The following is speculative, but sleep deprivation caused by nocturia and sleep disturbances due to CPPS effects on the enteric nervous system (and thus in the end on the HPA axis and on sickness behaviour) is probably an important cause of the severe discomfort and psychological effects seen in CPPS. Especially in non-retired individuals who cannot recover lost sleep during daytime because of work duties. The exact directionality of effects is likely complicated. Are the problem driven by HPA axis disturbances or enteric effects, mediated by the vagus nerve, or by the sleep disturbance caused by nocturia. Regardless of the ultimate cause it is well worth finding strategies for getting a good nights sleep. Strategies such as avoiding caffeinated products, chocolate, alcohol, strawberries and other products know to be diuretic. Especially in the evening and late afternoon.
Prostatit, sömn, cytokiner, CPPS, kroniskt bäckenbottensmärtsyndrom, kronisk abakteriell prostatit, NIHIIIb, immunförsvaret, nokturi.
Showing posts with label nocturia. Show all posts
Showing posts with label nocturia. Show all posts
Sunday, February 14, 2010
The importance of sleep
While this may seem an off topic it is not. Disrupted sleep is a common feature in CPPS and other disease. Why is sleep important? Because regular and normal sleep is important for immunocomptence. In an elegant study it was shown that: “Species that have evolved longer sleep durations appear to be able to increase investment in their immune system an be better protected from parasites” and “suggest that sleep has a much wider role in disease resistance than is currently appreciated”.(1)
So undisturbed sleep is important for psychological, urological (2) and immunological health. This is also why elite athletes pay much attention to get regular and adequate (about 8 hours) sleep to keep at the top. You should take the same care.
While studies on sleep and immunity etc on humans are somewhat contradictory due to methodological differences and the complexity of the studies, some general associations have been shown.
Mild sleep deprivation is associated with increased activity of e.g the HPA axis and the autonomic sympatho-adrenal system. The first signs of alterations are changes in emotional perception. And there is a connection between disturbed sleep (i.e. apnoea) and psychiatric illness (e.g. ADHD, depression, schizophrenia). And conversely certain disease, notably chronic inflammatory diseases, is associated with sleep disturbances.(3-8)
Well known cytokines in sleep and health are IL-1 and IL-6. Sleep deprivation increases diurnal levels of IL-6, IL-1 and TNF-alfa and decreases cortisol levels thus causing daytime sleepiness, fatigue, disrupted concentration and other problems. IL-6 peaks during normal sleep (and promotes slow wave sleep, aka stage 3 and 4 sleep). (9-10) But too much will cause bad sleep.
As aspirin decreases IL-6 (11) it may both improve sleep during infection and likely worsen sleep in healthy individuals if taken in the evening. (IL-6 peaks around 1900 and 0500, and is at its lowest around 0800 and 2100.) Other cytokines do also affect sleep.
Vagus nerve signaling is important for activation of the immune system, and insults to vagus nerve afferents may activate the immune system in the absence of verifiable infection / pathogens and cause sleep disruption. Severing of the nerve diminishes this response. (12-13)
Obesity, metabolic syndrome and diabetes are associated with increased risk of sleep disturbances and obstructive sleep apnea.
Effects of sleep disruption differ depending on amount of disruption and if it occurs during deep sleep (also called restorative sleep, slow wave sleep, stage 3 and 4) or during REM sleep. A few days of sleep deprivation has been shown to increase viable bacteria in blood and lymphatic systems. Early (14) and slow wave sleep (SWS) is correlated with a shift towards Th1 immunity and late and REM sleep with a Th2 / immunosuppressive shift. Frequent arousals are correlated with increased cortisol, epinephrine (adrenaline) and norepinephrine (noradr…) levels. (15)
During infection time in SWS is increased, while duration of REM slep is decreased in “severe inflammatory states” (chronic fatigue, cancer and auto-immune disease). Shift work is associated with increased infection and prolonged sleep loss in military is associated with changes in “hormonal patterns”.(16)
(See by the way the site www.cfs-recovery.org, if it is still on line, where a chronic fatigue sufferer tells his tale of years of failed attempts to get a diagnosis (wow he must have been a hypochondriac… [this is a sarcasm]) and appropriate treatment, before finally testing himself for sleep apnoea, despite no snoring!! After which he fast recovered… Especially notice the many odd symptoms and problems he got!)
Prostatit, sömn, cytokiner, CPPS, kroniskt bäckenbottensmärtsyndrom, kronisk abakteriell prostatit, NIHIIIb, immunförsvaret, nokturi.
