What a "Heart-Healthy" Diet Does to Your Cholesterol Levels

It's the butter that is bad for you, not the bread... right? (Photo from flickr.com)

What happens when you follow the American Heart Association's dietary recommendations? You know, a diet high in whole grain, vegetables, fruit and berries, but low in animal protein and fat, especially that nasty artery-clogging saturated fat.

According to conventional wisdom, you will be healthier in general. In particular, your cholesterol levels are supposed to improve – though it's never quite clear what "improvement" here means. Is it lower total cholesterol? Or perhaps lower LDL and higher HDL? And what about triglycerides and oxidized LDL?

Fortunately, a few years ago the Journal of the American Heart Association published a study that looked at what happens to cholesterol levels while on the officially heart-healthy diet (link). In contrast to many other studies, the participants in this one were healthy and had normal cholesterol levels to begin with. The idea was to see whether adopting an optimal diet would make them even healthier.

Study design and composition of diets

The study included 37 healthy women and consisted of two phases. During the first phase, the women followed a low-fat, low-vegetable diet for five weeks. After that, there was a three week washout period, followed by the second experimental diet. This second diet was the "optimal" diet, which was also low-fat but this time included lots of vegetables, fruit and berries. To make sure that the dietary guidelines were followed, the meals were supervised.

Both diets included 8 portions of grain products, 3-4 portions of low-fat or fat-free dairy products, and 2 portions of lean meat, chicken or fish. In the first phase, the subjects were given 2 portions of fruit and vegetables per day. In the second phase, the amount of fruit and vegetables was increased to 4-5 and 5-6 portions, respectively.

Dietary fats were replaced vegetable oils and spreads which contained minimal amounts of trans fats. The amount of total fat and saturated fat decreased, whereas the amount of polyunsaturated fats increased. To replace the lost calories, the subjects ate more carbohydrates and protein. Fiber intake also increased; in the second phase, it was nearly twice as much as at baseline.

Thus, both diets were very close to official recommendations: they included only moderate amounts of fat and animal protein, the fat was mostly from vegetable oils high in polyunsaturated fatty acids, dairy products were low in fat or fat-free, and grain products high in fiber were included. In addition, the second phase was high in veggies, fruits and berries.

HDL, LDL and triglycerides

After the low-fat, low-vegetable phase, total cholesterol was unchanged. On the other hand, triglycerides and HDL decreased, while LDL levels increased. The increase in LDL was apparently not statistically significant, which is probably due to the small sample size.

When the amount of vegetables, fruit and berries was increased, total cholesterol decreased. Triglycerides remained the same, but both HDL and LDL decreased:

Thus, reducing the amount of fat in the diet and replacing animal fats with vegetable oils did not change total cholesterol but did change the cholesterol profile: HDL and triglycerides decreased, while LDL increased. From the "good cholesterol, bad cholesterol" standpoint, adopting a low-fat diet actually changed things for the worse.

Things were not much better when vegetables, fruit and berries were added to the low-fat diet. Total cholesterol was clearly reduced, which by some standards is admittedly a positive change. Importantly, however, this change was not achieved through a decrease in "harmful" LDL but in "healthy" HDL.

The amount of triglycerides did decrease compared to baseline, but the reason is unclear. Generally, replacing fats with carbohydrates seems to increase triglycerides. Also, triglycerides decreased after the first phase, when the diet was low in vegetables, and did not decrease further after the second phase, so dietary antioxidants don't seem to be the explanation either. One thing that comes to mind is alcohol intake, which is not reported in the study. Perhaps the subjects reduced their alcohol intake while on the experimental diets? That would show up as a lower triglyceride score, but we can't know for sure.

Oxidized LDL and lipoprotein (a)

Both oxidized LDL and lipoprotein (a) are independently associated with a higher risk of atherosclerosis – more so than total cholesterol or LDL. In fact, oxidized LDL (ox-LDL) is believed to cause clogging of arteries and inflammation. Lipoprotein (a), also called Lp(a), is a known risk factor in many cardiovascular diseases, although its function is not entirely understood.

