Water And Weight Loss

Water helps to lose weight.
The liver's job is to convert the stored fat into energy, this metabolism of fat is directly influenced by the amount of water you drink. It directly affects your body fat and weight loss.

The liver also acts as a backup for the kidney, which needs plenty of water to work properly.The kidneys cannot function properly without enough water. When kidneys do not work to full capacity, some of their load is shifted on the liver. But if the liver has to do some of the kidney's work, it cannot do its job. It then can't metabolize fat quickly or efficiently so weight loss slows down.

So drinking water is important for losing weight. Water suppresses the appetite naturally and helps the body metabolize stored fat. Decrease in water intake will cause fat deposits to increase and an increase in water intake can actually reduce fat deposits.

Nonalcoholic Fatty Liver Disease

Nonalcoholic fatty liver disease (NAFLD) is milder form of NASH, in which the liver becomes enlarged and accumulates fat. Ready for a shocker? The prevalence of NAFLD is thought to be between 20 and 30 percent in the Western world, and rising. It's typically associated with insulin resistance and often with the metabolic syndrome. This has lead some researchers to believe it's caused by insulin resistance. It's a chicken and egg question, but I believe it's the other way around if anything.

There are certain animal models of human disease that are so informative I keep coming back to them again and again. One of my favorites is the LIRKO mouse, or liver-specific insulin receptor knockout mouse. The LIRKO mouse is missing its insulin receptor in the liver only, so it is a model of severe insulin resistance of the liver. It accumulates a small amount of fat in its liver in old age, but nothing that resembles NAFLD. So liver insulin resistance doesn't lead to NAFLD or NASH, at least in this model.

What else happens to the LIRKO mouse? It develops severe whole-body insulin resistance, impaired glucose tolerance, high fasting blood glucose and hyperinsulinemia (chronically elevated insulin). So insulin resistance in the liver is sufficient to cause whole-body insulin resistance, hyperinsulinemia and certain other hallmarks of the metabolic syndrome, while liver and whole-body insulin resistance are not sufficient to cause NAFLD or NASH. This is consistent with the fact that nearly everyone with NAFLD is insulin resistant, while many who are insulin resistant do not have NAFLD.

In all fairness, there are reasons why NAFLD is believed to be caused by insulin resistance. For example, insulin-sensitizing drugs improve NAFLD. However, that doesn't mean the initial metabolic 'hit' wasn't in the liver. One could imagine a scenario in which liver insulin resistance leads to insulin resistance in other tissues, which creates a positive feedback that aggravates NAFLD. Or perhaps NAFLD requires two 'hits', one to peripheral insulin sensitivity and another directly to the liver.

In any case, I feel that the most plausible mechanism for NAFLD goes something like this: too much n-6 from polyunsaturated vegetable oil (along with insufficient n-3), plus too much fructose from sweeteners, combine to cause NAFLD. The liver becomes insulin resistant at this point, leading to whole-body insulin resistance, hyperinsulinemia, impaired glucose tolerance and general metabolic havoc.

How to Fatten Your Liver

Steatohepatitis is a condition in which the liver becomes inflamed and accumulates fat. It was formerly found almost exclusively in alcoholics. In the 1980s, a new condition was described called nonalcoholic steatohepatitis (NASH), basically steatohepatitis without the alcoholism. Today, NASH is thought to affect more than 2% of the adult American population. The liver has many important functions. It's not an organ you want to break.

This week, I've been reading about how to fatten your liver. First up: industrial vegetable oil. The study that initially sent me on this nerd safari was recently published in the Journal of Nutrition. It's titled "Increased Apoptosis in High-Fat Diet–Induced Nonalcoholic Steatohepatitis in Rats Is Associated with c-Jun NH₂-Terminal Kinase Activation and Elevated Proapoptotic Bax". Quite a mouthful. The important thing for the purpose of this post is that the investigators fed rats a high-fat diet, which induced NASH.

