Category Archives: Weight Loss - Page 3

Protein, Satiety, and Body Composition

Posted by on January 25, 2011 62 comments

A number of studies have found protein to be the most satiating macronutrient, with fat moderately satiating, and carbs least satiating.

Thus, when people reduce carbs and increase protein, their appetite declines and they almost always reduce calorie intake. This can leads to rapid short-term weight loss. This is why most popular weight loss diets are high in protein: increasing protein causes dieters to quickly lose some weight, encouraging them to continue.

A 2005 editorial in the American Journal of Clinical Nutrition summarized the evidence that higher protein intake is helpful for weight loss:

The higher than usually recommended protein content of many popular diets, such as the Atkins Diet, The Zone, and The South Beach Diet, seems to point at possible solutions to the obesity epidemic. Many national dietary guidelines have, until recently, recommended that only 10–20% of the calorie content of the diet come from protein; however, 30–40% of the calorie content in the aforementioned diets comes from protein, at the expense of carbohydrates. Newer research indicates that the high-protein content of these diets may actually be the reason for their partial success in inducing weight loss, despite no restrictions in total calories (2)….

In this issue of the Journal, Weigle et al (3) showed that an increase in dietary protein from 15% to 30% of energy and a reduction in fat from 35% to 20%, at a constant carbohydrate intake, produces a sustained decrease in ad libitum calorie intake and results in significant weight loss….

Weigle et al’s results clearly showed that protein is more satiating than is fat, and previous studies have shown that protein is more satiating than is carbohydrate (4). Moreover, diets with a fat content fixed at 30% of calories produce more weight loss when high in protein (25% of energy) than when normal in protein (12% of energy): 9.4 compared with 5.9 kg after 6 mo; after 1 y, evidence was found to suggest that the high-protein diet, independent of the loss of total body fat, resulted in a significant loss of visceral fat (5). [1]

But there are downsides to high protein consumption. Various animal experiments have found that longevity is increased with protein restriction. Also, protein restriction promotes autophagy, which enhances immunity to intracellular bacteria and viruses. So higher protein intake may shorten lifespan and increase the risk of disease.

In a post on his blog (linked in this comment), Dennis Mangan introduced us to the “protein leverage hypothesis.” This hypothesis is put forward in a 2005 paper by SJ Simpson of Oxford University and D Raubenheimer of the University of Auckland [2].

The Satiating Power of Protein

The paper has some graphs which neatly illustrate the satiating power of protein. When animals are given a food formula with a lower protein fraction, they eat more total calories.

Here are some data from rats (b) and chickens (c). The numbers are in kiloJoules; divide by 4.18 to get calories. The animals were on feed formulas with a constant fat content, but different carb-protein ratios. Each data point represents a diet with a different P:C ratio.

If both macronutrients were equally satiating, then the animals would eat the same amount of calories regardless of their food’s protein-carb ratio. The data points would fall on a 45º line (say, for chickens, a constant 1000-kJ line connecting the 1000 kJ mark on the y-axis with the 1000 kJ mark on the x-axis).

But they don’t:  if a line were fitted to these points, it would be much closer to vertical than 45º. The rats, for instance, eat around 150 kJ protein and 75 kJ carb if given high-protein food, but 75kJ protein and 300 KJ carb if given high-carb food. That’s 225 kJ (54 calories) on a high-protein diet, but 375 kJ (90 calories) on a high-carb diet.

The chickens and rats act like protein dominates appetite control:

  • A shortage of protein makes them hungry, and it takes a lot of carbohydrate to satisfy that hunger. So they eat a calorie excess.
  • An excess of protein satisfies their hunger and causes them to quit eating while they are still in calorie deficit.

Evidence in Humans

The same sort of thing happens in humans:

Results a, b, and c are from “short-term” experiments that varied from 2 days to 6 months in length. Results d, e, f, and g are from “long-term” experiments.

