Study Finds that Carbs Prevent Energy Use

Supports Chapter 19: 'Healthy eating' is fattening

A few days ago, England’s Euro 2012 football team lost a quarter-final match to Italy on penalties. This scenario has happened so regularly that one might call it the ‘England finish’.

It has also happened so regularly that it hasn’t been difficult to see a pattern emerging for some years: England just run out of energy; they aren’t able to sustain 90 minutes of football.

The question is: Why? And the answer, which I have been convinced of for some years, was their rubbish carb-based diet. I am no lover of football, so have never watched a game, but commentaries on news bulletins spell out the form. To précis it, the England team always seem to start the game full of bounce, have most of the possession and often take the lead, then I all goes wrong. At half time they fill up on Jaffa cakes - and are so rubbish during the second half that they lose. But this, is exactly what I would expect. Carbs not only result in reactive hypoglycaemia (you run out of blood glucose), they also raise serotonin, a hormone that makes you sleepy and slows you down. This is why people are advised to have a carb meal before going to bed. But both of these conditions are the last thing you should eat if you have to work – or play football.

Now a study just published in the Journal of the American Medical Association finds another good reason why the carbs, so favoured by the England team’s nutritionists, are so devastating to their game: Carbs, it now appears, as well as everything else that is wrong with them, actively slow down the rate at which your body can use its energy.

Here is the abstract of the study – and an explanation as it is a bit convoluted:

Ebbeling CB, et al. Effects of Dietary Composition on Energy Expenditure During Weight-Loss Maintenance. JAMA 2012;307(24):2627-2634

ABSTRACT

Context Reduced energy expenditure following weight loss is thought to contribute to weight gain. However, the effect of dietary composition on energy expenditure during weight-loss maintenance has not been studied.

Objective To examine the effects of 3 diets differing widely in macronutrient composition and glycemic load on energy expenditure following weight loss.

Design, Setting, and Participants A controlled 3-way crossover design involving 21 overweight and obese young adults conducted at Children’s Hospital Boston and Brigham and Women’s Hospital, Boston, Massachusetts, between June 16, 2006, and June 21, 2010, with recruitment by newspaper advertisements and postings.

Intervention After achieving 10% to 15% weight loss while consuming a run-in diet, participants consumed an isocaloric low-fat diet (60% of energy from carbohydrate, 20% from fat, 20% from protein; high glycemic load), low–glycemic index diet (40% from carbohydrate, 40% from fat, and 20% from protein; moderate glycemic load), and very low-carbohydrate diet (10% from carbohydrate, 60% from fat, and 30% from protein; low glycemic load) in random order, each for 4 weeks.

Main Outcome Measures Primary outcome was resting energy expenditure (REE), with secondary outcomes of total energy expenditure (TEE), hormone levels, and metabolic syndrome components.

Results Compared with the pre–weight-loss baseline, the decrease in REE was greatest with the low-fat diet (mean [95% CI], –205 [–265 to –144] kcal/d), intermediate with the low–glycemic index diet (–166 [–227 to –106] kcal/d), and least with the very low-carbohydrate diet (−138 [–198 to –77] kcal/d; overall P=.03; P for trend by glycemic load=.009). The decrease in TEE showed a similar pattern (mean [95% CI], −423 [–606 to –239] kcal/d; −297 [–479 to –115] kcal/d; and −97 [–281 to 86] kcal/d, respectively; overall P=.003; P for trend by glycemic load<.001). Hormone levels and metabolic syndrome components also varied during weight maintenance by diet (leptin, P<.001; 24-hour urinary cortisol, P=.005; indexes of peripheral [P=.02] and hepatic [P=.03] insulin sensitivity; high-density lipoprotein [HDL] cholesterol, P<.001; non-HDL cholesterol, P<.001; triglycerides, P<.001; plasminogen activator inhibitor 1, P for trend=.04; and C-reactive protein, P for trend=.05), but no consistent favourable pattern emerged.

Conclusion Among overweight and obese young adults compared with pre–weightloss energy expenditure, isocaloric feeding following 10% to 15% weight loss resulted in decreases in REE and TEE that were greatest with the low-fat diet, intermediate with the low–glycemic index diet, and least with the very low-carbohydrate diet.

What it means

This is a study looking at weight loss, but in a different way from normal. Usually, scientists look at the amount of weight lost and/or for how long. This one is different; here they are considering how the different macronutrients affect energy usage. To make it confusing, the authors don't talk about energy usage, they talk in terms of 'decrease' in amount of energy used.

The study looks at two aspects of energy usage. A person has to use a certain amount of energy just to keep their body alive: These are things like the heart beating, brain working, keeping the body warm, etc, which they call “resting energy expenditure” (REE). This is relatively constant at approximately 1,500 kcals for an average-sized person. On top of that is the amount of energy we use when we do work or exercise. The total of the two is the total energy expenditure (TEE).