The most interesting result of the study is that the number of oxidized LDL particles and Lp(a) increased significantly as a result of following the low-fat diets. Oxidized LDL increased by a whopping 27% in the first phase. Even after vegetables, fruits and berries were added to the diet, ox-LDL levels were still 19% higher than at baseline. Similarly, Lipoprotein (a) was 7% higher after the first phase and 9% higher after the second phase compared to baseline.

What this means is that two important risk factors of atherosclerosis worsened markedly after following the very dietary recommendations that are supposed to reduce risk of atherosclerosis. Although plasma antioxidant capacity correlated with the intake of fruit, vegetables and berries, the antioxidants in them were clearly not enough to protect from these harmful changes.

The changes in total cholesterol, HDL, LDL and triglycerides were relatively small, which may be partly due to the short duration of the study. However, the 27% increase in ox-LDL demonstrates that diet can have a dramatic even in a short period of time.

Conclusion

The authors describe the results as "unexpected". According to them, a decreased intake of fat – especially saturated fat – should have led to a decrease in risk factors. They quote a number of studies where replacing saturated fatty acids with polyunsaturated fatty acids led to a "beneficial" decrease in total cholesterol. So why did the risk factors of atherosclerosis not see a similar "beneficial" change?

It is true that fats and oils high in polyunsaturated fatty acids generally tend to lower cholesterol (although the relationship between different fatty acids and cholesterol is more complicated than that). A completely different question is whether total cholesterol even matters, however. Even official recommendations acknowledge that the ratio of LDL to HDL is a better predictor of CVD than total cholesterol.

As was to be expected, the low-fat diets in this study did reduce total cholesterol. But if that decrease happens by reducing HDL and not changing or even increasing LDL, is the change really for the better? Most importantly, if the drop in total cholesterol comes with a marked increase in Lp(a) and oxidized LDL, can the results really be seen as beneficial?

Since the results of the study are incompatible with the cholesterol hypothesis and dietary recommendations, the authors came up with an alternative explanation. According to their hypothesis, high Lp(a) and ox-LDL may in fact be a sign of existing artherial damage being fixed and therefore a positive thing – but of course only in the case of low-fat diets. Right.

For anybody who has been keeping up with the gradual destruction of the cholesterol hypothesis, these results are not all that surprising. For example, we already know that polyunsaturated fatty acids oxidize much more easily than monounsaturated or saturated fats. It seems logical that LDL would be oxidized also.

What is somewhat surprising, however, is that the study was published in a journal that promotes the official dietary recommendations as heart-healthy.

For more information on cholesterol and diets, see these posts:

Which Oils and Fats Are Best for Cooking?
Carotenoids and Lipid Peroxidation: Can Vegetables & Fruit Reduce ALEs?
Sugar and AGEs: Fructose Is 10 Times Worse than Glucose
Anthocyanins from Berries Increase HDL and Lower LDL

Why Are Thin People Not Fat?

How do some people manage to stay thin despite eating a lot?

You probably know at least a couple of people who just don't seem to get fat no matter how much they eat. Some of them don't even do much exercise. But is it really true that some of us gain weight more easily than others, or do thin people just eat less calories?

Most of the studies on obesity and weight loss have been done on subjects who are overweight to begin with. A BBC Horizon documentary titled Why are thin people not fat? looked at the obesity problem from a different angle. They chose subjects who were naturally thin and stuffed them with excess calories. None of the participants had watched their food intake before, but their weight had remained roughly the same for years.

The subjects were told to eat at least double their usual calories and to avoid exercise for four weeks. The target energy intake for men was 5,000 kcal and somewhat less for women. The purpose was to find out whether naturally thin people would start gaining weight, given a sufficiently large amount of calories. It was no exercise in healthy eating either: the menu included processed, calorie-dense foods such as cakes and milkshakes. Precisely the kind of thing that should make one fat.

