Salt In Sweat Research Articles

Salt preferences of horses for types of NaCl offered

Salt (NaCl) is an essential nutrient for horses because their diet is low in sodium and they lose salt in sweat. Given the many types of salt block available, 342 horse owners were surveyed to see what type they offered their horses. The owners most often offered plain(30%) mineralized (29%) or Himalayan salt blocks. Next, adult mares were given two choice preference tests between plain (white) and mineralized (red) salt blocks, between mineralized and selenium (green) blocks, between plain and selenium, between Himalayan (pink) and plain and between Himalayan and selenium salt blocks. The horses preferred plain salt to Himalayan salt, but showed no preference between the other combinations.

“Wood-Bark Sign” in Dermoscopy of Aquagenic Syringeal Acrokeratoderma

“Wood-Bark Sign” in Dermoscopy of Aquagenic Syringeal Acrokeratoderma

Sodium Status and Replacement in Children and Adults Living with Cystic Fibrosis: A Narrative Review

Patients with cystic fibrosis (CF) have a two- to four-fold higher sodium chloride sweat content compared with healthy controls. This high sweat salt loss increases the risk for electrolyte disturbances, associated with subacute or chronic complications. Sodium status therefore needs to be adequately monitored and salt intake adjusted to individual needs. The lack of current evidence to formulate specific recommendations and assess sodium status is reflected in a variability of recommendations in international guidelines. This narrative review presents an overview of the current evidence. Infants with CF in particular are at risk for severe sodium deficiency, potentially leading to metabolic alkalosis due to low intake and high sweat losses. More research on the assessment of sodium status and efficacy of sodium chloride supplements in the population of patients with CF, especially given the changing era of CF transmembrane conductance regulator modulatory treatment, is warranted.

Low abundance of sweat duct Cl- channel CFTR in both healthy and cystic fibrosis athletes with exceptionally salty sweat during exercise.

To understand potential mechanisms explaining interindividual variability observed in human sweat sodium concentration ([Na(+)]), we investigated the relationship among [Na(+)] of thermoregulatory sweat, plasma membrane expression of Na(+) and Cl(-) transport proteins in biopsied human eccrine sweat ducts, and basal levels of vasopressin (AVP) and aldosterone. Lower ductal luminal membrane expression of the Cl(-) channel cystic fibrosis transmembrane conductance regulator (CFTR) was observed in immunofluorescent staining of sweat glands from healthy young adults identified as exceptionally "salty sweaters" (SS) (n = 6, P < 0.05) and from patients with cystic fibrosis (CF) (n = 6, P < 0.005) compared with ducts from healthy young adults with "typical" sweat [Na(+)] (control, n = 6). Genetic testing of healthy subjects did not reveal any heterozygotes ("carriers") for any of the 39 most common disease-causing CFTR mutations in the United States. SS had higher baseline plasma [AVP] compared with control (P = 0.029). Immunostaining to investigate a potential relationship between higher plasma [AVP] (and sweat [Na(+)]) and ductal membrane aquaporin-5 revealed for all groups a relatively sparse and location-dependent ductal expression of the water channel with localization primarily to the secretory coil. Availability of CFTR for NaCl transport across the ductal membrane appears related to the significant physiological variability observed in sweat salt concentration in apparently healthy humans. At present, a heritable link between healthy salty sweaters and the most prevalent disease-causing CFTR mutations cannot be established.

Autosomal recessive hyponatremia due to isolated salt wasting in sweat associated with a mutation in the active site of Carbonic Anhydrase 12

Genetic disorders of excessive salt loss from sweat glands have been observed in pseudohypoaldosteronism type I (PHA) and cystic fibrosis that result from mutations in genes encoding epithelial Na+ channel (ENaC) subunits and the transmembrane conductance regulator (CFTR), respectively. We identified a novel autosomal recessive form of isolated salt wasting in sweat, which leads to severe infantile hyponatremic dehydration. Three affected individuals from a small Bedouin clan presented with failure to thrive, hyponatremic dehydration and hyperkalemia with isolated sweat salt wasting. Using positional cloning, we identified the association of a Glu143Lys mutation in carbonic anhydrase 12 (CA12) with the disease. Carbonic anhydrase is a zinc metalloenzyme that catalyzes the reversible hydration of carbon dioxide to form a bicarbonate anion and a proton. Glu143 in CA12 is essential for zinc coordination in this metalloenzyme and lowering of the protein-metal affinity reduces its catalytic activity. This is the first presentation of an isolated loss of salt from sweat gland mimicking PHA, associated with a mutation in the CA12 gene not previously implicated in human disorders. Our data demonstrate the importance of bicarbonate anion and proton production on salt concentration in sweat and its significance for sodium homeostasis.

