Categories:

Lactate Paradox: High Altitude and Exercise

Also see:
Protective Altitude
Altitude Sickness: Therapeutic Effects of Acetazolamide and Carbon Dioxide
Carbon Dioxide as an Antioxidant
Ray Peat, PhD on Carbon Dioxide, Longevity, and Regeneration
Protective Carbon Dioxide, Exercise, and Performance
Exercise and Effect on Thyroid Hormone
Altitude Improves T3 Levels
Synergistic Effect of Creatine and Baking Soda on Performance
Exercise Induced Stress
Ray Peat, PhD: Quotes Relating to Exercise

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Quotes by Ray Peat, PhD:
“Fatigued cells take up water, and become heavier. They also become more permeable, and leak. When more oxygen is made available, they are less resistant to fatigue, and when the organism is made slightly hypoxic, as at high altitude, muscles have more endurance, and are stronger, and nerves conduct more quickly.”

“K. P. Buteiko believed that increased carbon dioxide in the body fluids sometimes caused cancers to disappear. In many studies over the last 40 years (and the trend can also be seen in insurance statistics published in 1912), it is clear that cancer mortality is much lower at high altitude. Under all conditions studied, the characteristic lactic acid metabolism of stress and cancer is suppressed at high altitude, as respiration is made more efficient. The Haldane effect shows that carbon dioxide retention is increased at high altitude.

Studying athletes at sea level and at high altitude, it was seen that less lactic acid is produced by maximal exercise at high altitude than at sea level. Since oxygen deficiency in itself tends to cause the formation of lactic acid, this has been called the “lactate paradox”; the expectation was that more lactic acid would be formed, yet less was produced. Something was turning off the production of lactic acid. Normally, it is oxidative respiration that turns off glycolysis and lactic acid production, so that in exercise beyond the ability of the body to deliver oxygen, and in cancer with its respiratory defect, glycolysis produces lactic acid. So, something is happening at high altitude which turns off glycolysis.

The Haldane effect is a term for the fact that hemoglobin gives up oxygen in the presence of carbon dioxide, and releases carbon dioxide in the presence of oxygen. It is the increased retention of carbon dioxide that accounts for the “lactate paradox.” Carbon dioxide activates the Krebs cycle, but it also combines with ammonium, and in doing so, deactivates glycolysis because ammonium activates a regulatory enzyme. At high elevation, carbon dioxide is retained, and lactic acid formation is suppressed. (This is called the Pasteur effect, but altitude physiologists haven’t begun thinking in these directions.) Comparing very low altitude (Jordan valley, over 1000 feet below sea level) with moderate altitude (620 meters above sea level), ACTH was increased in runners after a race only at the low altitude, indicating that the stress reaction was prevented by a moderate increase of altitude. (el-Migdadi, et aI., 1996.)

The perspective we get on cancer, from the high altitude studies, allows us to go beyond the specific issue of cancer, to the more general issue of stress and regeneration. In outline, stress alters the physical nature of the cellular substance in a way that activates the cell, in which case it will either die from exhaustion, or grow into new cells. The replacement of injured cells means that mutations need not accumulate, and this renewal with elimination of mutant cells has been observed in sun-damaged skin. Among the many layers of form-generating and form-sustaining systems, the balance of electrical fields has a basic place.”

“The production of lactic acid during lactic acid during intense muscle activity led some people to suggest that fatigue occurred when the muscle wasn’t getting enough oxygen, but experiments show that fatigue sets in while adequate oxygen is being delivered to the muscle. Underwater divers sometimes get an excess of oxygen, and that often causes muscle fatigue and soreness. At high altitudes, where there is relatively little oxygen, strength and endurance can increase.”

“The idea of the “oxygen debt” produced by exercise or stress as being equivalent to the accumulation of lactic acid is far from accurate, but it’s true that activity increases the need for oxygen, and also increases the tendency to accumulate lactic acid, which can then be disposed of over an extended time, with the consumption of oxygen. This relationship between work and lactic acidemia and oxygen deficit led to the term “lactate paradox” to describe the lower production of lactic acid during maximal work at high altitude when people are adapted to the altitude. Carbon dioxide, retained through the Haldane effect, accounts for the lactate paradox, by inhibiting cellular excitation and sustaining oxidative metabolism to consume lactate efficiently.”

“Mild hypoxia, as at high altitude, suppresses lactic acid production (“the lactate paradox”), and increases the amount of carbon dioxide in tissues.”

Clin Physiol. 1990 May;10(3):265-72.
Limiting factors for exercise at extreme altitudes.
West JB.
Man can only survive and do work in the severe oxygen deprivation of great altitudes by an enormous increase in ventilation which has the advantage of defending the alveolar PO2 against the reduced inspired PO2. Nevertheless the arterial PO2 on the summit of Mt Everest at rest is less than 30 Torr, and it decreases with exercise because of diffusion limitation within the lung. One of the consequences of the hyperventilation is that the marked respiratory alkalosis increases the oxygen affinity of the haemoglobin and assists in loading of oxygen by the pulmonary capillary. Although ventilation is greatly increased, it is a paradox that cardiac output for a given work level is the same in acclimatized subjects at high altitude as at sea level. Stroke volume is reduced but not because of impaired myocardial contractility because this is preserved up to extreme altitudes. Indeed the normal myocardium is one of the few tissues whose function is unimpaired by the very severe hypoxia. There is evidence that oxygen delivery to exercising muscle is diffusion limited along the pathway between the peripheral capillary and the mitochondria. At the altitude of Mt Everest, maximal oxygen uptake is reduced to 20-25% of its sea level value, and it is exquisitely sensitive to barometric pressure. Seasonal variations of barometric pressure affect the ability of man to reach the summit without supplementary oxygen. In spite of the greatly reduced aerobic capacity, anaerobiosis is greatly curtailed, and it is predicted that above 7500 m, there is no rise in blood lactate on exercise. The paradoxically low lactate is possibly related to plasma bicarbonate depletion.

Eur J Appl Physiol Occup Physiol. 1996;74(3):195-205.
Lactate during exercise at high altitude.
Kayser B.
In acclimatized humans at high altitude the reduction, compared to acute hypoxia, of the blood lactate concentration (la) at any absolute oxygen uptake (VO2), as well as the reduction of maximum la (lamax) after exhaustive exercise, compared to both acute hypoxia or normoxia, have been considered paradoxical, and these phenomena have therefore become known as the “lactate paradox”. Since, at any given power output and VO2, mass oxygen transport to the contracting locomotor muscles is not altered by the process of acclimatization to high altitude, the gradual reduction in [la-]max in lowlanders exposed to chronic hypoxia seems not to be due to changes in oxygen availability at the tissue level. At present, it appears that the acclimatization-induced changes in [la-] during exercise are the result of at least two mechanisms: (1) a decrease in maximum substrate flux through aerobic glycolysis due to the reduced VO2max in hypoxia; and (2) alterations in the metabolic control of glycogenolysis and glycolysis at the cellular level, largely because of the changes in adrenergic drive of glycogenolysis that ensue during acclimatization, although effects of changes in peripheral oxygen transfer and the cellular redox state cannot be ruled out. With regard to the differences in lactate accumulation during exercise that have been reported to occur between lowlanders and highlanders, both groups either being acclimatized or not, these do not seem to be based upon fundamentally different metabolic features. Instead, they seem merely to reflect points along the same continuum of phenotypic adaptation of which the location depends on the time spent at high altitude.

