Lean Liver With A Low-Carb Diet
Generally people are suspicious of low-carb diets — not because of the carbs, but because of the fat. They worry:
Fat makes you fat!
My triglycerides and cholesterol will go up!
My arteries will clog!
The food pyramid says I should cut down on fat and eat more grains!
Your doctor, mother, grandmother, next door neighbour and even governments have been telling you that fat is bad and a low-carb/high-fat diet might help you lose weight now, but you’re putting your health at risk.
Once, even I thought that although people could (maybe, temporarily) lose weight on low-carb diets, they’d be harming their health in the process.
So let’s answer this question definitively: Are you putting yourself at risk by going on a low-carb diet?
No.
In fact, there’s a good chance you’re making yourself healthier.
The truth about low carbohydrate (aka high fat) diets
Over the last decade, many studies have found that if you eat a diet that is lower in carbohydrate and higher in fat:
- You will lose weight.
- Your triglycerides will go down.
- Your HDL (“good”) cholesterol will go up.
- Your cardiovascular health will improve.
Not convinced? I’m not surprised. It seems that every week there’s a new “healthy” way to eat. It’s normal to feel suspicious.
Let’s look more closely at how a diet higher in carbohydrates leads to fat gain, and how that results in higher blood triglycerides.
Fat doesn’t make you fat; carbohydrates make you fat
For years you’ve heard “fat makes you fat”. It’s a nice short clear concise statement that just seems to make perfect sense… on the surface, until you look at how fat storage is regulated.
People imagine when they eat a spoonful of lard that it goes unchanged into a fat cell on their left thigh, or right next to their belly button, in a very FedExy delivery sort of way. Fat to fat.
Meanwhile, people imagine that if they eat a spoonful of sugar it ends up in your blood or muscle, and they “burn it off”. (Actually, most people probably don’t think much at all about all the sugar they consume, which is part of the problem.)
But your body is complicated. It does a lot of processing and regulation of the nutrients you give it. Where nutrients end up is often different than where you might expect. And your diet and activity can affect where nutrients end up — the same nutrients can end up in different places, depending on what else you eat, and how active you are.
Eat more fat, and you won’t necessarily store more fat, but eat more carbohydrate, and you’ll definitely stash that fat away unless you’re running a marathon or climbing Everest.
How sugar creates fat
All carbohydrates (at least, the ones we can digest) break down to two simple sugars after digestion: fructose and glucose. Along with insulin, fructose and glucose regulate fat storage.
And how do you get more insulin? More blood glucose means more insulin. Great!
Glucose increases fat storage in two ways:
- directly; and
- indirectly through insulin.
Candy anyone?
Directly, more blood glucose means more glucose in the liver. If there is a bunch of glucose hanging out in the liver, the body responds by storing those carbs.
While carbs can be stored as glycogen (which can be used as fuel), that “glycogen tank” fills up pretty quickly. When there’s too much carbohydrate to use immediately, the body stores the rest as fat.
Yup, your body can make fat from carbohydrates. This process even has a name: de novo lipogenesis. How can this be? Mostly because two enzymes acetyl-CoA carboxylase (ACC) and fatty acid synthase (FAS) go up when glucose is around.
Indirectly, having more glucose in your blood releases more insulin into your blood, thanks to your pancreas, which secretes insulin in response to a meal — and in proportion to the amount of carbohydrate. Once released, insulin decreases three processes:
- glycogenolysis (breakdown of glycogen);
- gluconeogenesis (making of glucose); and
- lipolysis (breakdown of fat).
In other words, insulin released in response to high blood glucose tells the body to stop breaking down fat.
Insulin also has anabolic (muscle-building) effects: it increases glycogen storage and protein synthesis, which is why you want to consume some carbohydrate (which increases insulin production) immediately after a tough workout.
But here’s the catch: these anabolic effects only work if you combine insulin release with heavy exercise. If you’re just sitting around and you let the insulin rip, it’ll use its superpowers for fat-storing evil.
