Artifical Sweeteners Make You Fat

It seems counter-intuitive, but it might be true.  Artificially sweetened drinks could be contributing to the obesity epidemic.

Ordering a Diet Coke may make you feel less guilty about an afternoon snack, but there’s little data to show that switching to diet drinks does anything to help control weight in the long run.  Some data even shows an increase in weight gain among frequent users.

Five artificial sugar substitutes have been approved by the U.S. Food and Drug Administration: sucralose, aspartame, acesulfame, neotame and saccharin.  A 2007 review in the European Journal of Clinical Nutrition (61:691-700) looked at epidemiological, laboratory, and clinical studies of their usefulness and ultimately decided that the data is just not clear enough to say much of anything.  Since scientific findings are mixed, there’s no official recommendation about using artificial sweeteners as a tool to lose weight or to limit the addition of new pounds of fat.

With simple logic, replacing a 140-calorie Coke with one that contains no calories should stave off one twenty-fifth of a pound of body fat.  Over time, that should add up.  By always drinking a Diet Coke with a meal rather than the 140-calorie version, over 25 meals a dieter should prevent the addition of one extra pound.

The problem with using simple logic is that the human body isn’t that simple.  It’s a highly complex product of nature with innate intelligence beyond what we perceive with our minds.

Sweet natural foods like fruit supply the body with a ready to use form of energy, and that energy induces changes in the brain and body.  But artificial sweeteners uncouple the sweet taste from energy content.  It confuses our brain’s regulatory centers that help us to accurately assess how many calories we’ve consumed.  We throw an artificial wrench in the bio-computer.

At Purdue University in Indiana, researchers found that saccharin-fed rats took in more food overall and gained more weight than rats fed sugar sweetened food.  The usually saccharin-fed rats also had a smaller rise in core body temperature after eating sugary foods later. Basically that means they burned calories less efficiently, ate more, and gained weight when given artificial sweeteners in place of sugar.

In humans, a San Antonia Heart Study found that consuming more diet drinks over a 7-year period was associated with weight gain.  Drinking more than 21 servings of diet drinks in a week rather than none doubled the risk of being overweight or obese.  21 servings a week is about 3 servings per day, or 24 ounces.  Sound like a lot?  Its not when you realize that an average bottle of Coke from the soda machine contains 2.5 servings, or 20 ounces.

Another report, the Multi-Ethnic Study of Atherosclerosis, looked at 6814 adults and found that daily consumption of diet drinks was associated with a 67% greater risk for type 2 diabetes.

Both studies of observational data must be taken with a grain of salt though, because it’s possible that people first gained weight and then switched to diet drinks.  It’s a little bit of “which came first, the chicken or the egg?”  Given the animal studies, the possibility that there’s more to the biochemistry of artificial sweeteners than we realized must be seriously considered.

The best bet?  Avoid unnecessary synthetic chemicals whenever you can, and that includes in your no-calorie drinks.

Drink water.  Add a slice of fresh lemon or cucumber with nothing else.  It’s delicious!

What is Cholesterol Myth (part 4)

One point to remember is that the studies in the Harvard review didn’t differentiate between omega-6 and omega-3 poly-unsaturated fats. The latter is protective against heart disease while the former is of questionable merit. Could it be that using oils like canola that have higher levels of omega-3 rather than something like lard, which is predominately saturated fat, is really what matters? Is it not the reduction of saturated fat but rather the addition of omega-3? Again, I think it’s a concerted effort of both together. Those saturated fat calories have to be replaced with something – might as well be healthy, protective fats instead of sugar, white bread, hydrogenated oils and junk food.

My take is that we should be eating less saturated fat and cholesterol, and that means less animal fat. All saturated fat isnt the same though, and saturated fat from plant sources, like coconuts, is better than animal sources because it contains primarily medium chain fatty acids rather than long ones.  The Yogis may have had this one right, too. In the old Hatha Yoga Pradipka, the gurus recommended that aspirants not eat “fish, goat, or other meat” and not consume “oil.” (I:59) On the other hand, they did promote coconuts and even minimal amounts of dairy products for a Yoga diet. (I:62)

While the latter may seem a contradiction, I believe this should be taken within the context of moderation. We need fat. We need cholesterol. They’re paramount to proper bodily functioning. But as with so many things, the middle path of moderation is the key. We have to find the right balance.

The American Heart Association (AHA) agrees, too. They don’t recommend no saturated fat, but rather that the intake is less than 10% of dietary energy for those without heart disease or diabetes. It drops to a recommended 7% of the diet with those conditions.

What’s 10%? If a normal diet is 2000 calories, then 10% is 200 calories.

A large egg contains 1.5 grams of saturated fat, and at 9 calories per gram, that’s  13.5 calories from saturated fat. (It also contains about 200 grams of cholesterol, so within the <300 grams of actual cholesterol per day recommended by the AHA.)