Eur J Appl Physiol Occup Physiol. 1991;63(5):315-22.
Effect of beta-adrenergic blockade on plasma lactate concentration during exercise at high altitude.
Young AJ, Young PM, McCullough RE, Moore LG, Cymerman A, Reeves JT.
When unacclimatized lowlanders exercise at high altitude, blood lactate concentration rises higher than at sea level, but lactate accumulation is attenuated after acclimatization. These responses could result from the effects of acute and chronic hypoxia on beta-adrenergic stimulation. In this investigation, the effects of beta-adrenergic blockade on blood lactate and other metabolites were studied in lowland residents during 30 min of steady-state exercise at sea level and on days 3, 8, and 20 of residence at 4300 m. Starting 3 days before ascent and through day 15 at high altitude, six men received propranolol (80 mg three times daily) and six received placebo. Plasma lactate accumulation was reduced in propranolol- but not placebo-treated subjects during exercise on day 3 at high altitude compared to sea-level exercise of the same percentage maximal oxygen uptake (VO2max). Plasma lactate accumulation exercise on day 20 at high altitude was reduced in both placebo- and propranolol-treated subjects compared to exercise of the same percentage VO2max performed at sea level. The blunted lactate accumulation during exercise on day 20 at high altitude was associated with reduced muscle glycogen utilization. Thus, increased plasma lactate accumulation in unacclimatized lowlanders exercising at high altitude appears to be due to increased beta-adrenergic stimulation. However, acclimatization-induced changes in muscle glycogen utilization and plasma lactate accumulation are not adaptations to chronically increased beta-adrenergic activity.

High Alt Med Biol. 2003 Winter;4(4):431-43.
Persistence of the lactate paradox over 8 weeks at 3,800 m.
Pronk M, Tiemessen I, Hupperets MD, Kennedy BP, Powell FL, Hopkins SR, Wagner PD.
The arterial blood lactate [La] response to exercise increases in acute hypoxia, but returns to near the normoxic (sea level, SL) response after 2 to 5 weeks of altitude acclimatization. Recently, it has been suggested that this gradual return to the SL response in [La], known as the lactate paradox (LP), unexpectedly disappears after 8 to 9 weeks at altitude. We tested this idea by recording the [La] response to exercise every 2 weeks over 8 weeks at altitude. Five normal, fit SL-residents were studied at SL and 3,800 m (Pbar = 485 torr) in both normoxia (PIO2 = 150 torr) and hypoxia (PIO2 = 91 torr approximately air at 3,800 m). Arterial [La] and blood gas values were determined at rest and during cycle exercise at the same absolute workloads (0, 25, 50, 75, 90, and 100% of initial SL-VO2Max) and exercise duration (4, 4, 4, 2, 1.5, and 0.75 min, respectively) at each time point. [La] curves were elevated in acute hypoxia at SL (p < 0.01) and at 3,800 m fell progressively toward the SL-normoxic curve (p < 0.01). On the same days, [La] responses in acute normoxia showed essentially no changes over time and were similar to initial SL normoxic responses. We also measured arterial catecholamine levels at each load and found a close relationship to [La] over time, supporting a role for adrenergic influence on [La]. In summary, extending the time at this altitude to 8 weeks produced no evidence for reversal of the LP, consistent with prior data obtained over shorter periods of altitude residence.

Fed Proc. 1986 Dec;45(13):2953-7.
Lactate during exercise at extreme altitude.
West JB.
Maximal exercise at extreme altitude results in profound arterial hypoxemia and, presumably, extreme tissue hypoxia. The best evidence available indicates that the resting arterial PO2 on the summit of Mount Everest is about 28 torr and that it falls even further during exercise. Nevertheless, some 10 climbers have now reached the summit without supplementary oxygen. Paradoxically, blood lactate for a given work rate at high altitude in acclimatized subjects is essentially the same as at sea level. Because work capacity decreases markedly with increasing altitude, maximal blood lactate also falls. Extrapolation of available data up to 6300 m indicates that a climber who reaches the Everest summit will have no increase in blood lactate. The cause of the low blood lactate during exercise at extreme altitude is not fully understood. One possibility is depletion of plasma bicarbonate in acclimatized subjects, which reduces buffering and results in large increases in H+ concentration for a given release of lactate. The consequent local fall in pH may inhibit enzymes, e.g., phosphofructokinase (EC 2.7.1.56), in the glycolytic pathway.

J Appl Physiol. 1991 Apr;70(4):1720-30.
Metabolic and work efficiencies during exercise in Andean natives.
Hochachka PW, Stanley C, Matheson GO, McKenzie DC, Allen PS, Parkhouse WS.
Maximum O2 and CO2 fluxes during exercise were less perturbed by hypoxia in Quechua natives from the Andes than in lowlanders. In exploring how this was achieved, we found that, for a given work rate, Quechua highlanders at 4,200 m accumulated substantially less lactate than lowlanders at sea level normoxia (approximately 5-7 vs. 10-14 mM) despite hypobaric hypoxia. This phenomenon, known as the lactate paradox, was entirely refractory to normoxia-hypoxia transitions. In lowlanders, the lactate paradox is an acclimation; however, in Quechuas, the lactate paradox is an expression of metabolic organization that did not deacclimate, at least over the 6-wk period of our study. Thus it was concluded that this metabolic organization is a developmentally or genetically fixed characteristic selected because of the efficiency advantage of aerobic metabolism (high ATP yield per mol of substrate metabolized) compared with anaerobic glycolysis. Measurements of respiratory quotient indicated preferential use of carbohydrate as fuel for muscle work, which is also advantageous in hypoxia because it maximizes the yield of ATP per mol of O2 consumed. Finally, minimizing the cost of muscle work was also reflected in energetic efficiency as classically defined (power output per metabolic power input); this was evident at all work rates but was most pronounced at submaximal work rates (efficiency approximately 1.5 times higher than in lowlander athletes). Because plots of power output vs. metabolic power input did not extrapolate to the origin, it was concluded 1) that exercise in both groups sustained a significant ATP expenditure not convertible to mechanical work but 2) that this expenditure was downregulated in Andean natives by thus far unexplained mechanisms.