People tend to gravitate toward a protein intake of 1520 kJ (360 calories). This can be construed as the “normal” human protein intake, and tends to occur near a carb+fat intake of 8000 kJ (1900 calories). So the “normal” protein fraction of the diet is 360/2260 or 16%. This is consistent with epidemiological data, which finds that nearly everyone worldwide eats near 15% protein.

A line fit to the data has the same steep slope as the animal experiments, but note something interesting. The short-term experiments have a very steep slope, but the long-term experiments have a slope much closer to 45º.

This has to happen. Otherwise, a high-protein diet would lead to permanent calorie deficit which, over time, would lead to starvation. A low-protein diet would lead to permanent calorie excess which, over time, would lead to obesity.

Since we know people neither starve nor become obese due to small adjustments in protein fraction, they must adjust their calorie intake. In the long run, protein no longer controls calorie intake. So there is great protein leverage in the short-term, but much less protein leverage in the long term.

Simpson and Raubenheimer try to develop protein leverage into a theory of obesity. It’s not a very good theory, so I’ve relegated it to an appendix.

Instead, I’d like to talk about what this satiating power of protein means for Perfect Health Dieters.

Implications for Perfect Health Dieters

We have a fairly broad healthy protein range, 200 to 600 calories per day, which brackets the “normal” protein intake of 360 calories. What happens if you shift from 360 calories protein to either the low-protein or high-protein ends of the range?

IF YOU REDUCE PROTEIN: 

At low-protein intake, your appetite goes up and total calories go up. You gain a little weight, in the form of adipose mass. This causes leptin levels to increase. As we discussed in “How Does a Cell Avoid Obesity?”, higher leptin (a) lowers appetite and (b) increases thermogenesis, or destruction of fat as waste heat.

Adipose mass increases until the actions of leptin counterbalance the influence of protein leverage.

You reach equilibrium at a slightly higher fat mass and slightly higher leptin levels than on the “normal” protein intake.

IF YOU INCREASE PROTEIN:

At high protein intake, appetite goes down and total calories decrease. You start to lose adipose mass. This causes leptin levels to go down. This (a) increases appetite and (b) decreases thermogenesis, or heat generation.

Adipose mass decreases until a new equilibrium is reached. Equilibrium is reached at a slightly lower weight and slightly lower leptin than on the “normal” protein intake.

IN SHORT:

The main effect of changing the protein content of the diet is a modest change in body composition.

  • High-protein diets make you leaner and a little lighter.
  • Low-protein diets give you a slightly higher adipose reserve and make you slightly heavier.

The effect is probably small; probably just a few pounds either way. But if you’re looking for to win a bodybuilding competition and you have to become extremely lean and “cut,” you’d do well to adopt a high-protein diet.

It’s probably not a surprise, then, that people with the leanest bodies tend to be healthy but high-protein dieters. Here’s a picture of Anthony Colpo:

I think Anthony has a healthy body, but I don’t think you need to be this lean to be healthy. He would be equally healthy with a few more pounds of adipose tissue.

Conclusion

In the book we say that higher protein intake makes it easier to add muscle, and thus that it may be favored by athletes. Based on today’s post, we can adduce two other reasons to eat a high protein diet:

  1. A more chiseled body. If you want a lean, “cut” look, like Anthony Colpo, high protein will help.
  2. A controlled appetite. In a recent post, Don Matesz stated that he liked a high-protein diet because it helped him auto-regulate his calorie intake. If your goal is “effortless” (willpower-less) calorie restriction, then high protein may help – at least for a while.

However, there are reasons to restrict protein as well. Lower protein intake is likely to extend lifespan, and can increase immunity against intracellular bacteria and viruses, which are behind many late-life diseases.

Is it possible to achieve a lean, muscular body while still gaining the longevity and immunity advantages of low protein intake? And can one lose weight comfortably without assistance from a high-protein diet?  Those will be the topics of Thursday’s post.