The documentary begins by mentioning a similar experiment done on Vermont prison inmates in 1967. The inmates were grossly overfed with the purpose of studying the hormonal changes that happen when a person becomes obese. The prisoners who signed up were promised an earlier release.

Each inmate was supposed to increase their body weight by 25 percent. However, as the experiment progressed, it turned out that no matter how high the energy intake got, some of the inmates could not reach their targets. Despite eating and eating, they just didn't gain enough weight. One of them could not increase his body weight more than 18%, even though his daily calorie intake reached a whopping 10,000 kcal.

For years, experts argued over the results of the Vermont prison study. According to the classical model of calories in, calories out, such high intakes should have led to a dramatic weight gain, especially since exercise was forbidden during the experiment. So how did some of the inmates stay thin?

This is the question that the BBC experiment tries to answer. I recommend watching the whole documentary, but here's a summary of the results:

• All participants had trouble reaching their energy intake goals
• Energy-dense foods such as chocolate made reaching the goals easier
• Some of the subjects gained more weight than others
• One of the subjects gained almost no weight but increased his muscle mass
• All subjects returned to their normal weights after the experiment

These results confirm the observations from the Vermont prison study: despite very high calorie intakes, some people have a harder time gaining weight than others. The documentary also explains how naturally thin people are able to stay thin:

• Appetite has a genetic basis
• Age, weight, and diet of the mother during pregancy influence the child's weight
• Eating habits learned during childhood carry on until adulthood
• Naturally thin people avoid excess calories instinctively
• People have a certain "natural weight" towards which the body aims
• Basal metabolic rate plays a strong role in energy expenditure
• The feeling of hunger is related to the number of fat cells
• The number of fat cells can grow but never diminish

There's a lot of debate these days over the importance of basal metabolic rate (BMR) in the calories in, calories out model. It's interesting to note that nobody eats the exact same amount of calories per day, and yet weight remains in a very narrow range (at least in healthy, thin subjects). The one subject who stuck to his 5,000 kcal intake but gained almost no weight supports the idea that there is a kind of setpoint that the body tries to maintain regardless of calorie intake.

It also looks like in some people, the mechanisms to preserve the natural weight setpoint are stronger than in others. Increased heat production is obviously one way to maintain weight during increased energy intake. Some people (Michal Eades comes to mind) have also argued that as the number of calories eaten increases, the body starts to burn them by increasing small, almost involuntary movements such as tapping your fingers, moving your legs, etc. – physical activity which is not considered exercise but still uses up extra energy. I think this theory makes sense.

The last two points of the list are especially interesting. There are two key attributes to fat tissue: the size and number of fat cells. The number of fat cells in your body is typically pretty much determined during adolescence. Thus, eating affects first and foremost the size of your fat cells. As you store and burn energy, the fat cells in your body grow and shrink accordingly.

That's not all there is to it, however. If you keep eating even after the fat cells have grown to their maximum size, at some point the body will begin to produce new fat cells to store all that extra energy. The tendency to produce more fat cells probably depends on the individual.

The problem is that according to our current understanding, the number of fat cells can only be increased, never decreased. This means that any new fat cells produced as a result of (prolonged) overeating will always stay with you. What's worse, as the purpose of fat cells is precisely to store energy, the body will now send more signals of hunger to your brain to keep those fat cells filled up. Obviously this makes following diets that rely only on cutting back on calories very difficult.

The overall message of the documentary is that being naturally thin is a combination of many factors, some of which are genetically determined and some a result of the environment. Of course, individual choice also plays a role, but the studies on small children given unlimited candy show that even before we have the capability to think rationally about our food choices (kids will eat as much candy as they desire), there are differences among people.