J Appl Physiol. 1991 May;70(5):1963-76.
Skeletal muscle metabolism and work capacity: a 31P-NMR study of Andean natives and lowlanders.
Matheson GO, Allen PS, Ellinger DC, Hanstock CC, Gheorghiu D, McKenzie DC, Stanley C, Parkhouse WS, Hochachka PW.
Two metabolic features of altitude-adapted humans are the maximal O2 consumption (VO2max) paradox (higher work rates following acclimatization without increases in VO2max) and the lactate paradox (progressive reductions in muscle and blood lactate with exercise at increasing altitude). To assess underlying mechanisms, we studied six Andean Quechua Indians in La Raya, Peru (4,200 m) and at low altitude (less than 700 m) immediately upon arrival in Canada. The experimental strategy compared whole-body performance tests and single (calf) muscle work capacities in the Andeans with those in groups of sedentary, power-trained, and endurance-trained lowlanders. We used 31P nuclear magnetic resonance spectroscopy to monitor noninvasively changes in concentrations of phosphocreatine [( PCr]), [Pi], [ATP], [PCr]/[PCr] + creatine ([Cr]), [Pi]/[PCr] + [Cr], and pH in the gastrocnemius muscle of subjects exercising to fatigue. Our results indicate that the Andeans 1) are phenotypically unique with respect to measures of anaerobic and aerobic work capacity, 2) despite significantly lower anaerobic capacities, are capable of calf muscle work rates equal to those of highly trained power- and endurance-trained athletes, and 3) compared with endurance-trained athletes with significantly higher VO2max values and power-trained athletes with similar VO2max values, display, respectively, similar and reduced perturbation of all parameters related to the phosphorylation potential and to measurements of [Pi], [PCr], [ATP], and muscle pH derivable from nuclear magnetic resonance. Because the lactate paradox may be explained on the basis of tighter ATP demand-supplying coupling, we postulate that a similar mechanism may explain 1) the high calf muscle work capacities in the Andeans relative to measures of whole-body work capacity, 2) the VO2max paradox, and 3) anecdotal reports of exceptional work capacities in indigenous altitude natives.

High Alt Med Biol. 2006 Summer;7(2):105-15.
Work capacity of permanent residents of high altitude.
Marconi C, Marzorati M, Cerretelli P.
Tibetan and Andean natives at altitude have allegedly a greater work capacity and stand fatigue better than acclimatized lowlanders. The principal aim of the present review is to establish whether convincing experimental evidence supports this belief and, should this be the case, to analyze the possible underlying mechanisms. The superior work capacity of high altitude natives is not based on differences in maximum aerobic power (V(O2 peak)), mL kg(-1)min(-1)). In fact, average V (O2 peak) of both Tibetan and Andean natives at altitude is only slightly, although not significantly, higher than that of Asian or Caucasian lowlanders resident for more than 1 yr between 3400 and 4700 m (Tibetans, n = 152, vs. Chinese Hans, n = 116: 42.4 +/- 3.4 vs. 39.2 +/- 2.6 mL kg(-1)min(-1), mean +/- SE; Andeans, n = 116, vs. Caucasians, n = 70: 47.1 +/- 1.7 vs. 41.6 +/- 1.2 mL kg(-1)min(-1)). However, compared to acclimatized lowlanders, Tibetans appear to be characterized by a better economy of cycling, walking, and running on a treadmill. This is possibly due to metabolic adaptations, such as increased muscle myoglobin content and antioxidant defense. All together, the latter changes may enhance the efficiency of the muscle oxidative metabolic machinery, thereby supporting a better prolonged submaximal performance capacity compared to lowlanders, despite equal V(O2 peak). With regard to Andeans, data on exercise efficiency is scanty and controversial and, at present, no conclusion can be drawn as to the origin of their superior performance.

Cor Vasa. 1981;23(5):359-65.
Heart rhythm disturbances in the inhabitants of mountainous regions.
Mirrakhimov MM, Meimanaliev TS
The authors studied 513 males, permanently living in the high-mountain regions of Tian Shan and the Pamirs (2800 – 4000 m above sea level). A control group consisted of 404 males permanently living at low altitudes (780-900 m above sea level) in the Kemin District, Kirghiz SSR. The probands’ ages were 30-59 years. In all of them the resting electrocardiograms were recorded; 110 exercise tests were made in the high mountains, and 35 tests, at the low altitudes. The prevalence of heart rhythm disturbances was statistically significantly higher in the inhabitants of the high-mountain regions (12.1%) than in the low-altitude inhabitants (2.9%; p less than 0.0001). The most frequent disturbance was the 1st-degree a-v block (6 per cent). In the high mountains cardiac arrhythmias are usually associated with right ventricular hypertrophy, caused by high-altitude hypoxia. During exercise heart arrhythmias appeared conspicuously less frequently in the high mountain than in the low altitude inhabitants.

Acta Physiol Scand. 2000 Dec;170(4):265-9.
The ‘lactate paradox’, evidence for a transient change in the course of acclimatization to severe hypoxia in lowlanders.
Lundby C, Saltin B, van Hall G.
The metabolic response to exercise at high altitude is different from that at sea level, depending on the altitude, the rate of ascent and duration of acclimatization. One apparent metabolic difference that was described in the 1930s is the phenomenon referred to as the ‘lactate paradox’.Acute exposure to hypoxia results in higher blood lactate accumulation at submaximal workloads compared with sea level, but peak blood lactate remain the same. Following continued exposure to hypoxia or altitude, blood lactate accumulation at submaximal work and peak blood lactate levels are paradoxically reduced compared with those at sea level. It has recently been shown, however, that, if the exposure to altitude is sufficiently long, blood lactate responses return to those seen at sea level or during acute hypoxia. Thus, to evaluate the ‘lactate paradox’ phenomenon in relation to time spent at altitude, five Danish lowland climbers were studied at sea level, during acute exposure to hypoxia (10% O2 in N2) and 1, 4 and 6 weeks after arrival in the basecamp of Mt Everest (approximately 5400 m, Nepal). Basecamp was reached after 10 days of gradual ascent from 2800 m. Peak blood lactate levels were similar at sea level (11.0 +/- 0.7 mmol L-1) and during acute hypoxia (9.9 +/- 0.3 mmol L-1), but fell significantly after 1 week of acclimatization to 5400 m (5.6 +/- 0.5 mmol L-1) as predicted by the ‘lactate paradox’. After 4 weeks of acclimatization, peak lactate accumulation (7.8 +/- 1.0 mmol L-1) was still lower compared with acute hypoxia but higher than that seen after 1 week of acclimatization. After 6 weeks of acclimatization, 2 days after return to basecamp after reaching the summit or south summit of Mt Everest, peak lactate levels (10.4 +/- 1.1 mmol L-1) were similar to those seen during acute hypoxia. Therefore, these results suggest that the ‘lactate paradox’ is a transient metabolic phenomenon that is reversed during a prolonged period of exposure to severe hypoxia of more than 6 weeks.