________________
(1) Preston BT, Capellini I, McNamara P, Barton RA, Nunn CL. Parasite resistance and the adaptive significance of sleep. BMC Evol Biol 9:7, 2009 jan 9
(2) Nolan TE, Metheny WP, Smith RP. Unrecognized association of sleep disorders and depression with chronic pelvic pain. South Med J. 1992 Dec;85(12):1181-3.
(3) Chang PP, Ford DE, Mead LA, Cooper-Patrick L, Klag MJ. Insomnia in young men and subsequent depression. The Johns Hopkins Precursors Study. Am J Epidemiol. 146(2):105-14, 1997.
(4) Plante DT, Winkelman JW. Sleep disturbance in bipolar disorder: therapeutic implications. Am J Psychiatry. 165(7):830-43, 2008.
(5) Peppard PE, Szklo-Coxe M, Hla KM, Young T. Longitudinal association of sleep-related breathing disorder and depression. Arch Intern Med. 166(16):1709-15, 2006.
(6) Ellenbogen JM, Hulbert JC, Jiang Y, Stickgold R. The sleeping brain's influence on verbal memory: boosting resistance to interference. PLoS ONE. 2009;4(1):e4117. Epub 2009 Jan 7.
(7) Meerlo P, Sgoifo A, Suchecki D. Restricted and disrupted sleep: effects on autonomic function, neuroendocrine stress systems and stress responsivity. Sleep Med Rev 12(3):197-210, 2008.
(8) Schroder CM, O'Hara R. Depression and Obstructive Sleep Apnea (OSA). Ann Gen Psychiatry. 2005 Jun 27;4:13.
(9) Opp MR. Cytokines and sleep. Sleep Med Rev 9:355-364, 2005.
(10) Kapsimalis F, Basta M, Varouchakis G, Gourgoulianis K, Vgontzas A, Kryger M. Cytokines and pathological sleep. Sleep Med 9(6):603-614, 2008.
(11) von Känel R, Kudielka BM, Metzenthin P, Helfricht S, Preckel D, Haeberli A, Stutz M, Fischer JE. Aspirin, but not propranolol, attenuates the acute stress-induced increase in circulating levels of interleukin-6: a randomized, double-blind, placebo-controlled study. Brain Behav Immun. 22(2):150-157, 2008.
(12) Johnston GR, Webster NR. Cytokines and the immunomodulatory function of the vagus nerve. Br J Anaesth. 102(4):453-462, 2009
(13) Van Der Zanden EP, Boeckxstaens GE, de Jonge WJ. The vagus nerve as a modulator of intestinal inflammation. Neurogastroenterol Motil. 21(1):6-17, 2009.
(14) Refers to the first 1-3 hours of sleep, while late refers to the following 3-5 hours.
(15) Lorton D, Lubahn CL, Estus C, Millar BA, Carter JL, Wood CA, Bellinger DL. Bidirectional communication between the brain and the immune system: implications for physiological sleep and disorders with disrupted sleep. Neuroimmunomodulation 13:357-374, 2006.
(16) Majde JA, Krueger JM. Links between the innate immune system and sleep. J Allergy Clin Immunol 116:1188-1198, 2005.
So undisturbed sleep is important for psychological, urological (2) and immunological health. This is also why elite athletes pay much attention to get regular and adequate (about 8 hours) sleep to keep at the top. You should take the same care.
While studies on sleep and immunity etc on humans are somewhat contradictory due to methodological differences and the complexity of the studies, some general associations have been shown.
Mild sleep deprivation is associated with increased activity of e.g the HPA axis and the autonomic sympatho-adrenal system. The first signs of alterations are changes in emotional perception. And there is a connection between disturbed sleep (i.e. apnoea) and psychiatric illness (e.g. ADHD, depression, schizophrenia). And conversely certain disease, notably chronic inflammatory diseases, is associated with sleep disturbances.(3-8)
Well known cytokines in sleep and health are IL-1 and IL-6. Sleep deprivation increases diurnal levels of IL-6, IL-1 and TNF-alfa and decreases cortisol levels thus causing daytime sleepiness, fatigue, disrupted concentration and other problems. IL-6 peaks during normal sleep (and promotes slow wave sleep, aka stage 3 and 4 sleep). (9-10) But too much will cause bad sleep.
As aspirin decreases IL-6 (11) it may both improve sleep during infection and likely worsen sleep in healthy individuals if taken in the evening. (IL-6 peaks around 1900 and 0500, and is at its lowest around 0800 and 2100.) Other cytokines do also affect sleep.