References

[1] Astrup A. The satiating power of protein—a key to obesity prevention? Am J Clin Nutr. 2005 Jul;82(1):1-2. http://pmid.us/16002791.

[2] Simpson SJ, Raubenheimer D. Obesity: the protein leverage hypothesis. Obes Rev. 2005 May;6(2):133-42. http://pmid.us/15836464.

Appendix: The Protein Leverage Hypothesis as a Theory of Obesity

To the satiating power of protein, the protein leverage hypothesis adds two premises:

  1. That any increase in total calorie consumption leads to weight gain which induces insulin resistance in the liver, which in turn upregulates gluconeogenesis. Contrariwise, any decrease in calorie consumption reverses insulin resistance in the liver and downregulates gluconeogenesis.
  2. That the loss of protein associated with gluconeogenesis is treated by the brain’s appetite control centers exactly the same as a decreased intake of protein, and therefore that ongoing gluconeogenesis increases appetite immensely.

The theory of obesity is that once someone starts eating a low-protein diet, their appetite goes up. So they eat a larger amount of total calories, and gain weight. The weight gain causes them to become insulin resistant in the liver. Once that occurs gluconeogenesis is no longer inhibited by insulin, and the liver converts protein to glucose willy-nilly. The loss of protein stimulates appetite. But the person has to eat a lot of excess calories to get enough protein to replace the protein lost in gluconeogenesis. So weight goes up even more. There is a vicious spiral.

If these premises were correct, then:

  • Weight would be unstable. Weight would spiral out of control upward if people ate low-protein diets, and people would wither away once they started eating high-protein diets.
  • Low-carb diets would be extremely obesogenic. Every 1 calorie reduction in carb intake below the body’s daily needs of 600 calories would induce the eating of an extra 1 calorie of protein for purposes of gluconeoegenesis, and on the order of 4 extra calories of fat (by the leverage hypothesis: the P:F ratio stays constant). So each reduction of carb intake by 1 calorie leads to an extra ~5 P+F calories and an increase in total energy intake of 4 calories. Zero-carb diets would induce ravenous appetite, consumption of an extra 3,000 calories per day above the amount needed for weight stability, and obesity and metabolic syndrome would rapidly follow.

Neither is the case.

Why We Get Fat: Food Toxins

Posted by on January 20, 2011 88 comments

Erich asked about the link between omega-6 fats and obesity. It’s a good question and also a good way to introduce the first step of the Perfect Health Diet weight loss program:  removal of toxic foods from the diet.

Vegetable Oils With Fructose or Alcohol

These toxic foods are particularly dangerous in combination. We discuss this mix of toxins in the book (pp 56-59).

If you feed lab animals high doses of polyunsaturated fat (either omega-6 or omega-3 will do) along with high doses of either fructose or alcohol, then fatty liver disease develops along with metabolic syndrome. Metabolic syndrome is a major risk factor for obesity, and it’s not very difficult to induce obesity on these diets.

Both sugar and vegetable oils are individually risks for obesity:

  • Stephan did a nice post a few years back, “Vegetable Oil and Weight Gain,” discussing a couple of studies showing that both rats and humans get fatter the more polyunsaturated fat they eat.
  • Dr. Richard Johnson and colleagues did a review of the evidence for sugar (fructose) as a cause of obesity in the American Journal of Clinical Nutrition a few years ago. [1]

What the animal studies show us is that when fructose and vegetable oils are consumed together, they multiply each other’s obesity-inducing effects.

Here are a few pictures illustrating the correlation between polyunsaturated fat consumption, fructose consumption, and obesity.

Here is the Johnson et al chart showing historical fructose consumption in the UK and US [1]:

Here is Stephan’s chart showing historical polyunsaturated fat consumption in the US:

And here are obesity rates in the US:

Cereal Grains

It’s a common observation that the toxic grains, especially wheat, can produce a potbelly or “beer belly.” Rice doesn’t seem to do that.