Anytime a study mentions a "high-fat diet", I immediately look to see what they were actually feeding the animals. To my utter amazement, there was no information on the composition of the high-fat diet in the methods section, only a reference to another paper. Apparently fat composition is irrelevant. Despite the fact that a high-fat diet from coconut oil or butter does not produce NASH in rats. Fortunately, I was able to track down the reference. The only difference between the standard diet and the high-fat diet was the addition of a large amount of corn oil and the subtraction of carbohydrate (dextrin maltose).

Corn oil is one of the worst vegetable oils. You've eaten corn so you know it's not an oily seed. To concentrate the oil and make it palatable, manufacturers use organic solvents, high heat, and several rounds of chemical treatment. It's also extremely rich in n-6 linoleic acid. The consumption of corn oil and other n-6 rich oils has risen dramatically in the US in the last 30 years, making them prime suspects in NASH. They have replaced the natural (more saturated) fats we once got from meat and milk.

Next up: fructose. Feeding rats an extreme amount of fructose (60% of calories) gives them nonalcoholic fatty liver disease (NAFLD), NASH's younger sibling, even when the fat in their chow is lard. Given the upward trend of US fructose consumption (mostly from high-fructose corn syrup), and the refined sugar consumed everywhere else (50% fructose), it's also high on my list of suspects.

Here's my prescription for homemade foie gras: take one serving of soybean oil fried french fries, a basket of corn oil fried chicken nuggets, a healthy salad drenched in cottonseed oil ranch dressing, and wash it all down with a tall cup of soda. It's worked for millions of Americans!

Real Food VI: Liver

Liver was a highly regarded food among many hunter-gatherer and traditional agricultural societies. It's not surprising once you realize it's quite literally the most nutritious food in the world. It's because the liver is a storage depot, into which important nutrients are deposited in case of later need. A modest 4-oz serving of calf's liver contains 690% of your RDA of B12, 610% of preformed vitamin A, 215% of folate, 129% of B2, 24.5 g protein, and the list goes on. The nutrients found in liver are particularly important for development, but are also helpful for continued health in adulthood.

Preformed vitamin A is one of the nutrients Weston Price suggested was responsible for the glowing health of the cultures he studied in his book Nutrition and Physical Degeneration. It's an essential nutrient, but it's different from most vitamins (except D) because it acts like a hormone, entering cells and altering gene transcription. Thus, it has its hand in many important bodily processes.

"Vitamin A" from plant sources such as carrots is actually a group of vitamin A precursors called carotenes, which the body inefficiently converts to actual vitamin A. The efficiency of conversion varies around 10%, depending on the carotene and how much fat is ingested along with it. Nutrition labels in the US do not reflect this. When a nutrition label on a plant-based product says "30% vitamin A", you can assume you will get about 3% of your RDA from it. This doesn't apply to eggs, dairy and liver, which contain preformed vitamin A.

I'm not sure how this happened, but somewhere along the line we decided in the US that muscle is the only proper animal tissue to eat. We are missing out on the most nutritious parts of the animal, and our health is suffering.

I recommend purchasing organic calf's liver, 100% grass-fed if possible. Chicken livers are also nutritious but ruminant livers are the most concentrated in vitamins by far.

Here is a recipe for a liver pate. I recognize that many people don't like the taste of liver, which is why I chose this recipe because it is very mild.

Ingredients

• 1/2 to 1 lb calf's liver, chopped into 1-in strips
  
• 3 eggs
• 1/2 stick butter
• 1/2 onion
• 1-2 carrots (optional)
• Sage and/or rosemary (optional)
• Salt to taste
  

Recipe

1. Saute the onions and carrots in 1 tbsp butter until they're soft.
2. Add liver and herbs and cook until the liver is just done.
3. Crack the eggs right into the pan and stir them until they're cooked.
4. Turn off the heat, add the remaining butter.
5. Blend until smooth.

Enjoy!

More Liver

It's time to celebrate your liver. It's a hard-working organ and it deserves some credit.

One of the liver's most important overall functions is maintaining nutrient homeostasis. It controls the blood level of a number of macro- and micronutrients, and attempts to keep them all at optimal levels.

