The Color Purple Gains New Significance

Purple Corn Color May
Help Prevent Obesity

Anthocyanin pigments suppress obesity- and
diabetes-inducing effects of a high-fat diet in mice
By Richard P. Huemer, M.D.

I think it [angers] God if you walk by the
color purple in a field somewhere and don’t notice it.

— Alice Walker, The Color Purple

n The Color Purple, Shug helps Celie come to a new appreciation of the Deity, transcending her notion of an elderly, white-bearded male. Celie then realizes how her limited understanding has separated her from divine manifestations: “I been so busy thinking ’bout [that old white man] I never truly notice nothing God make. Not a blade of corn (how it do that?) not the color purple (where it come from?). Not the little wildflowers. Nothing.”

Ah, yes. Where does the color purple come from, and why is some corn colored purple? How does the corn do that? Moreover, aside from the stimulus to our sense of curiosity and wonder, why should we give a hoot?

We should care about this because obesity and its fellow traveler, type 2 diabetes, have reached epidemic proportions. Diabetes is growing increasingly prevalent worldwide; even children are now getting what used to be called adult-onset diabetes, in alarming numbers. It’s no point of pride that there are more obese Americans, percentage-wise, than ever before. As it turns out, the substance that gives some varieties of corn their purple color—it’s cleverly called purple corn color—may have benefits for the prevention of obesity and type 2 diabetes, if the surprising results of a certain mouse experiment are any indication.

What Color Is Your Lard?

A leading expert on purple corn color (PCC) is Dr. Takanori Tsuda, a scientist at Doshisha University in Kyoto, Japan. His research focuses on anthocyanins, a category of flavonoids that constitute the largest group of water-soluble pigments in the plant kingdom. Certain anthocyanins are the principal constituents of PCC, whose main use has been as a coloring agent for foods, such as soft drinks and confections, in Japan. Such foods are typically fattening, owing to their high caloric content, but because of PCC, the purple-colored ones may be less fattening than the others.

In 2003, Tsuda and his colleagues conducted a simple experiment to see what the effects of PCC would be on lab mice that were fed a high-fat diet.1 The young male mice were divided into four dietary groups: (1) a standard diet (the controls); (2) the standard diet plus PCC (0.2% by weight), which we’ll call the PCC diet; (3) a high-fat diet containing 30% lard by weight, which we’ll call the HF diet; and (4) the high-fat diet plus PCC (again 0.2% by weight), which we’ll call the HF+PCC diet. The HF diet, obviously, was meant to be the bad one—and it was. The question was, would the PCC in the HF+PCC diet tend to offset the harmful effects of all that lard? It seemed like a tall order, but . . .

PCC Prevented Lard-Induced Weight Gain

The PCC delivered! After 12 weeks, during which the mice were fed ad libitum (i.e., they were allowed to eat as much as they wanted of their respective diets), the researchers found that the HF mice were fat (no surprise), but the HF+PCC mice were not—their weight gain was no greater than that of the controls, i.e., it was normal! (The same was true of the PCC mice.) This was not because PCC affected food intake: the lard-fed mice (HF and HF+PCC) ate the same amounts of food (in terms of grams, not of calories). The standard-fed mice (controls and PCC) also ate the same amounts, but at a higher overall intake (more grams, but fewer calories) than the lard-fed mice.

Thus the PCC had no effect on food intake—only the lard did. The lard caused both groups of mice that ate it to eat less (in grams) than the other two groups, but it caused the HF mice—and only the HF mice—to gain more weight. And where did that weight wind up? In adipocytes (fat cells), of course. By contrast, the adipocytes in the other three groups, including HF+PCC, were normal.

In short, PCC normalized the weight-gain effects of a high-fat diet, effectively wiping them out. That in itself is stunning. But that’s not all the PCC normalized, as you will see shortly.

Obesity Causes a Host of Ills

A high-fat diet causes a variety of other physiological effects, all of them bad. Some contribute to the development of insulin resistance, the precursor to type 2 diabetes, and among these are hyperglycemia and hyperinsulinemia, or high blood levels of glucose and insulin, respectively. They can cause no end of trouble.