Dehydration and rehydration in competative sport

Dehydration, if sufficiently severe, impairs both physical and mental performance, and performance decrements are greater in hot environments and in long-lasting exercise. Athletes should begin exercise well hydrated and should drink during exercise to limit water and salt deficits. Many athletes are dehydrated to some degree when they begin exercise. During exercise, most drink less than their sweat losses, some drink too much and a few develop hyponatraemia. Athletes should learn to assess their hydration needs and develop a personalized hydration strategy that takes account of exercise, environment and individual needs. Pre-exercise hydration status can be assessed from urine frequency and volume, with additional information from urine color, specific gravity or osmolality. Changes in hydration status during exercise can be estimated from the change in body mass: sweat rate can be estimated if fluid intake and urinary losses are also measured. Sweat salt losses can be determined by collection and analysis of sweat samples. An appropriate, individualized drinking strategy will take account of pre-exercise hydration status and of fluid, electrolyte and substrate needs before, during and after a period of exercise.

Development of hydration strategies to optimize performance for athletes in high‐intensity sports and in sports with repeated intense efforts

Hypohydration - if sufficiently severe - adversely affects athletic performance and poses a risk to health. Strength and power events are generally less affected than endurance events, but performance in team sports that involve repeated intense efforts will be impaired. Mild hypohydration is not harmful, but many athletes begin exercise already hypohydrated. Athletes are encouraged to begin exercise well hydrated and - where opportunities exist - to consume fluid during exercise to limit water and salt deficits. In high-intensity efforts, there is no need, and may be no opportunity, to drink during competition. Most team sports players do not drink enough to match sweat losses, but some drink too much and a few may develop hyponatremia because of excessive fluid intake. Athletes should assess their hydration status and develop a personalized hydration strategy that takes account of exercise, environment and individual needs. Pre-exercise hydration status can be assessed from urine markers. Short-term changes in hydration can be estimated from the change in body mass. Sweat salt losses can be determined by collection and analysis of sweat samples. An appropriate drinking strategy will take account of pre-exercise hydration status and of fluid, electrolyte and substrate needs before, during and after exercise.

Development of Individual Hydration Strategies for Athletes

Athletes are encouraged to begin exercise well hydrated and to consume sufficient amounts of appropriate fluids during exercise to limit water and salt deficits. Available evidence suggests that many athletes begin exercise already dehydrated to some degree, and although most fail to drink enough to match sweat losses, some drink too much and a few develop hyponatremia. Some simple advice can help athletes assess their hydration status and develop a personalized hydration strategy that takes account of exercise, environment, and individual needs. Preexercise hydration status can be assessed from urine frequency and volume, with additional information from urine color, specific gravity, or osmolality. Change in hydration during exercise can be estimated from the change in body mass that occurs during a bout of exercise. Sweat rate can be estimated if fluid intake and urinary losses are also measured. Sweat salt losses can be determined by collection and analysis of sweat samples, but athletes losing large amounts of salt are likely to be aware of the taste of salt in sweat and the development of salt crusts on skin and clothing where sweat has evaporated. An appropriate drinking strategy will take account of preexercise hydration status and of fluid, electrolyte, and substrate needs before, during, and after a period of exercise. Strategies will vary greatly between individuals and will also be influenced by environmental conditions, competition regulations, and other factors.

Establishing sweat salt levels in normal healthy adults

Establishing sweat salt levels in normal healthy adults

Nutrition for Soccer Players

Nutrition for Soccer Players

Acid in the airways. Focus on “Hyperacidity of secreted fluid from submucosal glands in early cystic fibrosis”

cystic fibrosis (CF) is caused by defects in an anion channel called CF transmembrane conductance regulator (CFTR) that is found primarily in the apical membranes of epithelial cells. Most CF symptoms, such as high salt in sweat and obstruction of the pancreatic ducts, intestine, or vas deferens

Blood pressure and the cystic fibrosis gene: evidence for lower pressure rises with age in female carriers.