There is epidemiological evidence for this effect. Here, for instance, is obesity prevalence by country from the World Health Organization Global Infobase:

Note the low obesity prevalence in the rice eating countries of China, India, Japan, Indonesia, and southeast Asia; and in sub-Saharan Africa, where a diversity of starch sources are eaten, including manioc/cassava, sorghum, millet, rice, maize, and wheat. The highest obesity prevalence is found in wheat-eating countries.

This correlation persists within countries. In the China Study, the correlation of wheat consumption with BMI was 56%, whereas the correlation of total calorie intake with BMI was only 13%. (Since total calorie intake is correlated with muscle mass, total calorie intake may be completely uncorrelated with fat mass. It’s not how much you eat, but how much wheat!)

Similar outcomes occur in mice. I can’t find any mouse studies comparing wheat to rice, but I did find one comparing wheat to rye [4]. Wheat was far more obesity-inducing than rye:

Body fat percentage was 20.2% in the wheat group, 13.7% in the rye group; fasting insulin was 126 pM in the wheat group, 90 pM in the rye group; and fasting cholesterol, triglycerides, and free fatty acids were higher in the wheat group.

In short:  wheat made mice fatter, more insulin resistant, and more dyslipidemic than rye.

Just for fun here’s a picture comparing fat tissue in the rye (left) versus wheat (right) fed mice:

I believe that rice would have done even better than rye, but I was unable to find a paper directly comparing rice vs wheat or rye.

Why We Get Fat

This brings me to a point of difference with Gary Taubes. Although glucose is toxic in high doses, the body has an extensive machinery for disposing of excess glucose. As we discussed in our last post, all tissues of the body participate in glucose disposal. Dietary glucose is not likely to do much damage unless the body’s glucose-disposal machinery has been damaged by other toxins first.

Obesity is caused not by carb calories per se, but by natural plant toxins. Plants, not carbs, make you fat!

It’s possible, by the way, that differing toxicities among grains could be responsible for epidemiological evidence favoring “whole grains” over “refined grains.” In America, products made with refined grains are usually 100% wheat; but products made with whole grains are often of mixed origin (“7 grain bread”). Since wheat is the most obesity-inducing grain, dilution of wheat content may be masking the toxicity of whole grains.

Conclusion

Certain toxic foods seem to be very effective at causing obesity:  vegetable oils, fructose, and wheat. Along with malnourishment (for instance, by choline deficiency) and infectious disease, food toxins are why we get fat.

The first step in any weight loss effort, therefore, ought to be removal of these toxic foods from the diet. Removing these toxins may not cure obesity; but without this step a cure is unlikely.

References

[1] Johnson RJ et al. Potential role of sugar (fructose) in the epidemic of hypertension, obesity and the metabolic syndrome, diabetes, kidney disease, and cardiovascular disease. Am J Clin Nutr. 2007 Oct;86(4):899-906. http://pmid.us/17921363.

[2] Andersson U et al. Metabolic effects of whole grain wheat and whole grain rye in the C57BL/6J mouse. Nutrition. 2010 Feb;26(2):230-9. http://pmid.us/19647415.

How Does a Cell Avoid Obesity?

Posted by on January 18, 2011 53 comments

I am optimistic that everyone can acquire an attractive and healthy body composition, including women of a certain age. I’ll discuss what I think is the best strategy for that in future blog posts. First, some ground work.

Obesity and weight regulation is a complicated subject, and I have to confess upfront that I am not thoroughly conversant with the literature. I still learn new things every time I delve into the journals. Occasionally, I will I write posts (like today’s) that look into journal articles and molecular pathways related to obesity. This helps me explore ideas and learn. Hopefully you’ll have some fun following along.

A good starting point for an investigation into obesity would seem to be the issue of how weight regulation works in a healthy person. How does our body keep itself at its ideal weight?