Thus, blood sugar makes body fat in two ways:
- directly, by triggering fat manufacture through de novo lipogenesis; and
- indirectly, by triggering insulin that reduces fat breakdown.
Together both processes cause fat accumulation by having you make more fat while using less fat.
Okay, so we can see how excess carbohydrate can make you fat, but we still have that little problem of whether low carb diets are actually healthy.
Well, one way to judge the “healthiness” of a diet is to look at particular markers of metabolic health, such as blood lipids.
Lower carbs improve blood lipids
Blood lipids — aka blood fats — are the form of fat that circulates in your bloodstream. Your body packages fats in various ways in order to transport it throughout the system. For instance:
- Triglycerides are molecules made up of three (“tri”) fatty acids and a glycerol group.
- The “cholesterol” that your doctor tests for is actually not the true form of cholesterol (which is a waxy lipid), but a protein that transports fat, known as a lipoprotein. Cholesterol can’t travel well in your blood on its own, because it’s not water-soluble. Your cholesterol hitches a ride on lipoproteins just like tubing down a river. There are several types of lipoproteins, but you’re probably most familiar with high-density lipoprotein (HDL, aka the “good cholesterol”) and low-density lipoprotein (LDL, aka the “bad cholesterol”).
When you get a blood test for lipids, the lab usually looks for both triglycerides and circulating lipoproteins. High blood lipids tell your doctor that you’re probably at higher risk for cardiovascular and metabolic diseases.
It seems to make sense that if you don’t want fat in your bloodstream, then you shouldn’t eat fat. If your doctor thought your cholesterol was too high, s/he’d probably tell you to quit eating fat. Yep, it’s the avocado — not the immortal white sliced bread or “healthy” low fat bran muffin — that’s causing your health problems.
Wrong.
What really happens to your triglycerides, cholesterol and heart health on a low carb/high fat diet? Let’s explore.
Triglycerides and carbohydrates
In fact, the relationship between dietary carbohydrate and blood fat is the opposite of what well-meaning health professionals have been telling us for years.
- The higher your carbohydrate intake (especially if the carbs are processed/refined), the higher your blood triglycerides (unless you’re very active and in the process of losing weight).
- The lower your carbohydrate intake, the lower your blood triglycerides.
Seems a bit strange. More carbs… not more fat… means more blood triglycerides? How the heck does that happen?
Let’s review quickly.
- Your body doesn’t have a lot of carbohydrate storage (after all, nobody complains about their glycogen rolls).
- If you consume excess carbohydrate, your liver makes fat out of it via de novo lipogenesis.
- As the liver makes more fat, you end up with more triglycerides in your blood.
Cholesterol and carbohydrates
Low-carbohydrate diets also increase HDL-C, or the “good cholesterol”. HDL-C transports cholesterol from the rest of the body either back to the liver or to hormone-making glands such as the ovaries and testes.
Higher HDL-C means lower cardiovascular risk. How this happens is still being sorted out, but it’s likely more to do with the increase in dietary fat rather than decrease in carbohydrates.
When you eat a high-fat, low-carb diet, you thus lower your triglycerides while increasing HDL-C. You get an improved ratio of triglycerides to HDL-C ratio, which some experts argue is one of the more reliable markers of cardiovascular disease. Better ratio means lower disease risk. Seems like another win for the low-carb/high-fat diet.
However, while studies consistently find less triglyceride and more HDL-C with low-carb diets, nearly every study also finds more low density lipoprotein cholesterol (LDL-C), aka the “bad cholesterol”, which is a risk factor for cardiovascular disease.
Hmm… what does that mean? That low carb diets are only kinda good for your blood lipids?
Cholesterol: Size matters
To understand the role of LDL, you have to understand that not all LDL-C is created equal. Most people think that LDL-C is one thing. It’s actually a group of lipoproteins that come in different sizes:
- large VLDL (36–60 nm)
- medium VLDL (27–35 nm)
- small VLDL (23–27nm)
- large LDL (21.2–23 nm)
- medium LDL (19.8–21.2)
- small LDL (18–19.8 nm)
As the particles get smaller, they get denser.
