trying to eat the right things (recommended by their caring governments) and they still couldn't manage to lose weight. He thought, there is a problem with the healthy food! Well, yes of course there is!! Chandon summed up the problem as "if people think something is healthy, they think it has fewer calories and eat more of it". Never mind that the root of the problem is not really about quantities of calories but qualities of calories! According to Chandon, "Today it's almost impossible to buy food that's not saying it's healthy. The paradox of low fat food and high fat people is not going to go away. I think it's going to get worse." And the greatest mistake was to believe that it was solely our fault when it is clear that it wasn't.

The BBC documentary also makes a pretty good job showing how the sugar lobby once threatened the World Health Organization of withdrawing their 406 million funding if they set a limit on sugar, so they didn't. See how food policy gets dictated? As Professor Simon Capewell from the University of Liverpool puts it, putting the food industry at the policy table is like putting Dracula in charge of the blood bank. Their money resources are of massive proportions and they are able to stop dissent by tactics such as menace of removing food jobs in the constituency areas of politicians if they carry on with a policy that will affect the food industry. It is really a laser-like precision to remove dissent against the Giants - The Food Industry.

The conflict of interest is massively outrageous. Instead of admitting that the Food Industry is part of the problem, it is put to provide for a solution. "From your shareholder perspective, would you like to suggest how we take forward food policy in this country?" How is that for a bias?

Not remotely interested on health, but on business profiting, the Food Industry is capitalizing on the obesity epidemic and your suffering by manufacturing processed foods which are dubiously marketed as healthier. Saying that a cereal "contains calcium" in glowing letters in front of a cereal box is outrageous to say the least, when in fact it is full of sugar that will cause you osteoporotic bones.

Or how about the health-epitome Olympic Games celebrated in London last year courtesy of your sponsors: chocolate brands, sugary drinks, etc. Or the UK government endorsed Cadbury's sporting campaign where you have to eat a ton of chocolate in order to get a basketball for free. It is a profit scheme in the middle of a health catastrophe which only has an obligation to the shareholders and their profits.

A study which analyzed the relationship between research funding and outcome in the area of nutrition related with soft drinks, milk and fruit juice illustrates these points:
Of 206 relevant studies, 111 declared their source of funding. Of this 111, more than half (53 per cent) were funded in full or in part by the food industry. 52 studies had no funding from the food industry. [...] In studies which were interventional in nature (which usually meant giving a beverage to individuals to assess its effects), 37 per cent of non-industry-funded intervention studies showed evidence of adverse effects. In contrast 0 out of 16 (0 per cent) industry-funded intervention studies found evidence of adverse effect. Studies funded entirely by industry were more than 7 ½ times more likely to report favorable results than those which received no industry funding.
Go Low Carb

It is recognized that the change in diet since the Agricultural Revolution, Industrial Revolution and the Modern Age has systemically destroyed our health and that the mismatch between our ancient physiology and current diet is at the root of many so-called diseases of civilization: coronary heart disease, obesity, hypertension, type-2 diabetes, cancer, autoimmune disease, osteoporosis, etc. which are virtually absent in hunter-gatherers and non-westernized populations.[11] Most of the human genome has ancestral genes that adapted for over millions of years to a caveman diet.

Low-carb ketogenic diets are effective for weight loss, seizure disorders, and a host of other neurological diseases. Attention has focused on the use of low carb diets and their efficacy in controlling metabolic diseases including obesity and fatty liver.[12] A ketogenic diet has led to significant weight loss and histological improvement of fatty liver disease [13]. A ketogenic diet - a diet based on animal fats - is the one thing that could put an end to this nightmare. (For more information on the ketogenic diet, check out the threads in Sott.net's forum "Life Without Bread" and "Ketogenic Diet"). And considering that there is no evidence for concluding that animal saturated fat is associated with an increased risk of cardiovascular disease, then there is simply no good reason at all to fear animal fat [14].

Notes

[1] Linda Wasserbach York et al. Nonalcoholic Fatty Liver Disease and Low-Carbohydrate Diets Annu. Rev. Nutr. 2009. 29:365 - 79
[2] European Association for the Study of the Liver (2011, April 2). New data show non-alcoholic fatty liver disease will reach epidemic status in the US. ScienceDaily. Retrieved February 3, 2013, from http://www.sciencedaily.com­ /releases/2011/04/110402163427.htm
[3] Erin Marie McCarthy. The Role of Diet and Nutrient Composition in Nonalcoholic Fatty Liver Disease. Journal of the Academy of Nutrition and Dietetics. 2012;112:401-409.
[4] Schugar et al. Low-carbohydrate ketogenic diets, glucose homeostasis, and nonalcoholic fatty liver disease. Curr Opin Clin Nutr Metab Care 2012, 15: 374-380.
[5] The Endocrine Society (2011, February 25). Fatty liver may herald impending Type 2 diabetes. ScienceDaily. Retrieved February 3, 2013, from http://www.sciencedaily.com­ /releases/2011/02/110224091613.htm
[6] Lanaspa et al. Uric Acid Stimulates Fructokinase and Accelerates Fructose Metabolism in the Development of Fatty Liver. PLoS One. 2012; 7(10): e47948.
[7] Rebollo et al. Way back for fructose and liver metabolism: bench side to molecular insights. World J Gastroenterol 2012 December 7; 18(45):6552-6559
[8] Lustig et al. The toxic truth about sugar. Nature 2012 Feb 1;482(7383):27-9
[9] Zivkovic et al. Comparative review of diets for the metabolic syndrome: implications for nonalcoholic fatty liver disease. Am J Clin Nutr 2007; 86:285-300.
[10] Welsh et al. Caloric Sweetener Consumption and Dyslipidemia Among US Adults. JAMA, April 21, 2010 - Vol 303, N. 15, 1490-1497.
[11] Carrera-Bastos P., Fontes-Villalba M., et al. The western diet and lifestyle and diseases of civilization. Research Reports in Clinical Cardiology. 2011:2, 15-35.
[12] Schugar et al. Low-carbohydrate ketogenic diets, glucose homeostasis, and nonalcoholic fatty liver disease. Curr Opin Clin Nutr Metab Care 2012, 15: 374-380.
[13] Tendler et al. The Effect of a low-carbohydrate, ketogenic diet on nonalcoholic fatty liver disease: a pilot study. Dig Dis Sci (2007) 52: 589-593.
[14] Siri-Tarino PW, Sun Q, Hu FB, Krauss RM. Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. Am J Cln Nutr. 2010 Mar;91(3):535-46