If you cook the egg in 2 tablespoons of canola oil, that’s another 2 grams of saturated fat. (Canola oil is primarily poly-unsaturated with a high level of healthy omega-3.) So if you fry an egg (okay, I recommend boiling, but…) in canola oil, you’ll get another 18 calories for a total of 31.5 calories of saturated fat from an egg sandwich for breakfast. And that’s less than a quarter of the 200 calories advocated by the AHA.

And what if you cook it in butter? (gasp!) If you use two tablespoons of butter, that’s 14 grams, so another 126 calories from saturated fat. One egg cooked in two tablespoons of butter provides 140 calories from saturated fat, well within the dietary guidelines for cholesterol provided by the AHA. That means, of course, little dairy, meat products or other forms of saturated fat for the rest of the day.

And that’s the problem. Most people would not only eat bacon or sausage with that fried egg, but they might also include a glass of milk or cream in their coffee. Then they would butter their toast. And then they would have cheese for lunch on top of their hamburger. And then have pot roast for supper. (Yes, SUPPER. I’m from the rural Midwest where we also warsh our clothes rather than wash them.)

If you’re considering following Dr. Ornish’s low-fat diet (which I highly recommend) because you have known cholesterol deposits in your blood vessels and heart disease, then the AHA guidelines for the average well person are too high. As noted in my last post, it’s Ornish’s cure-with-diet-and-no-drugs program that has reversed the build-up of cholesterol in the arteries of the heart and decreased heart attacks, hospitalizations, and angioplasties by 2.5 times! It’s those gnarly cholesterol build-ups that destabilize and rupture in a heart attack.

Cholesterol is not the entire answer. It’s not that simple. The human body is complex. Some people have stable cholesterol plaques that never rupture. What makes them rupture? That’s a whole different topic. The point is that when they’re there, that other thing that makes them rupture comes along and ruptures them. And if they’re not present within the blood vessel wall to rupture, then that other thing can’t do so much damage.

Bottom line:

Limit intake of saturated fat, which the body sees as cholesterol, from animal products like meat, milk, cheese and butter. Most people should strive for obtaining only 10% of their calories from animal sources.

Replace most animal fats with olive oil and canola oil.

Avoid hydrogenated fat, partially hydrogenated fat, and trans fat like the plague. They increase LDL cholesterol and reduce HDL cholesterol levels in the blood and lead to disease-causing inflammation – provoking heart attacks from two angles. That means no commercially prepared cookies, crackers,and other baked goods, commercially prepared fried foods, and most margarines.

In the next post, I’ll go over, point-by-point, the “facts” Dr. Ravnskov presents on his website.

References:

Mozffarian D, Micha R, Wallace S. Effects on coronary heart disease of increasing polyunsaturated fat in place of saturated fat: a systematic review and meta-analysis of randomized controlled trials. PLoS Med. 2010 Mar 23;7(3):e1000252.

American Heart Association Dietary Guidelines: Revision 2000

NIH’s National Cholesterol Education Program:  Third Report

What Cholesterol Myth? (part 3)

There’s some people out there, smart ones even, who don’t believe that elevated cholesterol levels are dangerous for your health. One reader recently read The Cholesterol Myth by U. Ravnskov, MD, PhD and wrote to ask my opinion on his anti-cholesterol rhetoric. Is the whole cholesterol thing a scam, a phony issue, a myth?

The mainstream story goes like this:  Animal products and some tropical oils have high levels of saturated fat. Eating a lot of saturated fat increases blood cholesterol levels. Having elevated blood cholesterol increases the chance of dying from a heart attack.

But, well, does it? Does eating saturated fat in the form of meat and whole milk and cheese and eggs and all that other good stuff really lead to heart attacks? Ravnskov’s point is that there is surprisingly little support from good randomized and controlled clinical trials to prove it.

But since Ravnskov stepped down from his soapbox there’s been some new evidence supporting the role of dietary intake of saturated fat (and that means cholesterol as the body sees it) in the development of heart disease. A Harvard study reviewed the literature to date (as of June, 2009) and pooled the existing research to look for an overall effect of replacing saturated fat with poly-unsaturated fat in the form of vegetable and fish oils.

They found that people who replaced saturated fat in their diets with poly-unsaturated fat had a 19% reduced risk of heart disease troubles like heart attacks. For each 5% energy increase of poly-unsaturated fat in the diet substituting for saturated fat, there was a 10% reduction in risk.  It was “dose dependent” so a little reduction of saturated fat helped a little and a big reduction helped a lot. The longer people stuck to the diet change, the greater the benefit that was seen.

The risk of heart disease was reduced by 24% for each 1 mmol/l reduction in total cholesterol. This finding is consistent with results of observational studies of total cholesterol levels and the risk of heart disease.