Your doctor will tell you how much LDL-C you have, but not what size or type it is. Having more small but dense LDL particles is a higher risk factor for cardiovascular disease than having more large, but less dense, LDL. Smaller LDL-C can penetrate the blood vessel wall and cause plaques.
There are a few studies showing that lower-carbohydrate diets increase the size of LDL, thus improving cardiovascular health, but until a few more studies that look specifically at LDL size and carbohydrate intake are published, I think the jury is still out. However, research shows that lower triglycerides correlate to bigger, less dense LDL, which is good.
So let’s review what happens metabolically with a low-carb, high-fat diet. There won’t be an exam on this — just remember that when you eat fewer carbs and more fat:
- You use more fat productively and store less of it.
- You use less carbohydrate and store less of it too — either as glycogen or as fat.
Fat Metabolism (storing and breaking down of fat) |
Fat oxidation (breakdown of fat) increases |
Muscle triglyceride stores increase |
Muscle triglyceride utilization during exercise increases (in other words, more fat used as fuel) |
Very low density lipid cholesetrol (VLDL-C) increases |
Fatty acid binding protein and fatty acid translocase (FAT/CD36) increases |
Ketone body production and utilization increases |
Muscle lipoprotein lipase increases |
b-Hydroxyacyl-CoA dehydrogenase |
Carnitine acyltransferase I increases |
3-Oxoacid CoA thiolase increases |
Carbohydrate metabolism |
Carbohydrate oxidation (carbohydrate breakdown) decreases |
Muscle glycogen storage decreases |
Muscle glycogen rate of utilization during exercise decreases |
Gluconeogenesis (making of new glucose) decreases |
Phosphoenolpyruvate carboxykinase decreases |
Hexokinase decreases |
Pyruvtate dehydrogenase decreases |
This week’s review
This week’s review looks at how a low-carbohydrate diet affects liver triglycerides in obese people with fatty livers.
Yes, I know it seems like a very special subpopulation, but it is another study showing the safety and possible benefits of low-carbohydrate diets — and in fact, the results are more broadly applicable than you might think.
Fatty liver disease
We are beginning to realize that inflammation as well as high circulating blood fats and glucose don’t just affect the heart — they affect all organs in the body. One organ that is particularly damaged is the liver.
The liver is the processing centre for the body, and it’s uniquely vulnerable to the consequences of metabolic syndrome (high blood sugar, high blood fats, lots of inflammation, and insulin resistance). (Just FYI: If you’re carrying excess body fat, and your liver enzymes are elevated, talk to your doctor — you could be in big trouble and not even realize it.)
In NAFLD, excess fat accumulates in and around the liver. If the diseases progresses far enough, you can end up with cirrhosis, which is essentially trading in your liver for a big bag of scar tissue. This is bad news.
And fatty liver isn’t just restricted to hardcore drinkers. Non-alcoholic fatty liver disease (NAFLD), aka hepatic steatosis, is an emerging problem.
In fact, autopsies on people who died of other causes (such as auto accidents) have shown that about 15 to 20% of people — even quite young people — have fatty livers. Among morbidly obese people about to undergo bariatric surgery, the rate of fatty liver can be as high as 80%!
Given that about 1/3 of the U.S. population is now obese, and that fatty liver goes up as body fat goes up, it’s pretty clear that fatty liver is a little-known, but quite prevalent and serious, health problem. So any insights we gain about its treatment are probably widely applicable.
Can a low-carb, high-fat diet help NAFLD?
This study looked at whether people with NAFLD could manage, or even reverse, their health problems with diet. In addition, this study explores the metabolic improvements that can occur with a low-carb diet (beyond simply losing weight/fat).
Methods
Eighteen people with NAFLD and an average BMI of 35 went on either a low-carbohydrate or low-calorie diet for 2 weeks.