“Many people experience exhilaration when they go to very high altitudes, and it is known that people generally burn calories faster at high altitude. It has been found that, during intense exercise (which always produces a lactic acid accumulation in the blood), a lower peak accumulation of lactate occurs at high altitude, and this seems to be caused by a reduction in the rate of glycolysis, or glucose consumption (B. Grassi, et al.)” –Ray Peat, PhD

J Appl Physiol. 1995 Jul;79(1):331-9.
Maximal rate of blood lactate accumulation during exercise at altitude in humans.
Grassi B, Ferretti G, Kayser B, Marzorati M, Colombini A, Marconi C, Cerretelli P.

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By Team FPS – August 27, 2012

Glucose, Brain Lactate, and Panic Attacks

Am J Psychiatry. 1995 May;152(5):666-72.
Proton magnetic resonance spectroscopy investigation of hyperventilation in subjects with panic disorder and comparison subjects.
Dager SR, Strauss WL, Marro KI, Richards TL, Metzger GD, Artru AA.
OBJECTIVE:
The purpose of this study was to investigate differential effects of hyperventilation on brain lactate in patients with panic disorder and comparison subjects as a possible mechanism for explaining previous observations of an excess rise in brain lactate among panic disorder subjects during lactate infusion.
METHOD:
Seven treatment-responsive patients with panic disorder and seven healthy comparison subjects were studied with proton magnetic resonance spectroscopy to measure brain lactate during controlled, voluntary hyperventilation over a period of 20 minutes. Hyperventilation was regulated with the use of capnometry to maintain end-tidal PCO2 at approximately 20 mm Hg during the period of hyperventilation. Blood lactate was measured prior to and at the end of hyperventilation.
RESULTS:
At baseline the two groups had similar brain lactate levels. Panic disorder subjects exhibited significantly greater rises in brain lactate than comparison subjects in response to the same level of hyperventilation. Blood lactate levels before and after 20 minutes of hyperventilation were not significantly different between groups.
CONCLUSIONS:
Controlled hyperventilation increases brain lactate and does so disproportionately in subjects with panic disorder. This increase in brain lactate may result from decreased cerebral blood flow due to hypocapnia, and individuals with panic disorder may have greater sensitivity to this regulatory mechanism.

Am J Psychiatry. 1995 May;152(5):692-7.
Effect of chloride or glucose on the incidence of lactate-induced panic attacks.
George DT, Lindquist T, Nutt DJ, Ragan PW, Alim T, McFarlane V, Leviss J, Eckardt MJ, Linnoila M.
OBJECTIVE:
This study was designed to test the hypothesis that the addition of chloride to a lactate infusion would reduce the frequency of panic attacks.
METHOD:
The subjects included 14 healthy volunteers and 20 patients meeting the DSM-IV criteria for panic disorder. All subjects received an infusion of lactate dissolved in 0.9% sodium chloride and an infusion of lactate dissolved in 5% dextrose in water on separate days in a random-order, double-blind procedure. Blood pressure, heart rate, and panic symptoms were measured at 3-minute intervals during the infusions. The occurrence of panic attacks was ascertained through the subjects’ reports of losing control, panicking, or “going crazy” and the presence of at least four Research Diagnostic Criteria symptoms of a panic attack.
RESULTS:
Fifteen (75%) of the patients with panic disorder reported a panic attack during one of the infusions or both; no healthy volunteers had a panic attack. The patients with panic disorder were significantly more likely to have a panic attack during the lactate/sodium chloride infusion than during the infusion of lactate/5% dextrose in water. The number of panic attack symptoms reported at 3-minute intervals did not differ between the two types of infusion.
CONCLUSIONS:
The coadministration of glucose resulted in a reduced sensitivity to the panicogenic effects of lactate. The hypothesis that adding chloride to the infusion would reduce the frequency of lactate-induced panic attacks was not supported.

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By Team FPS – August 27, 2012

Red Light Improves Mental Function

Also see:
Light is Right
Fat Deficient Animals – Activity of Cytochrome Oxidase
Glucocorticoids, Cytochrome Oxidase, and Metabolism
“Curing” a High Metabolic Rate with Unsaturated Fats
PUFA, Aging, Cytochrome Oxidase, and Cardiolipin
Blue Light, Cytochrome Oxidase, and Eye Injury
Get a “Chicken Light” and Amp Up Your Energy!
Using Sunlight to Sustain Life
The Therapeutic Effects of Red and Near-Infrared Light (2015)
The Therapeutic Effects of Red and Near-Infrared Light (2017)
The Benefits of Near Infrared Light
Significant Improvement in Cognition in Mild to Moderately Severe Dementia Cases Treated with Transcranial Plus Intranasal Photobiomodulation: Case Series Report.
LED Light Therapy Could Radically Change Our Treatment of Brain Disease
MECHANISMS OF LOW LEVEL LIGHT THERAPY
LaserLessons

BR40 250W Bulb and 10'' Metal Brooder

“Getting a generous amount of light on the head has beneficial effects on mental function, by increasing the activity of cytochrome oxidase (Rojas, et al., 2012) and reducing inflammation.” -Ray Peat, PhD

J Alzheimers Dis. 2012;32(3):741-52. doi: 10.3233/JAD-2012-120817.
Low-level light therapy improves cortical metabolic capacity and memory retention.
Rojas JC, Bruchey AK, Gonzalez-Lima F.
Cerebral hypometabolism characterizes mild cognitive impairment and Alzheimer’s disease. Low-level light therapy (LLLT) enhances the metabolic capacity of neurons in culture through photostimulation of cytochrome oxidase, the mitochondrial enzyme that catalyzes oxygen consumption in cellular respiration. Growing evidence supports that neuronal metabolic enhancement by LLLT positively impacts neuronal function in vitro and in vivo. Based on its effects on energy metabolism, it is proposed that LLLT will also affect the cerebral cortex in vivo and modulate higher-order cognitive functions such as memory. In vivo effects of LLLT on brain and behavior are poorly characterized. We tested the hypothesis that in vivo LLLT facilitates cortical oxygenation and metabolic energy capacity and thereby improves memory retention. Specifically, we tested this hypothesis in rats using fear extinction memory, a form of memory modulated by prefrontal cortex activation. Effects of LLLT on brain metabolism were determined through measurement of prefrontal cortex oxygen concentration with fluorescent quenching oximetry and by quantitative cytochrome oxidase histochemistry. Experiment 1 verified that LLLT increased the rate of oxygen consumption in the prefrontal cortex in vivo. Experiment 2 showed that LLLT-treated rats had an enhanced extinction memory as compared to controls. Experiment 3 showed that LLLT reduced fear renewal and prevented the reemergence of extinguished conditioned fear responses. Experiment 4 showed that LLLT induced hormetic dose-response effects on the metabolic capacity of the prefrontal cortex. These data suggest that LLLT can enhance cortical metabolic capacity and retention of extinction memories, and implicate LLLT as a novel intervention to improve memory.