Now all the problems our body has to solve, had to be solved about 2 billion years earlier by the first eukaryotic cells. Formed by the merger of fat-eating mitochondria with glucose-eating bacteria, single-celled eukaryotes had to regulate their various metabolic pathways to keep themselves from becoming too fatty or too lean (and to control the urge of mitochondria to eat their hosts!). Then, when multi-cellular organisms developed, these cellular-level mechanisms were the building blocks available for organism-level weight regulation.

So we can simplify the subject a bit by looking at individual cells. And here CarbSane gets a huge “hat tip” for finding a fascinating paper that neatly summarizes how an individual human muscle cell controls its fat and glucose levels.

Obese Cells on High-Carb Diets

The paper dates from 2004, looks at muscle cells, and has the latinate title of “Substrate cycling between de novo lipogenesis and lipid oxidation: a thermogenic mechanism against skeletal muscle lipotoxicity and glucolipotoxicity.” [1]

We can (loosely) translate “de novo lipogenesis” as “fat creation from glucose,” “lipotoxicity” as “too much fat” and “glucolipotoxicity” as “too much glucose in a cell that has too much fat.” So the paper is examining cells that are:

  1. fat;
  2. eating a high-carb diet; and
  3. disposing of excess glucose by converting it to fat.

Sounds familiar! How do these cells control their weight?

Cells Follow the Same Strategy as the Body

Glucose can be toxic and it feeds bacteria, so excess glucose is removed from the body as quickly as possible. First, it’s stored as liver and muscle glycogen; beyond that it is mostly converted to fat by de novo lipogenesis.

The main organs which do that conversion are the liver and adipose tissue, but this paper points out that muscle cells do it too:

The recent recognition that de novo lipogenesis might have relevance for lipid homeostasis in skeletal muscle stems from the realization that Sterol regulatory element binding protein-1c (SREBP-1c), a member of the family of transcription factors that regulate the expression of genes involved in lipid storage in liver and adipose tissue, is also present in skeletal muscle at a level close to that observed in the liver,41,42 … [M]ost fascinating are the very recent demonstrations that glucose alone (in the absence of insulin) can stimulate de novo lipogenesis in skeletal muscle cells….

[I]t is clear that de novo lipogenesis, although low in skeletal muscle, can be markedly stimulated in muscle cells, particularly under conditions of high glucose (and/or high insulin) concentrations. [1]

So muscle cells convert glucose to fat just as liver cells do. Indeed, they convert glucose to fat even without any insulin stimulation, just to get rid of it – but they dispose of glucose most aggressively when stimulated by insulin.

The likely reason for this is to help the body avoid glucose toxicity:

Extrapolated to conditions of postprandial elevation in blood glucose and insulin (particularly after a high-carbohydrate meal), de novo lipogenesis in skeletal muscle, like in the liver, could also contribute to blood glucose homeostasis by disposing some of the excess circulating glucose as muscle triglycerides, particularly if the glycogen stores are full. In other words, de novo lipogenesis in myocytes may provide another sink for glucose disposal through skeletal muscles. [1]

Insulin gets the muscle cells to take in more glucose and do more of this glucose-to-fat conversion. So insulin is a glucose disposal hormone. Muscle cells respond to it as an act of charity to the rest of the body.

But if muscle cells are storing fat that they manufacture from glucose, they risk becoming obese. How do they get rid of excess fat?

That gets us to the other latinate phrase in the title, “lipid oxidation,” also known as fat burning, and a key hormone, leptin. The authors write:

It is now well established that the adipocyte-derived hormone leptin, which is well known for its central role in body weight regulation in part via its control over thermogenesis, 52–55 also plays an important role in blood glucose homeostasis and in the protection of insulin-sensitive tissues against excessive ectopic lipid storage by regulating the partitioning of fatty acid away from storage towards oxidation. 56–58 [1]

Leptin is released by adipose cells in proportion to the amount of fat they are storing. High leptin levels mean “I’m obese, help me lose weight”; low leptin levels mean “I’m skinny, please don’t waste any fat, we may need it.”