Here we have three different diets with same amount of calories, but with different ratios of carbs, proteins and fats. In this respect it is similar to the Dunlop & Lyon study of 1932 and Kekwick & Pawan’s 1956 study, both of which found that the lowest carb diet was the best for weight loss. With a similar finding, this latest study tells us why. When they ate the 60% carb diet, the participants used the least energy. It even cut the amount of energy used to maintain the body (REE). The diet on which they used the most energy (both REE and TEE) was the diet which had the least carbs and most fats.

Diet and exercise

So, if you are counting calories and exercising to lose weight, as the ‘experts’ say you should, then, obviously, when you exercise, you want to use as much energy as possible. There isn’t much point in jogging lots of boring miles if you are not going to use up energy – and thus weight - right? But this study shows that if you eat the diet these incompetent ‘experts’ advise you to eat, you won’t lose as much as you would if your diet was high-fat, low-carb!

And if you are an England footballer, you really don’t want to have to eat a diet that destroys your ability to use all your energy. Or a nutritionist/dietician who insists on it!

Now, Statins May Increase Heart Attack Risk!

Supports Chapter 2: What's Behind The Screens?

It is widely believed that atherosclerosis, the 'furring up' of the arteries, narrows the coronary arteries and makes a heart attack more likely in two ways: Firstly, a clot in a partially blocked artery is more likely to block it completely, cutting off the blood supply downstream; and secondly, the atherosclerosis itself may block the artery with a similar result.

Many laymen have been led to believe that cholesterol is to blame for the blockage, or 'plaque', but this is hotly disputed. Much more likely, it seems, is that calcification of the artery wall, which hardens the artery wall making it less pliable, is the cause.

Statin Use Tied to Faster Plaque Buildup

A small observational American study of war veterans with diabetes and advanced coronary heart disease has found that those who regularly took statins had accelerated progression of calcification. This current analysis included 197 participants with type 2 diabetes from the Risk Factors, Atherosclerosis, and Clinical Events in Diabetes (RACED) study, a substudy of the Veterans Affairs Diabetes Trial (VADT) study.

Study participants who were frequent statin users were found to have significantly more coronary plaque advancement than those who were less frequent users (P<0.001), according to Aramesh Saremi, MD, and colleagues from the Phoenix VA Health Care System in Arizona.

The results remained the same even after adjusting for age, duration of diabetes, hypertension, cardiovascular events, baseline coronary artery calcium, race and ethnicity, blood pressure, total cholesterol/high density lipoprotein cholesterol (HDL-C), and body mass index, Saremi's team reported here at the annual meeting of the American Diabetes Association.

But Cam Patterson, MD, from the Center for Heart and Vascular Care at the University of North Carolina at Chapel Hill, and who was not involved in this study, warned that it would be a 'horrible mistake to infer that strict compliance with statin use is somehow causally associated with progression of atherosclerosis. Adding that he thought that such a conclusion is definitively a false one.

'The patients who were more compliant with statin therapy had much higher calcium scores at baseline, so these are obviously patients who had a substantially greater propensity for atherosclerosis to begin with,' Patterson said. He suggested that patients who already have vascular disease are more likely to be compliant with their statins.

Saremi does not disagree with Patterson; the progression of calcification may be linked to the healing of soft plaque initiated by statin therapy.

'It's important now to determine whether this progression of calcification leads to cardiovascular events.

She also suggested that if diabetics are put on statins earlier in the course of their disease, when their calcium scores are low, there may not be such a rapid advancement of calcification. But this is unsupported supposition.



In this substudy, 36 patients reported less frequent statin use, while 161 reported more frequent use. The mean age of patients was 61 and the average follow-up was 4.6 years.
In the unadjusted model, researchers found that every 10% increase in statin use was associated with a 0.41 mm³ increase in coronary calcium progression (P<0.01), which did not change much in the adjusted model: 0.33 mm³ increase (P=0.04).

When researchers excluded those with prior or new cardiovascular events, the risk for calcium progression remained the same.

Saremi and colleagues speculated that statins may enhance the density of calcification as part of the healing process, potentially contributing to plaque stabilization and decreased cardiovascular disease events . But this is more unsupported speculation (they don't like to give up on statins, even though statins have also been shown to increase diabetes risk). However, they did also suggest that the advancement of plaque in type 2 diabetics who frequently took statins may lessen the medication's overall benefit.

Reference:

Saremi A, et al. Progression of vascular calcification is increased with statin use in the Veterans Affairs Diabetes Trial (VADT)" ADA 2012; Abstract 426-P.