When pregnant mice were fed a diet moderately deficient in zinc, their offspring exhibited a malfunctioning immune system for the first six months of life. More alarming, the second and third generations also showed signs of poor immunity - even though they were fed a zinc-plentiful diet.
Jean Carper, writing in Jean Carper's Total Nutrition Guide, in reference to zinc studies done at U.C. Davis
If zinc deficiencies can carry over from generations in mice, as noted above, could the same be true for humans? Perhaps some of the conditions in humans we currently attribute to genetic defects were actually caused by deficiencies of zinc or other nutrients occurring in past generations.
Abnormal levels of zinc have been found in the eyes of people with:
Zinc has been found useful in treating myopia (nearsightedness).
Zinc and other nutritional requirements rise as children begin puberty in order to support sexual development. This is especially true for males, as sperm contains high amounts of zinc. A diet that provided sufficient calories and nutrients during childhood may no longer be sufficient for a child beginning puberty.
Many people who develop pectus excavatum or pectus carinatum have their deformities occur at puberty or just before, the same time they are susceptible to zinc deficiencies. As noted above, in monkeys, zinc deficiencies can cause rickets, which can cause pectus excavatum or pectus carinatum. A zinc deficiency occurring around puberty would logically explain why children often develop pectus deformities at this time. It would also explain why pectus deformities often occur along with stretch marks and other signs of zinc deficiencies such as poor wound healing. It would also explain why people with chest deformities have been found to have zinc deficiencies in their rib cartilage, as noted in the abstract excerpt below:
"In 71 patients with chest deformity,,,,cartilage of the ribs was removed intraoperatively. Analyses of trace elements showed a highly significant decrease in zinc....". The study also showed that the ribs also had abnormalities of collagen. As noted in the study above on chicks, zinc deficiencies were shown to cause abnormalities of collagen.
So if we look at zinc deficiencies as a possible factor in some cases of pectus excavatum, then there are logical explanations of why:
Humans with connective tissue disorders commonly have stretch marks, scoliosis, hypermobile joints, delayed wound healing, reduced collagen, and frequent infections. In fact, these features are often used as diagnostic criteria for many of the connective tissue disorders. But are they really signs of incurable connective tissue disorders, or, at least in some cases, are they signs of zinc deficiencies that may have an inherited component?
Here are some studies linking zinc deficiencies to connective tissue disorders:
As noted above, in a zinc deficiency study on in human volunteers, their collagen and the sponge of their connective tissue was impacted. The study states that, "an adverse effect of zinc restriction on total protein, total collagen, ribonucleic acid, and the activity of deoxythymidine kinase (a zinc-dependent enzyme) in the sponge connective tissue of the two volunteers in whom this test was done was noted."
Some patients with Marfan syndrome have what geneticists like to call "emerging Marfan syndrome". They don't have Marfan syndrome when they are born -- it "emerges" as they get older. Developing pectus excavatum or carinatum around puberty is a feature linked to Marfan syndrome. If Marfan syndrome was truly due only to an inherited mutated fibrillin gene, then why would it "emerge" at puberty or right before? Why would a mutation in the gene for fibrillin cause Marfans to be underweight? Why wouldn't the disorder show up right away if it was really caused only by genes? A zinc deficiency as a factor in Marfan syndrome and related connective tissue disorders would provide a logical explanation of why Marfans:
Perhaps "emerging Marfan syndrome" is really due to a treatable pre-puberty deficiency of zinc and other nutrients, with a genetic predisposition, rather than an incurable genetic disorder. If a zinc deficiency were a factor, then all of these unusual findings regarding emerging Marfan syndrome would have a completely logical explanation.
Mitral valve prolapse syndrome is another connective tissue disorder with possible links to zinc deficiencies. Some researchers feel MVP syndrome is a mild form of Marfan syndrome. MVP syndrome is more common in women than men. The characteristic features of the disorder include:
All of the above conditions associated with MVP syndrome have also in some way been linked to zinc deficiencies. Mitral valve prolapse is an age dependent condition, which interestingly, also usually first appears in women around puberty or a few years later, the same time that zinc requirements increase to support sexual development.
I had finger nails completely riddled with white spots growing up and so did other members of my immediate family. My husband's mother told me she had lots of white spots on her finger nails growing up. Her mother called them her "little friends". Some friends! Like his mother, my husband's fingers were riddled with white spots. Our kids had a few white spots on their nails, too, until we changed their diets. Now they only get the white spots back around holidays or vacations, when they don't eat as healthy as they should.
My husband and I were both very thin as children. We both have pectus excavatum (a feature of rickets), stretch marks and we both had problems with facial blemishes until we were about 40, when we changed our diets to get more zinc. Then our faces suddenly cleared up completely. (We started getting more zinc after I read the book Super Nutrition for Women.)
I've been diagnosed with a few variations of incurable inherited connective tissue disorders, including mitral valve prolapse syndrome. My husband, with many of the same symptoms as me, had a genetic exam once, too, and was completely ruled out from having any connective tissue disorder at all. Yet, if my problems were caused by an incurable genetic disorder, and my husband doesn't have one, then how come my husband has so many of the same features as me? How did the doctors who diagnosed me know I had an incurable disorder when they never checked me for a zinc deficiency, which has many identical symptoms?
I don't think I ever really had any incurable disorder at all. I think I was low in zinc for much of my life until I changed my diet, and that a tendency to be low in zinc ran in my family and my husband's family. I just probably had more of a deficiency than he did. I do wonder how many other people have been given a diagnosis of an incurable disorder (or from my email, no diagnosis at all!) when perhaps what they really had was a correctable nutritional deficiency, with a genetic predisposition.
I went to an Ehlers-Danlos syndrome meeting once (and only once because none of the people there had any interest in nutrition). One thing I remember from that meeting is that one of the people there who had been diagnosed with EDS had acne and his finger nails were riddled with white spots, just like I used to have. I do wonder sometimes if, like me, he actually had zinc and other nutritional deficiencies and not an incurable genetic disorder.
Related sections of interest:
Zinc Deficiency - very good article by Ananda S Prasad, Wayne State University School of Medicine. Dr. Prasad is one of the world's leading authorities on zinc.One very interesting point he makes in this article is "phytate in cereals markedly impairs the absorption of zinc and also iron."
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