For those who have to struggle to maintain or lose weight, things are more difficult – though not impossible by any means. It just means paying attention to your diet, venturing beyond governmental recommendations, and trying on yourself what works. I've had many overweight people tell me how difficult it is to lose weight, and then when I ask them if they've tried for example a basic low-carb diet, they've either tried it for a few weeks and quit, or they've deemed it "unhealthy", because all they can picture is Atkins on his deathbed and slices of bacon clogging their arteries.

Are you a naturally thin person who can eat and eat without gaining weight? Are you the exact opposite? Share your experiences in the comment section!

For more information on diet and weight loss, see these posts:

Alternate-Day Feeding and Weight Loss: Is It the Calories Or the Fasting?
Green Tea and Capsaicin Reduce Hunger and Calorie Intake
A High-Protein Diet Is Better than a High-Carbohydrate Diet for Weight Loss
Low-Carb vs. Low-Fat: Effects on Weight Loss and Cholesterol in Overweight Men

Soy Isoflavones and Chili Pepper for Hair Growth – Experiment Begins

The hotter the pepper, the more capsaicin it contains. (Photo by Andreas Adermark)

I've written so many posts on soy isoflavones and hair growth that I figured it's time to start another experiment to see for myself whether the claims are true.

Even though it looks like soy isoflavones alone are sufficient to increase dermal levels of IGF-1 and thus promote hair growth, the most effective combination seems to be isoflavones and capsaicin. If you haven't seen the pictures from that paper for some reason, I recommend taking a look at the latter link. This combination is the one I will be testing.

The soy isoflavones supplement I have is by NOW Foods. It contains 60 mg of isoflavones (genistein, daidzein and glycitein) per capsule. This is slightly less than the 75 mg used in the human study, but since I don't want to take 120 mg per day, it'll have to do.

As for capsaicin, I'm going with the natural route and adding chili pepper to my foods during the experiment. There are capsaicin supplements too, but since I like spicy foods anyway, I don't think supplements are worth the extra money in this case.

The only problem is that it's pretty difficult to estimate the amount of capsaicin; a tablespoon of ground chili will contain anywhere between 0.8 mg and 480 mg of capsaicin. In the study, 7 mg per day was consumed, so if I manage to eat a tablespoon, I should have decent odds of ingesting at least as much capsaicin.

As you can see, this is not an exact replica of the human study, but I think my own experiment will be very close to what other people might try at home. The study lasted for 5 months, which is how long you should give any treatment before realistically expecting results. I will post an update after I run out of capsules and we'll see what happens then.

Keep in mind that this is not the only thing I have going on at the moment that might affect hair growth. Though not technically experiments, I've been using ketoconazole and piroctone olamine shampoos regularly, because the science behind them looks pretty good. I'm also consuming some ground flax seeds every now and then, which could be beneficial for hair.

Since I started to use these three things, I've noticed a slight decrease in the number of hairs lost daily. Whereas I counted 60-80 before, I now seem to lose about 40-50 hairs daily. Both of these figures are within the normal range, so these additions to my health regiment are mostly about preventing (or at least delaying) any future hair loss. Still, if the hair growth promoting effect of isoflavones and capsaicin is as strong as the rodent and human studies show, I would expect some visible changes even in people without androgenic alopecia.

Lastly, my experiments with retinoids and an Ayurvedic topical called Nutrich oil are still running. I'm applying both of them on my temples, one on the left and the other on the right, to see if they increase hair growth. So far I have not noticed any dramatic changes, so I don't think they will obfuscate the results of this experiment too much.

I'll keep you updated on how things go. Meanwhile, if you've tried soy isoflavones or capsaicin, drop a comment and share your experiences!

For more information on hair growth, see these posts:

BioSil, JarroSil & Beer – Silicon Experiment Conclusion
Emu Oil vs. Hair Again® Topical Gel: Hair Growth Battle Conclusion
Eclipta Alba Extract Grows Hair Quicker than Minoxidil
Do Flax Lignans Reduce Hair Loss from MPB?