“Rats had a bright red laser beam shined on their heads for 15 minutes and then the respiratory enzymes of the Krebs cycle was studied. The changes were consistent with enhanced respiration. (A.T. Pikulev, et al., Radiobiology 24(1):29-34, 1984).” -Ray Peat, PhD

Radiobiologiia. 1984 Jan-Feb;24(1):29-34.
[Enzyme activity of glutamic acid metabolism and the Krebs cycle in the brain of rats laser-irradiated against a background of altered adrenoreceptor function].
[Article in Russian]
Pikulev AT, Dzhugurian NA, Zyrianova TN, Lavrova VM, Mostovnikov VA.
In the in vivo experiments it was demonstrated that the effect of a helium-neon laser (lambda = 632.8 nm), at the background of altered functional status of adrenoreceptors, changes the activity of some enzymes of the glutamic acid metabolism and the Krebs cycle. This may be attributed to both the direct effect of laser radiation and the indirect effect via the adrenergic system.

“Cytochrome oxidase in the brain can also be increased by mental stimulation, learning, and moderate exercise, but excessive exercise or the wrong kind of exercise (“eccentric”) can lower it (Aguiar, et al., 2007, 2008), probably by increasing the stress hormones and free fatty acids.” -Ray Peat, PhD

Neurosci Lett. 2007 Oct 22;426(3):171-4. Epub 2007 Sep 4.
Mitochondrial IV complex and brain neurothrophic derived factor responses of mice brain cortex after downhill training.
Aguiar AS Jr, Tuon T, Pinho CA, Silva LA, Andreazza AC, Kapczinski F, Quevedo J, Streck EL, Pinho RA.
Twenty-four adult male CF1 mice were assigned to three groups: non-runners control, level running exercise (0 degrees incline) and downhill running exercise (16 degrees decline). Exercise groups were given running treadmill training for 5 days/week over 8 weeks. Blood lactate analysis was performed in the first and last exercise session. Mice were sacrificed 48 h after the last exercise session and their solei (citrate synthase activity) and brain cortices (BDNF levels and cytochrome c oxidase activity) were surgically removed and immediately stored at -80 degrees C for later analyses. Training significantly increased (P<0.05) citrate synthase activity when compared to untrained control. Blood lactate levels classified the exercise intensity as moderate to high. The downhill exercise training significantly reduced (P<0.05) brain cortex cytochrome c oxidase activity when compared to untrained control and level running exercise groups. BDNF levels significantly decreased (P<0.05) in both exercise groups.

Neurochem Res. 2008 Jan;33(1):51-8. Epub 2007 Jul 6.
Intense exercise induces mitochondrial dysfunction in mice brain.
Aguiar AS Jr, Tuon T, Pinho CA, Silva LA, Andreazza AC, Kapczinski F, Quevedo J, Streck EL, Pinho RA.
There are conflicts between the effects of free radical over-production induced by exercise on neurotrophins and brain oxidative metabolism. The objective of this study was to investigate the effects of intense physical training on brain-derived neurotrophic factor (BDNF) levels, COX activity, and lipoperoxidation levels in mice brain cortex. Twenty-seven adult male CF1 mice were assigned to three groups: control untrained, intermittent treadmill exercise (3 x 15 min/day) and continuous treadmill exercise (45 min/day). Training significantly (P < 0.05) increased citrate synthase activity when compared to untrained control. Blood lactate levels classified the exercise as high intensity. The intermittent training significantly (P < 0.05) reduced in 6.5% the brain cortex COX activity when compared to the control group. BDNF levels significantly (P < 0.05) decreased in both exercise groups. Besides, continuous and intermittent exercise groups significantly (P < 0.05) increased thiobarbituric acid reactive species levels in the brain cortex. In summary, intense exercise promoted brain mitochondrial dysfunction due to decreased BDNF levels in the frontal cortex of mice.

================================
Light therapy and muscle endurance.

Photochem Photobiol. 2010 May-Jun;86(3):673-80. doi: 10.1111/j.1751-1097.2010.00732.x. Epub 2010 Apr 16.
In vivo low-level light therapy increases cytochrome oxidase in skeletal muscle.
Hayworth CR, Rojas JC, Padilla E, Holmes GM, Sheridan EC, Gonzalez-Lima F.
Low-level light therapy (LLLT) increases survival of cultured cells, improves behavioral recovery from neurodegeneration and speeds wound healing. These beneficial effects are thought to be mediated by upregulation of mitochondrial proteins, especially the respiratory enzyme cytochrome oxidase. However, the effects of in vivo LLLT on cytochrome oxidase in intact skeletal muscle have not been previously investigated. We used a sensitive method for enzyme histochemistry of cytochrome oxidase to examine the rat temporalis muscle 24 h after in vivo LLLT. The findings showed for the first time that in vivo LLLT induced a dose- and fiber type-dependent increase in cytochrome oxidase in muscle fibers. LLLT was particularly effective at enhancing the aerobic capacity of intermediate and red fibers. The findings suggest that LLLT may enhance the oxidative energy metabolic capacity of different types of muscle fibers, and that LLLT may be used to enhance the aerobic potential of skeletal muscle.

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By Team FPS – August 27, 2012

Stress, Portrait of a Killer – Full Documentary (2008)

Also see:
Stress and Aging: The Glucocorticoid Cascade Hypothesis
The Streaming Organism

Robert Sapolsky National Geographic Documentary Stanford University

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By Team FPS – August 26, 2012

Walt Disney 1946: The Story of Menstruation

https://youtu.be/_l9qhlHFXuM?t=11s

The Story of Menstruation is a 1946 10-minute animated film produced by Walt Disney Productions in 1946. It was commissioned by the International Cello-Cotton Company (now Kimberly-Clark) and was shown to approximately 105 million American students in health education classes.

It was one of the first commercially sponsored films to be distributed to high schools. It was distributed with a booklet for teachers and students called Very Personally Yours that featured advertising of the Kotex brand of products, and discouraged the use of tampons, where the market was dominated by the Tampax brand of rivals Procter & Gamble.

The Story of Menstruation is believed to be the first film to use the word vagina in its screenplay. Neither sexuality nor reproduction is mentioned in the film, and an emphasis on sanitation makes it, as Disney historian Jim Korkis has suggested: “a hygienic crisis rather than a maturation event.”

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By Team FPS – August 26, 2012

Hyperventilation and Breathe-More Myth

Hyperventilation (definition) is breathing more than the medical norm.
http://www.normalbreathing.com/i-hyperventilation.php
Hyperventilation can be defined as breathing more than 10 liters of air per minute at rest for a 70-lg person.

