"Study shows dieters had higher rates of heart disease"

This headline, in some newspapers back in 1994, was based on statements made by Blair at an American Heart Association meeting. He surveyed 12,025 Harvard alumni, and found that those who claimed they were always on a diet had a heart disease rate twice that of those who said they never dieted.

Before you start worrying, be aware that the increased risk of heart disease noted in this study has been reported previously, and is not a consequence of dieting as such. The explanation, and the solution, will become clear as you read on. In other words, it does not change the basic rule: fat people must lose weight in order to improve their health.

Ashley and Kannel (1974) noted that 10% weight gain increased the risk of heart disease by 30%, but a weight loss of 10% was only associated with a 20% decrease in risk. They concluded that repeated cycles of weight gain and loss could have a net negative effect. Hamm et al. (1989) also reported that the risk of heart disease was increased in men who gained and lost large amounts of weight, compared to those whose weight did not change, while Avons et al. (1983) found that successful weight loss was associated with a reduced risk of heart disease, but with an increase in mortality from heart disease (more sudden cardiac deaths).

Insurance company statistics still show that losing excess weight increases life expectancy, and so do many other scientific studies. The overall conclusion is that those who gain weight and then lose it again may not drop back to the level of heart disease risk applicable to the ideal weight they have re-achieved, but that they certainly are at less risk than if they had stayed fat. The benefit of losing weight is still positive, but may become less positive with each cycle of weight gain and loss!

Why the increased risk, and can we do anything about it? The answers to these questions also apply to the sudden deaths that occur in joggers and young athletes, since the same mechanism is involved.

Heart attacks are usually due to thrombosis of a coronary artery (arteries which supply the heart with blood). Generally, the thrombosis occurs at a site where the artery is already constricted or damaged by a fatty plaque (atherosclerosis). This takes many years to develop, and often gives symptoms of angina pectoris long before a true heart attack occurs; in such cases, cardiac surgery can provide relief. Drugs which dilate the coronary arteries are also useful.

The atherosclerotic plaque looks like a "repair" process, contains fat and cholesterol, and may contain other materials. Lipoproteins (which transport cholesterol and fat in the blood) normally diffuse through the arterial wall and into lymphatic vessels which surround arteries, and it is thought that atherosclerosis occurs when this diffusion is slowed down, as happens when the arterial wall is damaged. In this case, less stable lipoproteins, such as the Low Density Lipoproteins (LDL), may break down in the arterial wall, releasing their fat load. The more stable High Density Lipoproteins (HDL) remain intact, which is why HDL-cholesterol is "good", and LDL-cholesterol is termed "bad".

While high LDL levels, or high blood pressure forcing more LDL into the vessel wall, could result in atherosclerosis, by overloading the diffusion capacity, it is now thought that the arterial wall must first be damaged. Though it has been suggested that free radical oxidation of LDL can cause such damage (and that antioxidant vitamins can protect against this), it is generally thought that this damage is due to blood platelets starting to stick together, and then to the arterial wall (this is also the first stage of thrombosis). The substance which makes platelets stick together is our old "friend", Thromboxane A2, made in platelets from arachidonic acid (AA); the more they make, the "stickier" platelets will become, and if enough stick together, and firmly enough, thrombosis occurs!

So if blood platelets are repeatedly exposed to small amounts of AA, arterial damage can occur and will eventually result in atherosclerosis, which narrows the arteries and in turn provides sites where thrombosis could occur. Coronary arteries are very susceptible to atherosclerosis, because they are squeezed almost closed every time the heart beats, and if there are "sticky" platelets about, they are most likely to get stuck to the walls of the coronary arteries. If, however, platelets are suddenly exposed to large amounts of AA, as in the case of sudden death in joggers, thrombosis can occur in the absence of arterial disease.

How does this explain why dieting can increase the risk of heart disease? The composition of stored fat in humans reflects that of the fat eaten, and a conventional "normal" diet containing large amounts of animal products, particularly red meat, results in deposition of AA in stored fat reserves (Jones, 1993). During dieting, and during periods of prolonged exertion (as in jogging), the body draws on these fat reserves for energy, and large amounts of AA are released into the blood (Wilson et al., 1989; Phinney et al., 1991). As shown above, this can result in progressive arterial damage which will increase the ultimate risk of developing heart disease. If large quantities of trans fatty acids (from partially hydrogenated domestic oils) formed part of the "normal" diet, then fat stores also contain trans fatty acids (Willett et al., 1993) which will also be released into the circulation, and can aggravate the situation by blocking metabolism of essential fatty acids (Jones, 1993).

This scenario applies to those who have previously eaten "normal" food, but probably not to vegetarians (Phinney et al., 1990) or those who have regularly eaten much fish. Use of specialty essential fatty acid (EFA) products containing both omega-3 and omega-6 EFAs in the correct proportions also offers some protection.

Excessive amounts of AA have also been implicated in the occurrence of gallstones, which likewise can occur more frequently in dieters (Marks et al., 1992).