Leptin helps the body regulate its weight, by two mechanisms: 

  1. Leptin promotes fatty acid oxidation, or the burning of fats.
  2. Leptin triggers thermogenesis, “creation of heat,” which warms the body and causes it to lose energy.

In short, leptin causes the body – and individual muscle cells – to transform fat into waste heat, thereby slimming down the cells and the body.

What happens if you stimulate normal muscle cells with both leptin and insulin?  This situation occurs in a healthy person with too much fat (leading to high leptin) who has eaten a high-carb meal and has lots of extra blood glucose to get rid of (leading to high insulin). The insulin triggers the glucose-to-fat conversion pathway, the leptin triggers thermogenesis – but the effect is compounded because the insulin amplifies leptin activity:

[W]e found that leptin could directly stimulate thermogenesis in skeletal muscle via ObRb,62 and that this thermogenic effect of leptin, which requires PI3K activity (since it is inhibited by wortmannin), is potentiated by insulin, a potent activator of PI3K. [1]

This makes sense: the body really wants to get rid of the excess glucose, which is toxic, but high leptin means it’s already fat and doesn’t want to get fattier. So if you’ve got too much fat and too much glucose, you really, really want to turn up the waste heat generator.

So eating some carbs, by increasing after-meal insulin, will actually tend to increase fat oxidation and waste heat generation. That is, it will lead to more calories out, at least for a few hours after a meal. Whereas a zero-carb diet, by keeping insulin low after meals, might tend to tamp down postprandial waste heat generation.

If you read CarbSane’s post, you’ll see that this is what got her excited. (Maybe it would also excite Matt Stone, advocate of the carb-overfeeding-raises-body-temperature thesis.)

We shouldn’t jump to the conclusion that eating lots of carbs is good for weight loss, since carbs may also increase appetite and calories in, or have other effects such as generating a transient glucotoxicity. But we should keep this thought in the backs of our minds: Not every response to dietary carbs works against weight loss.

The paper notes that it’s not only leptin that stimulates thermogenesis. Other hormones – including adiponectin, which is also released by adipose cells, stimulate the same thermogenic pathways.

One can also entertain the interesting possibility that, in skeletal muscle, this substrate cycling is also activated in response to other hormones and neurotransmitters (eg, adiponectin, catecholamines) particularly since adiponectin, as well as adrenergic agonists, can also stimulate AMPK activity, glucose utilization and fatty acid oxidation in skeletal muscle or adipose tissue.61,66–69 This substrate cycling between de novo lipogenesis and lipid oxidation could therefore constitute a thermogenic effector in skeletal muscle. [1]

Adiponectin is a favorite hormone of Dr. Kenneth Tourgeman of the blog Nephropal. High adiponectin levels are associated with good health; obesity is associated with low levels of adiponectin. Adiponectin, among other effects, increases insulin sensitivity – thus it would tend to promote thermogenesis not only by its own action, but also indirectly by enhancing insulin amplification of leptin-induced thermogenesis.

What If The Cell Became Hormone Resistant?

As a thought experiment, we can imagine what would happen if our healthy muscle cell became metabolically damaged – if it became resistant to some of these hormones.

If it became leptin resistant, then it would no longer dispose of excess fat via thermogenesis. The fat would collect and the cell would become obese.

If the cell remained leptin resistant but insulin sensitive, it would gradually kill itself through obesity. So leptin resistance would naturally lead to insulin resistance as the cell protects itself against lipotoxicity.

Once the cell becomes insulin resistant, then it no longer disposes of excess glucose by fat conversion. Glucose levels might become elevated. This corresponds to the condition in the body as a whole that we call metabolic syndrome or prediabetes.