Hyperventilation is very common these days. The large majority of people believe that it is worthwhile as well as healthy to breathe in more deeply (to hyperventilate) and obtain extra air in the respiratory system, medical doctors have the opposite view in regard to deep breathing or overbreathing.

The main initial result of overbreathing is lowered CO2 saturation of the arterial blood, and this reduces transport of O2 to cells. Let us consider how.

Hyperventilation does not improve blood oxygenation, which remains about the same, 98-99%, as during normal breathing. And physicians are right that hyperventilation does not raise O2 saturation of the arterial blood.

Hyperventilation reduces CO2 levels in the lungs and arterial blood. This effect takes place within 1-2 minutes.

Low arterial CO2 constricts arteries and arterioles reducing blood flow and O2 delivery to all vital organs. Dozens of studies confirmed this effect of hyperventilation.

Low CO2 also reduces O2 release in tissues. In other words, hyperventilation leads to the suppressed Bohr effect: less O2 is discharged from red blood cells due to reduced CO2 in tissues.

Nearly all chronic diseases are either based on or accompanied by hyperventilation. You can see these studies on NormalBreathing.com. Click the link at the top of this post.

Do not believe in “breathing-more” or “deep-breathing” myth.

Hundreds of doctors applied hyperventilation test in their medical practice. Let us consider how.

Numerous studies have made use of the overbreathing test (deliberate hyperventilation) when health care professionals required their clients to respire faster and heavier for 2 or 3 minutes so that these patients can reveal their signs and weakest organs of the human body. This kind of deep breathing test was particularly common with those specialists who taught breathing techniques. Multiple clinical research studies discovered that deep breathing causes many health problems.

Certainly, because a lot of individuals with diseases (usually over 90 percent) can recognize their signs during the deep breathing test, these individuals knew the root of their complications.

Awareness concerning regular respiration patterns helped the sufferers to find out the leading causes of their health symptoms. Now they can monitor their routine breathing so that they can notice too heavy breathing in every day lifestyle.

Initially, it happened to be discussed to the patient that deep breathing actions triggering over-breathing cause a decrease in carbon dioxide levels in the alveoli. These deep breathing actions consisted of coughing, yawning, sighing, sneezing as well as chest breathing. All are signs and symptoms of hyperventilation. So as to become healthy, those abnormal behaviors must be quit or avoided.

Learn more about hyperventilation symptoms: http://www.normalbreathing.com/hyperventilation-symptoms.php

Secondly, it was very important for the individual to recognize the features of upper body as well as abdominal respiration. Without a doubt, diaphragmatic breathing is usually represented by the observing adjectives: easy, quiet, slow, as well as light. On the flip side, chest respiration happens to be bulky, loud, too fast, as well as irregular.

Because psychological stress is a routine result to anxiety resulting in hyperventilation, one has the ability to end this. A person can slow down breathing. This reduces minute ventilation, lowers pulse rate, as well as boosts alveolar carbon dioxide concentrations. As a result, relaxation happens to be a useful therapeutic device in slashing deep breathing or hyperventilation as well as in improving one’s wellness as many studies related to various medical conditions have actually validated.

Furthermore, relaxation methods that slow down breathing can often be useful in getting rid of the negative effects of stress, deep breathing, and their subsequent uncommon physiological adjustments. In particular, the decrease of strain in the muscular tissues, particularly of the chest region, causes more calmness as well as better respiration.

URL of this YouTube video: https://www.youtube.com/watch?v=xhusT_X2e48

Find out more from Dr Artour Rakhimov’s website NormalBreathing.com

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By Team FPS – August 25, 2012

Sodium Deficiency and Stress

Also see:
Aldosterone, Sodium Deficiency, and Insulin Resistance
The Randle Cycle
Free Fatty Acids Suppress Cellular Respiration
Aldosterone as an endogenous cardiovascular toxin
Aldosterone and Thrombosis
Low Sodium Diet: High FFA, Insulin Resistance, Atherosclerosis
Sodium and Mortality – An Inverse Relationship
Elevated Levels of Sodium Blunt Response to Stress, Study Shows

“The absorption and retention of magnesium, sodium, and copper, and the synthesis of proteins, are usually poor in hypothyroidism. Salt craving is common in hypothyroidism, and eating additional sodium tends to raise the body temperature, and by decreasing the production of aldosterone, it helps to minimize the loss of magnesium, which in turn allows cells to respond better to the thyroid hormone. This is probably why a low sodium diet increases adrenalin production, and why eating enough sodium lowers adrenalin and improves sleep. The lowered adrenalin is also likely to improve intestinal motility.” -Ray Peat, PhD

J Hypertens. 1993 Dec;11(12):1381-6.
Effect of dietary salt restriction on urinary serotonin and 5-hydroxyindoleacetic acid excretion in man.
Sharma AM, Schorr U, Thiede HM, Distler A.
OBJECTIVE:
To determine the effect of dietary salt restriction on urinary excretion of serotonin and its principal metabolite 5-hydroxyindoleacetic acid (5-HIAA) in man.
DESIGN:
We studied 16 healthy male volunteers (age range 20-28 years) who ate a standard diet containing 20 mmol/day NaCl, to which either 220 mmol/day NaCl or placebo was added as a supplement for 1 week each, according to a randomized, single-blind crossover design.
METHODS:
Urinary excretion of serotonin, 5-HIAA, noradrenaline and vanillylmandelic acid (VMA) were measured during the low- and high-salt periods using reverse-phase high-performance liquid chromatography.
RESULTS:
During the low-salt diet, 24-h urinary excretion of serotonin increased by 42%, accompanied by a 52% rise in the excretion of 5-HIAA. Salt restriction also increased noradrenaline excretion by 77% and VMA excretion by 40%. Regression analysis revealed a strong positive relationship between the excretion of serotonin and of noradrenaline (r = 0.84, P < 0.001) and between that of 5-HIAA and of VMA (r = 0.74, P < 0.001).
CONCLUSIONS:
Salt restriction stimulates the serotonergic system in man. Stimulation of this system, in conjunction with the sympathetic nervous system, may contribute to renal sodium conservation during dietary salt restriction in man.