Another downside of a high-fat diet is hyperleptinemia, or an excess of leptin. Leptin is a protein hormone that’s secreted primarily by adipocytes in response to excess fat storage. By suppressing appetite, increasing energy expenditure, and inhibiting the synthesis of fatty acids (the precursors to fats), leptin acts as the key hormone involved in the regulation of body weight. That sounds good! As is so often true, however, too much of a good thing is a bad thing. Hyperleptinemia appears to be a risk factor for cardiovascular disease, and there is evidence that it may play a role in the heightened risk of thrombosis (blood clots) associated with obesity.

High-fat diets also cause an increase in a proinflammatory, tumor-cell-killing protein called tumor necrosis factor-α (TNF-α), which is synthesized widely throughout the female reproductive tract (but men have it too). Among other things, excessive production of TNF-α in adipocytes can inhibit insulin signaling and the function of pancreatic β-cells, where insulin is produced in the first place. And that, of course, promotes diabetes.

PCC Prevented the Excesses—and the Fat

In the mouse study, the HF mice had substantial increases, compared with the controls, in blood glucose (56%) and insulin (68%), an enormous increase in leptin (672%), and a major increase in TNF-α (154%; this one was measured indirectly via the corresponding levels of mRNA, a nucleic acid that carries the code for the synthesis of a specific protein). In the HF+PCC mice, however, the PCC prevented these excesses from occurring: it normalized the levels of all four substances, keeping them at essentially the same levels as those of the control mice on the standard diet! Stunning again. The authors attributed these effects to PCC’s prevention of the accumulation of adipose tissue (fat).

And how did it do that? Well, PCC in the HF+PCC diet strongly suppressed the large increases in liver total lipids (74%) and liver triglycerides (167%) that occurred in the HF diet.* This came about in part through PCC’s suppression of an enzyme complex called fatty acid synthase (FAS), which catalyzes the synthesis of palmitic acid from excess glucose. Palmitic acid is one of the fatty acids from which fat molecules are subsequently synthesized (by other enzymes), so reducing palmitic acid reduces fats. These antifat effects of PCC were observed in both the liver and the adipose tissues of the mice.


*Curiously, there was no increase in liver cholesterol in that diet, nor were there any increases in serum cholesterol, serum triglycerides, or serum free fatty acids.


There was still more that PCC did, but we have to stop here. The authors stated,

In conclusion, dietary C3G-rich PCC significantly suppressed the development of obesity and ameliorated hyperglycemia induced by HF diet feeding in mice. Dietary PCC suppressed the mRNA levels of the enzymes included in the fatty acid and triacylglycerol [triglyceride] synthesis . . . Our findings provide a biochemical and nutritional basis for the use of PCC or anthocyanins as a functional food factor, which may have important implications for preventing obesity and diabetes.

PCC Has a Variety of Activities

The compound C3G (cyanidin 3-O-β-D-glucoside) mentioned in the quote above is the principal anthocyanin in purple corn (it’s also found in many other foods). Tsuda et al. used this compound, along with its precursor, cyanidin, in a subsequent study on the mechanisms by which PCC might combat obesity and diabetes.2 They found beneficial effects on a number of genes that are involved in fat metabolism, as well as increased secretion of a hormonelike protein called adiponectin. Like leptin (whose secretion was also increased in this study), adiponectin is produced by adipocytes. Its principal effect is to enhance insulin sensitivity in peripheral tissues; this tends to increase fatty acid oxidation (the “burning” of fatty acid fuels in our cells) and decrease the levels of fat in our muscles.

Combating obesity and diabetes is a major biochemical feat, but purple corn color’s benefits don’t stop there. Among the earliest findings by Tsuda et al. was that C3G and cyanidin have strong antioxidant activity—equivalent to or greater than that of vitamin E—in a variety of test systems.3 Other researchers have found that PCC may also have antibacterial and antimutagenic activities.4

Is Purple Corn the King of Corn?

