The high potassium, low sodium diet of the Gerson therapy has been observed experimentally to cure many cases of advanced cancer in man, but the reason was not clear. Recent studies from the laboratory of Ling indicate that high potassium, low sodium environments can partially return damaged cell proteins to their normal undamaged configuration. Therefore, the damage in other tissues, induced by toxins and breakdown products from the cancer, is probably partly repaired by the Gerson therapy throught this mechanism.

Theoretically, we humans should be better adapted physiologically to the diet our ancestors were exposed to during millions of years of hominid evolution than to the diet we have been eating since the agricultural revolution a mere 10,000 years ago, and since industrialization only 200 years ago. Among the many health problems resulting from this mismatch between our genetically determined nutritional requirements and our current diet, some might be a consequence in part of the deficiency of potassium alkali salts (K-base), which are amply present in the plant foods that our ancestors ate in abundance, and the exchange of those salts for sodium chloride (NaCl), which has been incorporated copiously into the contemporary diet, which at the same time is meager in K-base-rich plant foods. Deficiency of K-base in the diet increases the net systemic acid load imposed by the diet. We know that clinically-recognized chronic metabolic acidosis has deleterious effects on the body, including growth retardation in children, decreased muscle and bone mass in adults, and kidney stone formation, and that correction of acidosis can ameliorate those conditions. Is it possible that a lifetime of eating diets that deliver evolutionarily superphysiologic loads of acid to the body contribute to the decrease in bone and muscle mass, and growth hormone secretion, which occur normally with age? That is, are contemporary humans suffering from the consequences of chronic, diet-induced low-grade systemic metabolic acidosis? Our group has shown that contemporary net acid-producing diets do indeed characteristically produce a low-grade systemic metabolic acidosis in otherwise healthy adult subjects, and that the degree of acidosis increases with age, in relation to the normally occurring age-related decline in renal functional capacity. We also found that neutralization of the diet net acid load with dietary supplements of potassium bicarbonate (KHCO3) improved calcium and phosphorus balances, reduced bone resorption rates, improved nitrogen balance, and mitigated the normally occurring age-related decline in growth hormone secretion--all without restricting dietary NaCl. Moreover, we found that co-administration of an alkalinizing salt of potassium (potassium citrate) with NaCl prevented NaCl from increasing urinary calcium excretion and bone resorption, as occurred with NaCl administration alone. Earlier studies estimated dietary acid load from the amount of animal protein in the diet, inasmuch as protein metabolism yields sulfuric acid as an end-product. In cross-cultural epidemiologic studies, Abelow found that hip fracture incidence in older women correlated with animal protein intake, and they suggested a causal relation to the acid load from protein. Those studies did not consider the effect of potential sources of base in the diet. We considered that estimating the net acid load of the diet (i. e., acid minus base) would require considering also the intake of plant foods, many of which are rich sources of K-base, or more precisely base precursors, substances like organic anions that the body metabolizes to bicarbonate. In following up the findings of Abelow et al., we found that plant food intake tended to be protective against hip fracture, and that hip fracture incidence among countries correlated inversely with the ratio of plant-to-animal food intake. These findings were confirmed in a more homogeneous population of white elderly women residents of the U.S. These findings support affirmative answers to the questions we asked above. Can we provide dietary guidelines for controlling dietary net acid loads to minimize or eliminate diet-induced and age-amplified chronic low-grade metabolic acidosis and its pathophysiological sequelae. We discuss the use of algorithms to predict the diet net acid and provide nutritionists and clinicians with relatively simple and reliable methods for determining and controlling the net acid load of the diet. A more difficult question is what level of acidosis is acceptable. We argue that any level of acidosis may be unacceptable from an evolutionarily perspective, and indeed, that a low-grade metabolic alkalosis may be the optimal acid-base state for humans.

OBJECTIVE: Kidney stones are an adverse event with the ketogenic diet (KD), occurring in approximately 6% of children who are started on this therapy for intractable epilepsy. Potassium citrate (Polycitra K) is a daily oral supplement that alkalinizes the urine and solubilizes urine calcium, theoretically reducing the risk for kidney stones.

METHODS: Children who started the KD from 2000 to 2008 at Johns Hopkins Hospital, with at least 1 month of follow-up, were evaluated (N = 313). From 2000 to 2005, children were treated with daily Polycitra K at 2 mEq/kg per day only in the setting of identified hypercalciuria, whereas, since 2006, it has been started for all children empirically at KD onset.