Individuals homozygous for the autosomal recessive disorder CF are known to have low blood pressure, thought to be caused by greatly increased sweat salt loss. We examined whether carriers of the CF gene also have low blood pressure. Our pilot studies had suggested an effect limited to females, leading to 2 further studies in white females. In the first, blood pressure was measured in 232 known CF mutation carriers and compared with 246 mutation-negative control subjects. The carriers showed a significantly lower rate of increase in systolic blood pressure with age than the controls, especially after age 50 (3.5% per decade compared with 5.4% per decade, P=0.010). In a small substudy, sweat sodium and chloride levels were highest in those CF carriers with the lowest blood pressures. In the second study, CF carrier status was investigated in 563 normotensive females and in 607 women with essential hypertension diagnosed to test whether a lower incidence of carriers in the hypertensives suggested a protective effect. Twenty-five of the normotensives (4.4%) were carriers compared with 21 (3.5%) of the hypertensive group (P=0.45). Older CF carrier females had lower systolic and diastolic pressures than matched control subjects, with a tendency for blood pressure to increase less with age. This could result in significant reduction in stroke and heart disease. The effect on blood pressure is insufficient to prevent hypertension, though it remains conceivable that the severity might be ameliorated in carriers.

Prolactin, human nutrition and evolution, and the relation to cystic fibrosis

Cystic fibrosis (CF) is a lethal, genetically transmitted disease of Caucasian populations. Its prevalence is highest (ca 1:2000 live births) among Western and Central Europeans and their descendants. Major clinical symptoms are chronic, obstructive, pulmonary disease, impaired intestinal digestion and absorption and elevated concentration of salt in sweat. The last is important, not only for diagnosis, but because it is an example of an electrolyte transport defect present in other epithelial tissues. Numerous other clinical manifestations are generally present. The history of prolactin (PRL), especially its role in osmoregulation, is outlined and related to the symptomatology and electrolyte defect of CF. Data are presented showing the relation of PRL to regulation of sweat electrolytes and its presence and probable synthesis in the coil of the human sweat gland. The basic biochemical defect of CF has not yet been elucidated, but recent research has shown that it is probably an abnormality of a regulatory factor. We propose that PRL is a likely candidate. The large variety of functions of PRL, in particular the regulation of the transport of sodium and chloride across epithelial membranes, and the regulation of mucus production, can be matched to the major disease symptomatology. Additionally, every other one of the multiple abnormalities of CF can be associated with described activities of PRL. In lower vertebrates epithelial tissues regulated by PRL are phylogenetic progenitors of affected tissues in CF. In the human, these tissues contain cells of the Diffuse Neuroendocrine System, or APUD cells, that show PRL-like immunoreactivity, or overt synthesis of the hormone. Thus, the regulatory activity of these tissues could be paracrine. The geographic distribution and the dietary habits of early Caucasians are examined. It appears that the Neolithic revolution, with the necessity of adapting to agriculturally produced foods, i.e. milk and wheat, could have brought about the genetic selection of post-translational variants of PRL. It is suggested that the combination of two or more of these mutations in the same individual may be responsible for CF. This is illustrated with proposed models of CF inheritance. We conclude by postulating that PRL acts at the level of the target cell by triggering (in conjunction with a steroid) the gene expression of unique proteins; these act as intermediaries of PRL activity; two or more abnormalities of these proteins when present in an individual produce CF; the protein abnormalities are the consequence of nutritional and ecological pressure.

Cystic fibrosis--its biochemical detection.

We examine critically the biochemical methods capable of detecting and monitoring the end-organ disease processes in patients with cystic fibrosis. Although the diagnosis of cystic fibrosis is never justified on the basis of the sweat salt test alone, the original filter-paper technic (Gibson-Cooke, Pediatrics 23:545-549, 1959) for determining Na+ and Cl- concentrations in sweat remains the most discriminating method. We discuss the contributions for neonatal screening of the so-called cystic fibrosis protein, associated decreased enzymic activities in the homo- and heterozygous state, and immunoreactive trypsin. Because evidence of either intestinal malabsorption or a pancreatic lesion must be sought, we review the use and interpretation of some tests of pancreatic dysfunction (meconium albumin, duodenal juice components, serum pancreatic isoamylase, and trypsinogen), both in establishing and in confirming the diagnosis of cystic fibrosis.

A hypertensive syndrome with relative adrenal cortical overactivity.

The authors have used the concentration of salt in sweat as an objective test to demonstrate the existence of a group of hypertensive patients with clinical signs of hyperadrenocortical function. The significantly lower concentration of salt in the sweat of patients with this endocrine hypertensive syndrome distinguishes them from other hypertensive patients who show no significant difference from normal. That this difference reflects an adrenal pathway is further suggested by Conn's demonstration that hypoadrenal activity is associated with high concentrations, and hyperadrenal function with low concentrations of salt in sweat.