Purple is such a gorgeous color, it’s too bad there’s not a lot more of it in the natural world (surely it would be very difficult to walk by a field of purple and not notice it!). It’s no accident that purple has long been considered the color of royalty—they always take the best for themselves.

So is purple corn the king of corn? Perhaps, if the promise suggested by the studies discussed above comes to fruition. Time, and further research, will tell. Meanwhile, let us rejoice, with Celie, in our newfound appreciation for the color purple.

Obesity Is Bad for Your Lungs Too

Being overweight or obese—which about 65% of American adults are—puts people at increased risk of many diseases and disorders, including hypertension, hyperlipidemia, cardiovascular disease, peripheral vascular disease, type 2 diabetes, various cancers, osteoarthritis, obstructive sleep apnea, infertility, heartburn, and urinary stress incontinence. Researchers in Colorado have now provided a strong argument for adding asthma to that list.1 Asthma is an acute or chronic inflammatory respiratory disease that entails obstruction of the airways; it often arises from allergies, and it causes labored breathing, wheezing, and coughing. It afflicts about 7% of American adults.

The researchers’ objectives were to determine: (1) a precise numerical estimate of the impact of overweight and obesity on the risk for asthma; (2) whether the risk increases with weight; and (3) whether there are gender differences in these regards. They used a technique called meta-analysis, in which the data from similar studies are pooled and analyzed using rigorous statistical methods so as to yield results that are more robust and reliable than those of the individual studies.

For the meta-analysis, the researchers selected the seven best-designed and best-executed studies available, encompassing 333,102 adults. The results showed that the incidence of asthma was 51% greater in overweight and obese adults than in adults of normal weight. For men, the risk was 46% greater, and for women, it was 68% greater; this difference was not considered significant. In both sexes, the data showed a dose-response relationship: the greater the body mass index (BMI), the greater the risk for asthma. (The National Institutes of Health have defined overweight as a BMI between 25 and 30, and obesity as 30 or more.)

The risk for asthma in the overweight or obese is not very great to begin with, but in terms of absolute numbers, it becomes important: the researchers estimated that if overweight and obese people could achieve significant weight loss, this might prevent up to 250,000 new cases of asthma in the U.S. each year.

Here’s a nice final twist: the authors cited another study showing that being underweight is also a risk factor for asthma. Nothing is simple.

Reference

  1. Beuther DA, Sutherland ER. Overweight, obesity, and incident asthma: a meta-analysis of prospective epidemiologic studies. Am J Respir Crit Care Med 2007;175:661-6.

References

  1. Tsuda T, Horio F, Uchida K, Aoki H, Osawa T. Dietary cyanidin 3-O-β-D-glucoside-rich purple corn color prevents obesity and ameliorates hyperglycemia in mice. J Nutr 2003;133:2125-30.
  2. Tsuda T, Ueno Y, Aoki H, Koda T, Horio F, Takahashi N, Kawada T, Osawa T. Anthocyanin enhances adipocytokine secretion and adipocyte-specific gene expression in isolated rat adipocytes. Biochem Biophys Res Commun 2004;316:149-57.
  3. Tsuda T, Watanabe M, Ohshima K, Norinobu S, Choi S-W, Kawakishi S, Osawa T. Antioxidative activity of the anthocyanin pigments cyanidin 3-O-β-D-glucoside and cyanidin. J Agric Food Chem 1994;42:2407-10.
  4. Cevallos-Casals BA, Cisneros-Zevallos LA. A comparative study of antimicrobial, antimutagenic and antioxidant properties of phenolic compounds from purple corn and bilberry colorant extracts. Poster 14E-1, International Food Technologists Annual Meeting, Chicago, IL, 2003.


Dr. Richard P. Huemer received his M.D. from UCLA and did postdoctoral research in cancer immunology at CalTech. He has specialized in orthomolecular medicine for most of his career, has written and lectured extensively on alternative medicine, and has served on the editorial boards of professional journals. His published books include The Roots of Molecular Medicine: A Tribute to Linus Pauling and, with coauthor Jack Challem, The Natural Health Guide to Beating the Supergerms.

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