J Clin Endocrinol Metab. 1991 Nov;73(5):975-81.
Effects of sodium supplementation during energy restriction on plasma norepinephrine levels in obese women.
Gougeon R, Mitchell TH, Larivière F, Abraham G, Montambault M, Marliss EB.
We tested whether sodium restriction would counteract the decrease in sympathetic nervous system activity usually associated with marked energy restriction. The effects of two levels of energy restriction, with different sodium intakes, on plasma norepinephrine (NE) levels while supine and in response to standing were studied. Twenty-two healthy normotensive obese female subjects (body mass index, 34 +/- 1 kg/m2; weight, 90 +/- 2 kg) followed one of three 3-week protocols: 1) total fasting with 80 mmol/day NaCl, 2) a very low energy diet (VLED) containing 1.7 MJ, 93 g protein, and 90 mmol Na/day, with an additional 60 mmol/day NaCl supplement, or 3) total fasting without NaCl (0 Na fast). At the end of the baseline isocaloric diet and of total fasts or VLED, pulse, blood pressure, and plasma NE were measured after 4 h of recumbency and 5 and 10 min after assuming the upright posture. These measurements were repeated after 1 L physiological saline was infused into the 0 Na fast subjects. Cumulative negative sodium balance was observed only in the 0 Na fasting subjects. Supine blood pressure decreased from baseline with fasting, but not with the VLED. The decreases in systolic pressure and increases in heart rate on standing observed with all diets were greatest with the 0 Na fast. Supine plasma NE (vs. baseline value) declined (P less than 0.05) with the VLED, remained unchanged with the Na supplemented fast, but increased with the 0 Na fast (P less than 0.05). The upright plasma NE values were highest in the 0 Na fast subjects, but lower after the saline infusion as well as in the subjects on the VLED. Thus, the decrease in NE due to energy restriction with normal sodium intake was counteracted by moderate sodium restriction, and levels increased with zero sodium intake. Therefore, sodium depletion can override the suppressive effect of energy restriction and, instead, increase the activity of the sympathetic nervous system, as reflected by plasma NE.

J Card Fail. 2009 Dec;15(10):864-73.
Long-term effects of dietary sodium intake on cytokines and neurohormonal activation in patients with recently compensated congestive heart failure.
Parrinello G, Di Pasquale P, Licata G, Torres D, Giammanco M, Fasullo S, Mezzero M, Paterna S.
BACKGROUND:
A growing body of evidence suggests that the fluid accumulation plays a key role in the pathophysiology of heart failure (HF) and that the inflammatory and neurohormonal activation contribute strongly to the progression of this disorder.
METHODS AND RESULTS:
The study evaluated the long-term effects of 2 different sodium diets on cytokines neurohormones, body hydration and clinical outcome in compensated HF outpatients (New York Heart Association Class II). A total of 173 patients (105 males, mean age 72.5+/-7) recently hospitalized for worsening advanced HF and discharged in normal hydration and in clinical compensation were randomized in 2 groups (double blind). In Group 1, 86 patients received a moderate restriction in sodium (120mmol to 2.8g/day) plus oral furosemide (125 to 250mg bid); in Group 2, 87 patients: received a low-sodium diet (80mmol to 1.8g/day) plus oral furosemide (125 to 250mg bid). Both groups were followed for 12 months and the treatment was associated with a drink intake of 1000mL daily. Neurohormonal (brain natriuretic peptide, aldosterone, plasma rennin activity) and cytokines values (tumor necrosis factor-alpha, interleukin-6) were significantly reduced with a significant increase of the anti-inflammatory cytokine interleukin-10 at 12 months in normal, P < .0001) than low-sodium group. The low-sodium diet showed a significant activation of neurohormones and cytokines and worsening the body hydration, whereas moderate sodium restriction maintained dry weigh and improved outcome in the long term.
CONCLUSIONS:
Our results appear to suggest a surprising efficacy of a new strategy to improve the chronic diuretic response by increasing Na intake and limiting fluid intake. This counterintuitive approach underlines the need for a better understanding of factors that regulate sodium and water handling in chronic congestive HF. A larger sample of patients and further studies are required to evaluate whether this is due to the high dose of diuretic used or the low-sodium diet.

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By Team FPS – August 21, 2012

Low Sodium Diet: High FFA, Insulin Resistance, Atherosclerosis

Also see:
Aldosterone, Sodium Deficiency, and Insulin Resistance
The Randle Cycle
Free Fatty Acids Suppress Cellular Respiration
Aldosterone as an endogenous cardiovascular toxin
Aldosterone and Thrombosis
Sodium Deficiency and Stress

J Endocrinol. 2005 Jun;185(3):429-37.
Low salt intake modulates insulin signaling, JNK activity and IRS-1ser307 phosphorylation in rat tissues.
Prada PO, Coelho MS, Zecchin HG, Dolnikoff MS, Gasparetti AL, Furukawa LN, Saad MJ, Heimann JC.
A severe restriction of sodium chloride intake has been associated with insulin resistance and obesity. The molecular mechanisms by which the low salt diet (LS) can induce insulin resistance have not yet been established. The c-jun N-terminal kinase (JNK) activity has been involved in the pathophysiology of obesity and induces insulin resistance by increasing inhibitory IRS-1(ser307) phosphorylation. In this study we have evaluated the regulation of insulin signaling, JNK activation and IRS-1(ser307) phophorylation in liver, muscle and adipose tissue by immunoprecipitation and immunoblotting in rats fed with LS or normal salt diet (NS) during 9 weeks. LS increased body weight, visceral adiposity, blood glucose and plasma insulin levels, induced insulin resistance and did not change blood pressure. In LS rats a decrease in PI3-K/Akt was observed in liver and muscle and an increase in this pathway was seen in adipose tissue. JNK activity and IRS-1(ser307) phosphorylation were higher in insulin-resistant tissues. In summary, the insulin resistance, induced by LS, is tissue-specific and is accompanied by activation of JNK and IRS-1(ser307) phosphorylation. The impairment of the insulin signaling in these tissues, but not in adipose tissue, may lead to increased adiposity and insulin resistance in LS rats.

Physiol Res. 2000;49(2):197-205.
Low-salt diet alters the phospholipid composition of rat colonocytes.
Mrnka L, Nováková O, Novák F, Tvrzická E, Pácha J.
The effect of low-salt diet on phospholipid composition and remodeling was examined in rat colon which represents a mineralocorticoid target tissue. To elucidate this question, male Wistar rats were fed a low-salt diet and drank distilled water (LS, low-salt group) or saline instead of water (HS, high-salt group) for 12 days before the phospholipid concentration and fatty acid composition of isolated colonocytes were examined. The dietary regimens significantly influenced the plasma concentration of aldosterone which was high in LS group and almost zero in HS group. Plasma concentration of corticosterone was unchanged. When expressed in terms of cellular protein content, a significantly higher concentration of phospholipids was found in LS group, with the exception of sphingomyelin (SM) and phosphatidylserine (PS). Phosphatidylcholine (PC) and phosphatidylethanolamine (PE) accounted for more than 70% of total phospholipids in both groups. A comparison of phospholipid distribution in LS and HS groups demonstrated a higher percentage of PE and a small, but significant, decrease of PC and SM in LS group. The percentage of phosphatidylinositol (PI), PS and cardiolipin (CL) were not affected by mineralocorticoid treatment. With respect to the major phospholipids (PE, PC), a higher level of n-6 polyunsaturated fatty acids (PUFA) and lower levels of monounsaturated fatty acids were detected in PC of LS group. The increase of PUFA predominantly reflected an increase in arachidonic acid by 53%. In comparison to the HS group, oleic acid content was decreased in PC and PE isolated from colonocytes of the LS group. Our data indicate that alterations in phospholipid concentration and metabolism can be detected in rats with secondary hyperaldosteronism. The changes in phospholipid concentration and their fatty acid composition during fully developed effect of low dietary Na+ intake may reflect a physiologically important phenomenon with long-term consequences for membrane structure and function.

