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Metals

I have given some thought to the effects of different traditional processing surfaces on the metal contents of sugar cane syrup, and an opinion has attached itself to me. Here, I will set down the reasons for my interests in metals, and provide some values for iron, copper, and zinc in syrup, all being the facts that support my opinion. Development of this perspective has been a two-year personal odyssey, which I could not have made alone. Bruce Smith assayed the metals. Ken Christison has offered encouragement, provided for syrup samples to be sent to me, and chased down important information. For her part, my wife, Nedra, took me in when I was 24 and finished rearing me; without that, I likely would have made a different trip. I thank them all, but do not share with them any of the blame for mistakes.

Because of the nostalgic grip that my grandfather's sugar-mill yard has on me, I often mused wistfully about setting up a replica of this operation. Reality, however, dictated otherwise. On the one hand, I have a consuming and you-might-say pesky job that admits of too little free time. On the other hand, prospects for retirement seemed dim as my father had a disabling stroke at 54, his brother died at 58, and his father died at 45. And, each of the four of my father's mother's brothers (Jerry, George, Newt, and Noah) died in his forties. Thus, it was pretty well established that the Sutton men, and some Outlaws, didn't live long, and I saw no reason that I should expect to be an exception.

When my son, Will, moved from without the umbrella of my health insurance coverage, he sought other coverage. Obtaining new individual insurance required that Will have a physical examination, which revealed iron overload. In brief, Will was diagnosed with hemochromatosis and the fatigue that we had attributed to his medical-school regimen was explained now, in part, by disease. Despite its being the most common genetic disorder of Americans, hemochromatosis is not a household word and it seems that too few physicians appropriate proportionate attention to this illness. Hemochromatosis is deadly serious and will cause just about whatever will ail a person (e.g., 14% lifetime incidence of hepatic cancer). Fortunately, hemochromatosis is usually easily treated by periodic phlebotomy; if detected early and treated, the length and quality of life are normal. As a relevant aside, Will's disease, as implied, like most hemochromatosis in the U.S., is hereditary. Hemochromatosis can be acquired, however, from abnormally high iron intake (e.g., through beer brewed in cast-iron kettles).

Detection of disease is but one small payoff of biological research that your taxes support. For a small price (less than two hours of machine-shop time!) and a small inconvenience (mailing a cheek smear), single-nucleotide substitutions of the HFE gene responsible for hereditary hemochromatosis will be determined. In brief, Will is a homozygote for the most common and implicated mutation (C282Y/C282Y) of the gene product. My daughter Elizabeth also has exactly the same genetic makeup, but as a menstruating person, her iron never became elevated. My wife Nedra and I are both heterozygotes, a condition with which little risk is associated, and both of us monitor the relevant blood-iron parameters. Interestingly, my sister is a H63D heterozygote and my mother was homozygous for the wild-type allele. That means, of course, that my father was a compound heterozygote and his health condition probably related to his genes. Based on these and other analyses, the parsimonious explanation is that my father's H63D allele was inherited from his father. The summary conclusion is that I divorced the Grim Reaper and turned my attention to building a syrup factory for my retirement (. . . all the while religiously taking a statin, a beta-blocker, and various nutriceuticals). As my goal was to be authentic, I preferred to cook in cast iron.