RESULTS: Polycitra K was administered to 198 children preventatively overall, 4 (2.0%) of whom developed kidney stones, compared with 11 (10.5%) of 105 who did not receive Polycitra K (P = .003). Two children since 2006 refused Polycitra K, 1 of whom developed a kidney stone. Successful empiric administration of Polycitra K at KD onset resulted in a kidney-stone incidence of 0.9% (1 of 106) compared with administration only because of hypercalciuria, 6.7% (13 of 195; P = .02). Polycitra K resulted in less acidic urine (mean pH: 6.8 vs 6.2; P = .002) but not reduced serum acidosis. No adverse effects of oral citrates were reported.

CONCLUSIONS: Oral potassium citrate is an effective preventive supplement against kidney stones in children who receive the KD, achieving its goal of urine alkalinization. Universal supplementation is warranted.

BACKGROUND:There are few studies on the association between nutrient intake and telomere length, which may reflect cumulative oxidative stress and indicate biological ageing. In the present study, we evaluated longitudinal associations between the consumption of micronutrients, including antioxidant nutrients and B vitamins involved in one-carbon transfer pathways, and leukocyte telomere length (LTL).

METHODS:The study included 1958 middle-aged and older Korean men and women (age range at baseline: 40-69 years) from a population-based cohort. We collected dietary information at baseline using a semiquantitative food frequency questionnaire (June 2001 to January 2003) and assessed the consumption of micronutrients, including vitamins A, B1 , B2 , B3 , B6 , B9 (folate), C and E, as well as calcium, phosphorus, potassium, iron and zinc. We measured LTL using a real-time polymerase chain reaction at the 10-year follow-up examination (February 2011 to November 2012).

RESULTS:In the multiple regression model adjusted for potential confounders, LTL was positively associated with the consumption of vitamin C (P<0.05), folate (P = 0.05) and potassium (P = 0.05) in all participants. In the age-stratified analysis, the association between the consumption of vitamin C (P<0.01), folate (P<0.05) and potassium (P<0.05) with LTL was significant only among participants aged<50 years.

CONCLUSIONS:Our findings suggest that the earlier consumption of vitamin C, folate and potassium, which are abundant in fruits and vegetables, can delay biological ageing in middle-aged and older adults.

Beyond the well-known effects on blood pressure (BP) of the dietary approaches to stop hypertension (DASH) and the Mediterranean diets, a large number of studies has investigated the possible BP lowering effect of different dietary supplements and nutraceuticals, the most part of them being antioxidant agents with a high tolerability and safety profile. In particular relatively large body of evidence support the use of potassium, L-arginine, vitamin C, cocoa flavonoids, beetroot juice, coenzyme Q10, controlled-release melatonin, and aged garlic extract. However there is a need for data about the long-term safety of a large part of the above discussed products. Moreover further clinical research is advisable to identify between the available active nutraceuticals those with the best cost-effectiveness and risk-benefit ratio for a large use in general population with low-added cardiovascular risk related to uncomplicated hypertension.

Ascorbic acid (A) has been demonstrated to exhibit anti-cancer activity in association with chemotherapeutic agents. Potassium (K) is a regulator of cellular proliferation. In the present study, the biological effects of A and K bicarbonate, alone or in combination (A+K), on breast cancer cell lines were evaluated. The survival of cancer cells was determined by sulforhodamine B cell proliferation assay, while analysis of the cell cycle distribution was conducted via fluorescence-activated cell sorting. In addition, the expression of signaling proteins was analyzed upon treatment. The results indicated that there was a heterogeneous response of the different cell lines to A and K, and the best effects were achieved by A+K and A treatment. The interaction between A+K indicated an additive or synergistic effect. In addition, A+K increased the percentage of cells in the sub-G1 phase of the cell cycle, and was the most effective treatment in activating the degradation of poly(adenosine diphosphate-ribose) polymerase-1. In the breast cancer cell line MCF-7, A+K induced the appearance of the 18 kDa isoform of B-cell lymphoma-2-associated X protein (Bax), which is a more potent inducer of apoptosis than the full-length Bax-p21. The effects of A and K on the phosphorylation of extracellular signal-regulated kinase (ERK)1 and ERK2 were heterogeneous. In addition, treatment with K, A and A+K inhibited the expression of nuclear factor-κB. Overall, the results of the present study indicated that K potentiated the anti-tumoral effects of A in breast cancer cells in vitro.