J Lipid Res. 2003 Apr;44(4):727-32. Epub 2003 Jan 16.
Dietary sodium chloride restriction enhances aortic wall lipid storage and raises plasma lipid concentration in LDL receptor knockout mice.
Catanozi S, Rocha JC, Passarelli M, Guzzo ML, Alves C, Furukawa LN, Nunes VS, Nakandakare ER, Heimann JC, Quintão EC.
This study aimed at measuring the influence of a low salt diet on the development of experimental atherosclerosis in moderately hyperlipidemic mice. Experiments were carried out on LDL receptor (LDLR) knockout (KO) mice, or apolipoprotein E (apoE) KO mice on a low sodium chloride diet (LSD) as compared with a normal salt diet (NSD). On LSD, the rise of the plasma concentrations of TG and nonesterified fatty acid (NEFA) was, respectively, 19% and 34% in LDLR KO mice, and 21% and 35% in apoE KO mice, and that of plasma cholesterol was limited to the LDLR KO group alone (15%). Probably due to the apoE KO severe hypercholesterolemia, the arterial inner-wall fat storage was not influenced by the diet salt content and was far more abundant in the apoE KO than in the LDLR KO mice. However, in the less severe hypercholesterolemia of the LDLR KO mice, lipid deposits on the LSD were greater than on the NSD. Arterial fat storage correlated with NEFA concentrations in the LDLR KO mice alone (n = 14, P = 0.0065). Thus, dietary sodium chloride restriction enhances aortic wall lipid storage in moderately hyperlipidemic mice.

Metabolism. 2011 Jul;60(7):965-8. Epub 2010 Oct 30.
Low-salt diet increases insulin resistance in healthy subjects.
Garg R, Williams GH, Hurwitz S, Brown NJ, Hopkins PN, Adler GK.
Low-salt (LS) diet activates the renin-angiotensin-aldosterone and sympathetic nervous systems, both of which can increase insulin resistance (IR). We investigated the hypothesis that LS diet is associated with an increase in IR in healthy subjects. Healthy individuals were studied after 7 days of LS diet (urine sodium <20 mmol/d) and 7 days of high-salt (HS) diet (urine sodium >150 mmol/d) in a random order. Insulin resistance was measured after each diet and compared statistically, unadjusted and adjusted for important covariates. One hundred fifty-two healthy men and women, aged 39.1 ± 12.5 years (range, 18-65) and with body mass index of 25.3 ± 4.0 kg/m(2), were included in this study. Mean (SD) homeostasis model assessment index was significantly higher on LS compared with HS diet (2.8 ± 1.6 vs 2.4 ± 1.7, P < .01). Serum aldosterone (21.0 ± 14.3 vs 3.4 ± 1.5 ng/dL, P < .001), 24-hour urine aldosterone (63.0 ± 34.0 vs 9.5 ± 6.5 μg/d, P < .001), and 24-hour urine norepinephrine excretion (78.0 ± 36.7 vs 67.9 ± 39.8 μg/d, P < .05) were higher on LS diet compared with HS diet. Low-salt diet was significantly associated with higher homeostasis model assessment index independent of age, sex, blood pressure, body mass index, serum sodium and potassium, serum angiotensin II, plasma renin activity, serum and urine aldosterone, and urine epinephrine and norepinephrine. Low-salt diet is associated with an increase in IR. The impact of our findings on the pathogenesis of diabetes and cardiovascular disease needs further investigation.

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By Team FPS – August 21, 2012

Syphillis as Aids

Syphilis as Aids

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By Team FPS – August 20, 2012

Inflammation from Decrease in Body Temperature

Also see:
Melatonin Lowers Body Temperature
Menopausal Estrogen Therapy Lowers Body Temperature
Temperature and Pulse Basics & Monthly Log
Thyroid, Temperature, Pulse
Ray Peat, PhD on Thyroid, Temperature, Pulse, and TSH

“A slight decrease in temperature can promote inflammation (Matsui, et al., 2006). The thermogenic substances–dietary protein, sodium, sucrose, thyroid and progesterone–are antiinflammatory for many reasons, but very likely the increased temperature itself is important.” -Ray Peat, PhD

“For example, keeping cells in a well oxygenated state with thyroid hormone and carbon dioxide will shift the balance from estradiol toward the weaker estrone. The thyroid stimulation will cause the liver to excrete estrogen more quickly, and will help to prevent the formation of aromatase in the tissues. Low temperature is one of the factors that increases the formation of estrogen. Lactic acid, serotonin, nitric oxide, prostaglandins, and the endorphins will be decreased by the shift toward efficient oxidative metabolism.” -Ray Peat, PhD

J Neurosurg Anesthesiol. 2006 Jul;18(3):189-93.
Mild hypothermia promotes pro-inflammatory cytokine production in monocytes.
Matsui T, Ishikawa T, Takeuchi H, Okabayashi K, Maekawa T.
Hypothermia is often associated with compromised host defenses and infection. Deteriorations of immune functions related to hypothermia have been investigated, but the involvement of cytokines in host defense mechanisms and in infection remains unclear. We have previously shown that mild hypothermia modifies cytokine production by peripheral blood mononuclear cells. In this study, the effects of hypothermia on the monocytic production of several cytokines and nitric oxide (NO) were determined. Monocytes obtained from 10 healthy humans were cultured with lipopolysaccharide (LPS) under hypothermic (33 degrees C) or normothermic (37 degrees C) conditions for 48 hours. We performed flow cytometric analysis for simultaneous measurement of interleukin (IL)-8, IL-1beta, IL-6, IL-10, IL-12p70, and tumor necrosis factor (TNF)-alpha in culture supernatants. NO production was quantified as accumulation of nitrite in the medium by a colorimetric assay. Compared with normothermia, mild hypothermia raised the levels of IL-1beta, IL-6, IL-12p70, and TNF-alpha produced by monocytes stimulated with LPS. On calculating the ratios of these elevated cytokines to IL-10, however, only IL-12p70/IL-10 and TNF-alpha/IL-10 ratios were significantly elevated under hypothermic conditions. In contrast, hypothermia did not affect NO production. This study demonstrates that mild hypothermia affects the balance of cytokines produced by monocytes, leading to a pro-inflammatory state. Specifically, monocytic IL-12 and TNF-alpha appear to be involved in the immune alterations observed in mild hypothermia. However, the clinical significance of these phenomena remains to be clarified.

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By Team FPS – August 10, 2012