As you saw with the my brother's vitamin protocol which I shared last week, he gets extra zinc every morning.
He takes Zinc in his Nutrivene-D, but ever since he was a one year old, he has been deficient in zinc. This is commonly seen in people with Down syndrome (I will share an article below), due to the overexpression of the Cu/Zn Superoxide Dismutase gene on the third 21st chromosome. So, we have been supplementing with 25-30mg/day extra of Zinc since that time. If we keep him on that dosage of extra zinc, he never gets TOO much zinc (it can be tested via blood work - with a zinc free needle!) and he is not deficient anymore. If we go any lower - 15 mg/day - then he becomes deficient again.
We typically use Nutricology Zinc Citrate or Swanson Zinc Citrate. Another really good form of zinc to use is Opti-Zinc (that's not a brand, it's a form of zinc).
Thiel R.J., Fowkes S.W. Can cognitive deterioration associated with Down syndrome be reduced? Medical Hypotheses, 2005; 64(3):524-532 (full text can be viewed here)
Individuals with Down syndrome have signs of possible brain damage prior to birth. In addition to slowed and reduced mental development, they are much more likely to have cognitive deterioration and develop dementia at an earlier age than individuals without Down syndrome. Some of the cognitive impairments are likely due to post-natal hydrogen peroxide-mediated oxidative stress caused by overexpression of the superoxide dismutase (SOD-1) gene, which is located on the triplicated 21 st chromosome and known to be 50% overexpressed. However, some of this disability may also be due to early accumulation of advanced protein glycation end-products, which may play an adverse role in prenatal and postnatal brain development. This paper suggests that essential nutrients such as folate, vitamin B6, vitamin C, vitamin E, selenium, and zinc, as well as alpha-lipoic acid and carnosine may possibly be partially preventive. Acetyl-L-carnitine, aminoguanidine, cysteine, and N-acetylcysteine are also discussed, but have possible safety concerns for this population. This paper hypothesizes that nutritional factors begun prenatally, in early infancy, or later may prevent or delay the onset of dementia in the Down syndrome population. Further examination of this data may provide insights into nutritional, metabolic and pharmacological treatments for dementias of many kinds. As the Down syndrome population may be the largest identifiable group at increased risk for developing dementia, clinical research to verify the possible validity of the prophylactic use of anti-glycation nutrients should be performed. Such research might also help those with glycation complications associated with diabetes or Alzheimer’s.
Oral zinc supplementation in Down's syndrome subjects decreased infections and normalized some humoral and cellular immune parameters.
The effect of 4 months of oral zinc supplementation on immune functions in non-institutionalized young female and male Down's syndrome (DS) subjects was studied. Along with plasma levels of zinc, the immune parameters, measured before and after zinc treatment, were plasma levels of thymulin, the percentage and the absolute number of circulating white blood cells, total lymphocytes, lymphocyte subpopulations, the mitogen-induced lymphocyte proliferation, the production of interleukin-2, and the activity of stimulated granulocytes. Some immune parameters were significantly influenced by zinc treatment. In particular, a normalization of thymulin and zinc plasma levels were found in these subjects after zinc supplementation. At the end of the clinical trial, in vitro lymphocyte proliferation and polymorphonuclear activity also increased and reached normal values. Zinc administration exerted a positive clinical effect in these children, since a reduced incidence of infections was found.
The Role of Zinc in Down’s Syndrome (view the full text here)
This paper considers a single nutrient, zinc, and its place in supporting people with Down’s syndrome. The importance of zinc is suggested by the many disease states found in DS that have also been observed in subjects with zinc deficiency. These include diabetes mellitus, dwarfism, hypogonadism, atherosclerosis, vitamin A deficiency night blindness, cirrhosis of the liver, myeloid leukaemia (Milunsky, 1970), and hyperthyroidism and hypothyroidism (Napolitano et al, 1990). Fabris et al (1993) cite the importance of zinc in the homeostatic networks found to be altered in DS, namely nervous, neuroendocrine and immune, and their interrelationship, plus a reduced turnover of this mineral, leading to the hypothesis that zinc deficiency could be implicated in at least some of the DS phenotype.
“Zinc forms part of the composition of at least 160 different enzymes. Indeed, zinc is the most widely used mineral in enzymes” (Graham and Odent, 1986).
It is vital for protein, essential fatty acid and carbohydrate metabolism, and for DNA synthesis, and can be used to detoxify lead and mercury (ibid.). The body only has a small pool of biologically available zinc, and a rapid turnover, meaning that deficiency signs appear very quickly (Passwater and Cranton, 1983).