The Harvard review provides proof from randomized, controlled clinical trials – the gold standard for medical evidence that reducing saturated fat in the diet (and thus cholesterol) and replacing it with poly-unsaturated fat reduces heart attacks. It’s not a myth.

And nobody’s talking drugs here. This is about diet. It’s about what you put into your body.

But there’s one caveat. Because the trials included in this study looked only at replacing saturated with poly-unsaturated fat, it’s not possible from this evidence alone to distinguish between the benefits of reducing saturated fat and the benefits of increasing poly-unsaturated fat. It’s likely they work in concert.

Other studies looking at replacing saturated fat with carbohydrates weren’t so supportive. This may be because of the choice of carb. If participants were eating more refined grains and sugar, then the inflammatory condition inspired by their choices may have counterbalanced any beneficial effect of lowering saturated fat. We know that fructose without fiber (Dr. Lustig’s poison without its antidote) increases triglycerides and the small, dense (ie dangerous) form of LDL. That small form of LDL is what climbs up under the lining of blood vessel walls and forms atherosclerotic plaques of cholesterol that eventually rupture causing a heart attack.

What Cholesterol Myth? (part 2)

The only effective way to lower cholesterol is with drugs, but neither heart mortality or total mortality have been improved with drugs the effect of which is cholesterol-lowering only. On the contrary, these drugs are dangerous to your health and may shorten your life.

Whoa! What kind of nonsense is this? “The only effective way to lower cholesterol is with drugs.” That’s total hogwash. It’s about the diet, baby. What you put into your temple affects what happens inside that temple.

Many people I know just don’t care to eat right. They think they can eat whatever they want and then take a pill to fix it. I see it all the time, even in my own family. I watch my relatives eat fried pork chops, cheeseburgers, and french fries and then go fill their prescriptions for a statin. Poor strategy. ALL drugs have side effects.

But some people have a genetic variation which requires an additional boost from medicine on top of a strict diet. They have to weigh the risk of dying from a heart attack, the leading cause of death in the United States, to the risks of taking a drug which can have harmful side effects. This is an independent, personalized decision.

When it comes to improving mortality, there’s plenty of controversy about using a drug for primary prevention. That means that just because your blood level of cholesterol is high, if you don’t already have heart disease, then you’re probably not getting enough benefit for the risk. The data isn’t really there. But if you have already had a heart attack, then a cholesterol lowering drug may significantly reduce the chances you’ll have another one – or that a second one is fatal. Those drugs work partly by reducing cholesterol, but there is also an indication that they stabilize the cholesterol plaques, preventing that second factor which works in concert, like inflammation or infection, from exploding it.

See a related post of mine here about the potential for harm from cholesterol medications.

 

6  The modern cholesterol-lowering drugs, the statins, do prevent cardiovascular disease, but this is due to other mechanisms than cholesterol-lowering. Unfortunately, they also stimulate cancer in rodents, disturb the functions of the muscles, the heart and the brain and pregnant women taking statins may give birth to children with malformations more severe than those seen after thalidomide.

Um… why can’t it be both? They lower cholesterol and they work by other mechanisms such as stabilizing plaques.

While I’m far, far away from believing that statins should be added to the water supply, there are a few people whose risk-to-benefit ratio makes them useful tools in a total plan that should primarily include diet, exercise, good sleep, stress reduction and weight loss. The trick is to do every freakin’ thing you can to lower your cholesterol to safer levels, and take a drug as a very, very, very last resort. If possible, use it as a bridge for the absolute shortest time possible. They’re not candy. Theyre not a free pass that lets you eat whatever unhealthy food you want. They can be dangerous. It’s not something to take, or to prescribe, lightly.

 

7  Many of these facts have been presented in scientific journals and books for decades but are rarely told to the public by the proponents of the diet-heart idea.

I’m not sure what this means. Science is a long and difficult PROCESS. There are good studies and bad ones, or rather different studies with different kinds of bias and flaws. For almost everything, you can find a study that shows exactly the opposite of what another study shows. The trick is to gather as much information as you can, as much evidence as possible, and then interpret the whole big picture. And the conclusions drawn may very well change over time as data trickles in. That’s good. It means we’re learning. We can’t just snap our fingers and know everything about the human body in an instant. If we could, that would be really awesome.

8  The reason why laymen, doctors and most scientists have been misled is because opposing and disagreeing results are systematically ignored or misquoted in the scientific press.

Um, what I said above.

References:

Mozaffarian D, Micha R, Wallace S. Effects on coronary heart disease of increasing polyunsaturated fat in place of saturated fat: a systematic review and meta-analysis of randomized controlled trials. PLoS Med. 2010 Mar 23;7(3):e1000252.