High glucose levels, of course, lead to glucotoxicity or poisoning by excess glucose. The pancreatic beta cells, which produce insulin, are especially subject to glucose poisoning. Thus, prediabetes in the body, continued long enough, leads to loss of these cells and diabetes.

We can imagine two kinds of diabetes:

  • If the insulin resistance developed as a consequence of leptin resistance, then we’d have an obese diabetic.
  • If the insulin resistance developed without leptin resistance, then we’d have a skinny diabetic.

Conclusion

I like this paper a lot because it gives us a look at the key hormonal pathways involved in obesity, but in a very simple model – a single muscle cell.

It suggests that possible causes of obesity are leptin resistance and adiponectin deficiency, and that if we want to fix obesity, we may wish to look for a diet which increases leptin sensivity and/or adiponectin level.

References

[1] Dulloo AG et al. Substrate cycling between de novo lipogenesis and lipid oxidation: a thermogenic mechanism against skeletal muscle lipotoxicity and glucolipotoxicity. Int J Obes Relat Metab Disord. 2004 Dec;28 Suppl 4:S29-37.  http://pmid.us/15592483.

Dieter’s Dessert: Taro Coconut Cream Soup

Posted by on January 16, 2011 29 comments

Since we’ve started the topic of weight loss, it seems a good time to discuss the sort of dessert one should eat while on a calorie-restricted diet.

Almost any mix of a carbohydrate with a fat can serve as a dessert. Sweeter desserts use more sugar, less starch.

The following principles can guide the design of a Perfect Health Diet weight loss dessert:

  1. Ketogenic fats, such as those in coconut oil, are the best fat source. Ketones can evade certain kinds of metabolic damage, lower blood sugar levels, contribute to metabolic recovery.
  2. Dieters should maintain their regular carbohydrate and protein consumption, since the recommended Perfect Health Diet amounts are calibrated to meet nutritional needs and malnutrition must always be avoided.
  3. Dieters should avoid fructose, a toxin. Carbs are best obtained from starches or from fructose-free sugars like dextrose (the monosaccharide of glucose) or maltose (the disaccharide of glucose).

Here’s one dessert that meets those guidelines. It’s a common Asian-Pacific dessert: Taro Coconut Cream Soup.

First, gather your starches. Here we’re dicing some (already cooked) taro that was leftover from dinner:

Tapioca pearls make another nice addition to the soup. They are white before cooking, but will become transparent when fully cooked:

Put a can of coconut milk in a pot and warm it to the boiling point. You can add up to an equal amount of water if you prefer a less thick soup:

Add tapioca pearls and taro, and simmer for 10-15 minutes until the tapioca pearls are transparent. You may need to stir from time to time to make sure nothing sticks to the bottom:

Once it’s warm and the pearls are cooked, transfer some to a bowl. Here Paul has added a bit of coconut oil for some extra fat, some lemon juice, and cinnamon:

Lemon juice is beneficial to health, for reasons we’ll explain in an upcoming series on enhancing immune function. Lemon juice adds sweetness but has only 7 calories per fluid ounce. Cinnamon increases insulin sensitivity, which is probably desirable for weight loss. Both add to the flavor of the dessert.

There it is – a Perfect Health Diet dessert for those on a diet!

Shou-Ching is not on a diet, and decided to sweeten hers with some clover honey. She also included some leftover sweet potato chunks:

An Aside About Sweet Potatoes

Last week we had a discussion about different kinds of sweet potatoes and yams. So we bought a sampling.  Here, clockwise from upper right, are an American sweet potato (orange), a Korean sweet potato (large and yellow), and a Japanese sweet potato (small and yellow). The last two are botanically yams, not sweet potatoes; they are starchy and not nearly as sweet as the American sweet potato.

The Korean sweet potato is what we eat; it has a pleasant chestnut flavor. I thought the Japanese sweet potato was excellent also. American sweet potatoes are too sweet for my taste.