This paragraph briefly addresses with a minimum of jargon how genetic hemochromatosis is diagnosed; those not interested should skip to the next paragraph. Genes, which function in concert with the environment in the appropriate place and time, are the essence of an individual. Most genes in humans are present in two copies, one obtained from the mother and one from the father. Genes may exist in slightly different forms, so the two copies may be alike or they may be just a little different. Because of these different forms of the same gene, individuals can be distinguished by examining several genes. The information in genes, for the most part, is encoded by a string of nucleotides of four different kinds, which, for shorthand, are designated A, T, C and G. A gene is characterized, therefore, by its sequence or order of its, say, 1000, nucleotides. Thus, a gene sequence may be ATTATCCGAGC . . . . . A powerful and widely used technique, the polymerase chain reaction (PCR), permits one to selectively duplicate thousands of times any sequence that lies between two short target sequences. Specifically, by knowing the general sequence of the HFE gene, any portion of the gene can be amplified for sequence analysis. As a test of a protocol designed to teach our biology undergraduates theory and practice of PCR, my colleague and collaborator Lloyd Epstein collected my sloughed-off cheek cells and "fished out" a portion of my HFE gene from the nominal 35,000 genes in those cells. After amplification by PCR, he turned the sample over to another molecular biologist, Steve Miller, who analyzed the sequence (Slide 1). An examination of the sequence-start at the upper left-shows the first position to be occupied by a single red peak, which corresponds to a T here. The second position is occupied by a single black peak, which corresponds to a G, and the next two peaks are green, corresponding to As. Since PCR amplified both copies of my HFE genes, the single peak in each position indicates that the nucleotide in that position is the same in both copies, a situation that is generally true for all positions. In one position, however (exploded view, Slide 1), there are two peaks-one corresponding to a G and one to an A, meaning that the gene copy I inherited from one of my parents is different from that inherited from the other. In a normal person, only G would be present; in a carrier, both A and G are present, and in a susceptible person, both are A. Since my mother contained only G in this position, I must have inherited the A in this position from my father. The gene form I donated to both of my children was the defective one containing A, as did my spouse. Thus, both children have only A in that position and are susceptible to genetic (or hereditary) hemochromatosis.

It is well known that iron dissolves from cookware into acidic foods, and it is also known that diet can be a component of iron overload. The long cooking times for processing sugar cane syrup in a cast-iron kettle obviously raised questions about the iron content of the syrup. Therefore, I became interested in learning the iron content of syrup cooked in kettles, but also considered cooking in copper, as copper evaporators were also used. With Ken's help, I learned that the Food Code of the U.S. Department of Health and Human Services proscribes the use of copper cooking surfaces for juices with a pH below 6. The pH of sugar cane juice is about 5.3, or 5-fold more acidic than pH 6. (pH, or potential of Hydrogen, is the negative logarithm (base 10) of the molar concentration of H+ [or hydronium ion], which means that a small change in pH is a big change in acidity.) Thus, copper went on my list to measure, along with zinc (because galvanized iron is also proscribed).

(There are many factors that control the absorption of an ingested ion like iron, however, so how to figure in diet is at best problematic, as I see it, except in extreme cases. As an example, dietary iron from animal sources (coordinated with heme) is relatively readily taken up; dietary iron from plant sources (chelated to phytates) is only sparingly available. Dietary interactions also come into play-alcohol enhances uptake, as does orange juice (because Vitamin C reduces the ferric ion to the ferrous ion, which is the uptake species).

In the foregoing, I described why syrup making interests me, which is a continuation of my introduction. I also described why metals are of interest to me. Now, I present a condensed version of the findings (Table 1) in a self-explanatory format.



Table 1
 

The concentrations of copper, iron, and zinc in sugar cane syrup and sugar cane-syrup blends prepared by the batch method in antique cast iron kettles (n = 14) or by continuous evaporation in baffled linear evaporators constructed of copper (n = 3). In both cases, heat was provided by flame to the bottom of the vessel. Metal concentrations were determined using atomic absorption on a Perkin Elmer Zeeman 5100 furnace. Differences in metal contents as a function of processing equipment were not significant (P < 0.1). Cadmium was not detected (< 10 ppb) in any of the samples.
 

Metal Processing
Equipment
Concentration
mg/100g
(x sd)
Reference Values1 mg/100g RDA
mg
Sorghum Syrup Maple Syrup
Copper Cast Iron 0.05 0.05 0.13 0.07 0.4 - 4
Copper 0.12 0.07
Iron  Cast Iron 5.60 11.90 3.80 1.20 6 - 15
Copper 6.30 9.50
Zinc Cast Iron 1.14 1.20 0.41 4.16 5 - 19
Copper 1.25 0.70
1 The reference values and the RDAs are taken from the Nutrient Database, Release 13, of the United States Department of Agriculture. This database does not contain values for sugar cane syrup or sugar cane-syrup blends.