Fung TT, et al “Low-carbohydrate diets and all-cause and cause-specific mortality” Ann Intern Med 2010; 153: 289-298.

American Heart Association Dietary Guidelines: Revision 2000

http://www.nhlbi.nih.gov/guidelines/cholesterol/atp3full.pdf

Cholesterol Myth Points (part 1)

A reader asks for comments on some specific points:

 

“I was wondering what are your thoughts concerning these issues from a book, “The Cholesterol Myth?”

 

My comments in response to Ravnskovs cholesterol myth points are below in blue.

  1.  Cholesterol is not a deadly poison, but a substance vital to the cells of all mammals. There are no such things as good or bad cholesterol, but mental stress, physical activity and change of body weight may influence the level of blood cholesterol. A high cholesterol is not dangerous by itself, but may reflect an unhealthy condition, or it may be totally innocent.

Cholesterol is definitely NOT a deadly poison. It is a substance vital to all the cells of all mammals. It’s a matter of balance and of finding the optimum level of ingestion so that the body gets an overall benefit, not a negative effect. There are different forms of cholesterol and some are disease promoting, like the small LDL which is tiny enough to get underneath the lining of blood vessel walls and cause narrowing of arteries. Some are more helpful, like HDL, the “garbage truck” of the system that goes around to pick up all the excess poorly deposited cholesterol that it can. A sedentary lifestyle, stress, and excess weight can all lead to higher cholesterol levels. MOST data indicate that cholesterol is a serious risk factor for heart attacks. To be dangerous, that doesn’t mean it has to act “by itself.” For instance, the high cholesterol must first form a plaque in the lining of the blood vessel wall. Then a stimulus comes along, some form of inflammation or infection, which makes the cholesterol plaque explode. It is the explosion that is the heart attack. One factor without the other wouldn’t do much.

 

2  A high blood cholesterol is said to promote atherosclerosis and thus also coronary heart disease. But many studies have shown that people whose blood cholesterol is low become just as atherosclerotic as people whose cholesterol is high.

This statement is pretty simplistic for a few reasons.

  1. Blood cholesterol levels are affected by what you eat and when you eat it. Put most people on a low-fat diet for 3 weeks and the cholesterol level of their blood test will be low. But if before that 3 weeks someone was eating tons of saturated fat, then they’ve got years of cholesterol buildup stuck beneath the lining of the blood vessel wall. It WILL reverse on a low-fat diet, but it takes time. At a year you can see some regression. At five years you see more.
  2. There are genetic differences. Some people have more of the small LDL but yet their total cholesterol levels are not so terribly high. Or they process things differently so that low levels can still wreak havoc.
  3. There are other reasons for heart attacks. High cholesterol is a serious risk factor. It’s not everything.

 

3  Your body produces three to four times more cholesterol than you eat. The production of cholesterol increases when you eat little cholesterol and decreases when you eat much. This explains why the “prudent” diet cannot lower cholesterol more than on average a few per cent.

Yes, the body produces much, much more cholesterol from the intake of saturated fat than it gets from actually ingesting cholesterol itself. That’s part of why eggs and shellfish aren’t so evil. They may have relatively high levels of cholesterol, but ingested cholesterol is not nearly as important as saturated fat which the body turns into cholesterol. The body is efficient. If you eat a unit of cholesterol, then that’s one less unit the metabolic machinery of the body has to manufacture. That does NOT explain “why the prudent diet cannot lower the cholesterol more than on average a few percent.” In fact, it can. In the Lifestyle Heart Trial, LDL cholesterol dropped 40% without the help of any medication. That’s about as much as is seen with Lipitor, one of the most widely prescribed pharmaceuticals.

 

“Cholesterol-rich foods that are relatively low in saturated fatty acid content (notably egg yolks and, to a lesser extent, shellfish) have smaller effects on LDL cholesterol levels.” American Heart Association Dietary Guidellines: Revision 2000

“Saturated fat is the principal dietary determinant of LDL cholesterollevels.” American Heart Association Dietary Guidelines: Revision 2000.

 

4  There is no evidence that too much animal fat and cholesterol in the diet promotes atherosclerosis or heart attacks. For instance, more than twenty studies have shown that people who have had a heart attack havent eaten more fat of any kind than other people, and degree of atherosclerosis at autopsy is unrelated with the diet.

This one is simply not true. A recent meta-analysis of existing data shows that lowering saturated fat in the diet reduces the risk of having a heart attack by 20%.

Another recent large study examining the Atkins Diet found that people who eat animal fat, which is primarily saturated fat, are more likely to die sooner than those eating only vegetable fat, which is un-saturated fat, while on a low-carb diet.

 

“The major food components that raise LDL cholesterol are saturated fatty acids, trans-unsaturated fatty acids, and, to a lesser extent, cholesterol.” American Heart Association Dietary Guidelines: Revision 2000