The situation sounds grim; most of those who want to lose weight have been living on "normal" diets, oblivious to the fact that their metabolism (that of a vegetarian) cannot really cope with dietary AA or trans fatty acids. However, they do need to lose that weight, so how can it be done without putting them at risk of vascular damage or gallstones? A biopsy of adipose tissue before starting a diet is impracticable! However, a simple questionnaire on food preferences will certainly reveal what the patient likes to eat, and probably has been eating. If this is suspicious, which it probably will be in most cases, then the fat stores should be "flushed" out, to remove stored AA and trans fatty acids, before starting diet programs.

Since there is a constant turnover of fatty acids in the fat stores, putting a patient on a medium fat diet (30% - 50% calories from fat) in which the fat is derived only from vegetable oil (NOT partially hydrogenated) and fish for 14 - 28 days should remove most of the stored AA and trans fatty acids at a sufficiently gentle rate that they will do no harm. Use of an essential fatty acid supplement containing eicosapentaenoic acid (EPA) and gammalinolenic acid (GLA) in the correct proportions will help; EPA competes with AA for the enzyme that controls thomboxane formation, but the Thromboxane A3 produced by the platelets from EPA does NOT make them stick together; if anything, it makes them less sticky! Most of the GLA in the product will also ultimately be converted into Thromboxane A1, which is also non-thrombogenic, though the ratio of EPA TO GLA is rather critical to ensure that Thromboxane A2 production is indeed minimized.

Many commercial weight loss programs have a pre-diet stabilization phase, and some include such steps for patients whose previous dietary habits are known to place them at risk. Risks can also be reduced by ensuring that dieters receive appropriate essential fatty acid supplementation during the reduced caloric intake phases of their diet programs, and restricting or eliminating the use of red meat.

It could also improve patient compliance and long-term success rates if the patients were aware that they do not have an unlimited number of chances to lose weight, and they will be better off getting it right the first time!

So it appears that there is a direct link between yo-yo dieting and development of arterial disease, which in turn may result in coronary thrombosis. What of other major "diseases of civilization" that are associated with excess body weight?

The answer is that most have not been studied in a yo-yo diet situation, but we could use the known facts and speculate rather accurately.

An increase in blood pressure, of course, is itself damaging to blood vessels, and blood pressure does increase when body weight increases. So during the "increase" phase of the yo-yo cycle, the blood vessels are suffering further abuse. Of course, abused blood vessels will lose their elasticity, so that blood pressure will gradually increase anyway. So theoretically, yo-yo dieting may cause gradual and permanent increase in blood pressure.

The situation with diabetes is more difficult to understand. Obesity will push the body into a situation where it is no longer able to control blood sugar levels correctly, so that if the degree of obesity is sufficient, even insulin may be required, but there is no evidence that there will be a gradual deterioration in carbohydrate metabolism with each yo-yo cycle.

One thing that is clear, however, is that if the yo-yo dieter uses bad diets during the "decrease" phase of each cycle, then they are also going to suffer some physical damage.

The need for a high protein intake in diet programs is well documented (Bistrian et al., 1981; Vasquez et al., 1985; Pasquali et al., 1987), and Oi et al. (1987) quantified the requirements for an 1100 calorie diet. They found that the minimal protein intake required to prevent loss of lean body mass on this relatively mild diet was 1.26 g/kg ideal weight/day. Not surprisingly, they also reported that the high protein intake also improved rates of weight loss by about 1 lb per week in their subjects, when compared to rates of loss on a low-protein 1100 calorie diet. Such findings have also been reported by other researchers.

Davis and Phinney (1990) showed that the ability to perform both aerobic and anaerobic exercise was maintained by a high protein, low calorie diet, but that this ability fell significantly on low calorie diets which supplied only moderate amounts of protein, indicating impairment of muscle function.

The EAAs in protein play major roles in the brain (Cooper et al., 1986), and in the context of weight loss, tryptophan may be the most important (Wurtman, 1987) because of its role as a precursor for serotonin, which is involved in a number of behavioral functions, including satiety and mood. In fact, Anderson et al. (1990) found that women on conventional low calorie diets had low blood tryptophan levels, which would correlate with the clinical depression sometimes seen with badly designed low calorie diets. Wadden et al. (1985) also commented that some behavioral features (including preoccupation with food) which occur on very low calorie diets are absent with high protein, low calorie diets.

So what are the consequences for the yo-yo dieter if they just reduce their caloric intake and do not increase protein intake during the "decrease" phase of each cycle?

Firstly, they will gradually lose lean tissue from muscle and vital organs, including the heart. This will not be replaced during the "increase" phases of their cycles, so they will become physically weaker and, if it becomes extreme, may suffer actual tissue damage, particularly of the heart.

Secondly, they will be suffering from psychological events during the "decrease" phases which will, in fact, gradually lead to cheating (self-therapy of depressive states) and ultimately to abandonment of the "diet". Thus they start into their next "increase" phase. Which does make one wonder whether the yo-yo diet syndrome can somehow be connected with trying to diet on bad diets!