Here's a list of some of the liver's functions I'm aware of:

• Buffers blood glucose by taking it up or releasing it when needed
• A major storage site for glycogen (a glucose polymer)
  
• Clears insulin from the blood
• Synthesizes triglycerides
• Secretes and absorbs lipoprotein particles ("cholesterol")
• Stores important vitamins: B12, folate, A, D, E, K (that's why it's so nutritious to eat!)
• Stores minerals: copper and iron
  
• Detoxifies the blood
• Produces ketone bodies when glucose is running low
• Secretes blood proteins
• Secretes bile
• Converts thyroid hormones
• Converts vitamin D (D3 --> 25(OH)D3)
  

The liver is an all-purpose metabolic powerhouse and storage depot. In the next post, I'll give you a recipe for it...

The Liver: Your Metabolic Gatekeeper

As I've been learning more about the different blood markers of metabolic dysfunction, something suddenly occurred to me. Most of them reflect liver function! Elevated fasting glucose, low HDL cholesterol, high LDL cholesterol, high triglycerides and high fasting insulin all reflect (at least in part) liver function. The liver is the "Grand Central Station" of cholesterol and fatty acid metabolism, to quote Philip A. Wood from How Fat Works. It's also critical for insulin and glucose control, as I'll explain shortly. When we look at our blood lipid profile, fasting glucose, or insulin, what we're seeing is largely a snapshot of our liver function. Does no one talk about this or am I just late to the party here?!

I read a paper today from the lab of C. Ronald Kahn that really drove home the point. They created a liver-specific insulin receptor knockout (LIRKO) mouse, which is a model of severe insulin resistance in the liver. The mouse ends up developing severe whole-body insulin resistance, dramatically elevated post-meal insulin levels (20-fold!), impaired glucose tolerance, and elevated post-meal and fasting glucose. Keep in mind that this all resulted from nothing more than an insulin resistant liver.

LIRKO mice had elevated post-meal blood glucose due to the liver's unresponsiveness to insulin's command to take up sugar. Apparently the liver can dispose of one third of the glucose from a meal, turning it into glycogen and triglycerides. The elevated fasting glucose was caused by insulin not suppressing gluconeogenesis (glucose synthesis) by the liver. In other words, the liver has no way to know that there's already enough glucose in the blood so it keeps on pumping it out. This is highly relevant to diabetics because fasting hyperglycemia comes mostly from increased glucose output by the liver. This can be due to liver insulin resistance or insufficient insulin production by the pancreas.

One of the interesting things about LIRKO mice is their dramatically elevated insulin level. Their pancreases are enlarged and swollen with insulin. It's as if the pancreas is screaming at the body to pick up the slack and take up the post-meal glucose the liver isn't disposing of. The elevated insulin isn't just due to increased output by the pancreas, however. It's also due to decreased disposal by the liver. According to the paper, the liver is responsible for 75% of insulin clearance from the blood in mice. The hyperinsulinemia they observed was both due to increased secretion and decreased clearance. Interestingly, they noted no decline in beta cell (the cells that secrete insulin) function even under such a high load.

Something that's interesting to note about these mice is they have very low blood triglyceride. It makes sense since insulin is what tells the liver to produce it. Could this have something to do with their lack of beta cell dysfunction?

The really strange thing about LIRKO mice is that their blood glucose becomes more normal with age. Strange until you see the reason: their livers are degenerating so they can't keep up glucose production!

LIRKO mice reproduce many of the characteristics of type II diabetes, without degenerating completely into beta cell death. So insulin resistance in the liver appears to reproduce some elements of diabetes and the metabolic syndrome, but the full-blown disorders require other tissues as well. As a side note, this group also has a skeletal muscle-specific insulin receptor knockout which is basically normal. Interesting considering muscle tissue seems to be one of the first tissues to become insulin resistant during diabetes onset.

So if you want to end up like your good pal LIRKO, remember to drink high-fructose corn syrup with every meal! You'll have fatty liver and insulin resistance in no time!

I have a lot more to say about the liver, but I'll continue it in another post.