The low carb diet only had 20 g carbs/day (really low) but no specific caloric restriction (though dietary journals showed an average of 1500 cals/day), while the low cal diet was about 1200 cal/day for women and 1500 cal/day for men.
Blood samples were drawn before and after the diets. Researchers scanned everyone’s livers before the diets to confirm liver disease (using 1H-NMR spectra).
Results
Despite being a short study, both groups lost a fair bit of weight (4 kg for the low cal group and 4.6 kg for the low-carb group, on average) though because the severity of the diets, participants probably also lost some lean mass too.
Liver triglycerides went down with weight loss, but more in the low-carb dieters. Low-carb dieters also oxidized (burned) more liver and whole body fat than the low-calorie dieters.
Conclusion
In this study, a lower carbohydrate diet had a metabolic advantage over other diets due to more liver lipid oxidation, higher ketones and higher whole body fat oxidation.
Low carbohydrate diets in general have been shown to:
- lead to weight loss
- lead to fat loss
- improve blood triglycerides — a key risk marker for cardiovascular disease
- improve HDL-C — a key risk marker for cardiovascular disease
- increase or cause no change in LDL-C, though it seems to change the size distribution to a more favourable pattern (more large lower density LDL-C).
Bottom line
When judging the value of diets, we need to look beyond weight loss. Does a given diet improve metabolic markers and disease risk? In this case, the low-carb, high-fat diet scored a win.
Low-carbohydrate diets improve blood triglyceride and HDL-C levels as wells as improving liver triglyceride levels. And both blood and liver triglycerides correlates to dietary carbohydrate intake.
Keep the carbs down and the good fats up, and your liver will stay happy and healthy!
References
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- Wood RJ, Volek JS, Davis SR, Dell’Ova C, Fernandez ML. Effects of a carbohydrate-restricted diet on emerging plasma markers for cardiovascular disease. Nutr Metab (Lond). 2006 May 4;3:19.
- Samaha FF, Iqbal N, Seshadri P, Chicano KL, Daily DA, McGrory J, Williams T, Williams M, Gracely EJ, Stern L. 3. A low-carbohydrate as compared with a low-fat diet in severe obesity. N Engl J Med. 2003 May 22;348(21):2074-81.
- Stern L, Iqbal N, Seshadri P, Chicano KL, Daily DA, McGrory J, Williams M, Gracely EJ, Samaha FF. The effects of low-carbohydrate versus conventional weight loss diets in severely obese adults: one-year follow-up of a randomized trial. Ann Intern Med. 2004 May 18;140(10):778-85.
- Seshadri P, et al. A randomized study comparing the effects of a low-carbohydrate diet and a conventional diet on lipoprotein subfractions and C-reactive protein levels in patients with severe obesity. Am J Med. 2004 Sep 15;117(6):398-405. Erratum in: Am J Med. 2006 Feb;119(2):191
- Foster GD, Wyatt HR, Hill JO, McGuckin BG, Brill C, Mohammed BS, Szapary
PO, Rader DJ, Edman JS, Klein S. 6. A randomized trial of a low-carbohydrate diet for obesity.
N Engl J Med. 2003 May 22;348(21):2082-90.
- Volek JS, Fernandez ML, Feinman RD, Phinney SD. 7. Dietary carbohydrate restriction induces a unique metabolic state positively affecting atherogenic dyslipidemia, fatty acid partitioning, and metabolic syndrome. Prog Lipid Res. 2008 Sep;47(5):307-18. Epub 2008 Mar 15. Review.
- Siri-Tarino PW, Sun Q, Hu FB, Krauss RM. 8. Saturated fat, carbohydrate, and cardiovascular disease.
Am J Clin Nutr. 2010 Mar;91(3):502-9. Epub 2010 Jan 20. Review
- Farrell, Geoffrey C., Jacob George. Fatty liver disease: NASH and related disorders. Wiley-Blackwell, 2005