Vagus nerve signaling is important for activation of the immune system, and insults to vagus nerve afferents may activate the immune system in the absence of verifiable infection / pathogens and cause sleep disruption. Severing of the nerve diminishes this response. (12-13)
Obesity, metabolic syndrome and diabetes are associated with increased risk of sleep disturbances and obstructive sleep apnea.
Effects of sleep disruption differ depending on amount of disruption and if it occurs during deep sleep (also called restorative sleep, slow wave sleep, stage 3 and 4) or during REM sleep. A few days of sleep deprivation has been shown to increase viable bacteria in blood and lymphatic systems. Early (14) and slow wave sleep (SWS) is correlated with a shift towards Th1 immunity and late and REM sleep with a Th2 / immunosuppressive shift. Frequent arousals are correlated with increased cortisol, epinephrine (adrenaline) and norepinephrine (noradr…) levels. (15)
During infection time in SWS is increased, while duration of REM slep is decreased in “severe inflammatory states” (chronic fatigue, cancer and auto-immune disease). Shift work is associated with increased infection and prolonged sleep loss in military is associated with changes in “hormonal patterns”.(16)
(See by the way the site www.cfs-recovery.org, if it is still on line, where a chronic fatigue sufferer tells his tale of years of failed attempts to get a diagnosis (wow he must have been a hypochondriac… [this is a sarcasm]) and appropriate treatment, before finally testing himself for sleep apnoea, despite no snoring!! After which he fast recovered… Especially notice the many odd symptoms and problems he got!)
Prostatit, sömn, cytokiner, CPPS, kroniskt bäckenbottensmärtsyndrom, kronisk abakteriell prostatit, NIHIIIb, immunförsvaret, nokturi.
________________
(1) Preston BT, Capellini I, McNamara P, Barton RA, Nunn CL. Parasite resistance and the adaptive significance of sleep. BMC Evol Biol 9:7, 2009 jan 9
(2) Nolan TE, Metheny WP, Smith RP. Unrecognized association of sleep disorders and depression with chronic pelvic pain. South Med J. 1992 Dec;85(12):1181-3.
(3) Chang PP, Ford DE, Mead LA, Cooper-Patrick L, Klag MJ. Insomnia in young men and subsequent depression. The Johns Hopkins Precursors Study. Am J Epidemiol. 146(2):105-14, 1997.
(4) Plante DT, Winkelman JW. Sleep disturbance in bipolar disorder: therapeutic implications. Am J Psychiatry. 165(7):830-43, 2008.
(5) Peppard PE, Szklo-Coxe M, Hla KM, Young T. Longitudinal association of sleep-related breathing disorder and depression. Arch Intern Med. 166(16):1709-15, 2006.
(6) Ellenbogen JM, Hulbert JC, Jiang Y, Stickgold R. The sleeping brain's influence on verbal memory: boosting resistance to interference. PLoS ONE. 2009;4(1):e4117. Epub 2009 Jan 7.
(7) Meerlo P, Sgoifo A, Suchecki D. Restricted and disrupted sleep: effects on autonomic function, neuroendocrine stress systems and stress responsivity. Sleep Med Rev 12(3):197-210, 2008.
(8) Schroder CM, O'Hara R. Depression and Obstructive Sleep Apnea (OSA). Ann Gen Psychiatry. 2005 Jun 27;4:13.
(9) Opp MR. Cytokines and sleep. Sleep Med Rev 9:355-364, 2005.
(10) Kapsimalis F, Basta M, Varouchakis G, Gourgoulianis K, Vgontzas A, Kryger M. Cytokines and pathological sleep. Sleep Med 9(6):603-614, 2008.
(11) von Känel R, Kudielka BM, Metzenthin P, Helfricht S, Preckel D, Haeberli A, Stutz M, Fischer JE. Aspirin, but not propranolol, attenuates the acute stress-induced increase in circulating levels of interleukin-6: a randomized, double-blind, placebo-controlled study. Brain Behav Immun. 22(2):150-157, 2008.
(12) Johnston GR, Webster NR. Cytokines and the immunomodulatory function of the vagus nerve. Br J Anaesth. 102(4):453-462, 2009
(13) Van Der Zanden EP, Boeckxstaens GE, de Jonge WJ. The vagus nerve as a modulator of intestinal inflammation. Neurogastroenterol Motil. 21(1):6-17, 2009.
(14) Refers to the first 1-3 hours of sleep, while late refers to the following 3-5 hours.
(15) Lorton D, Lubahn CL, Estus C, Millar BA, Carter JL, Wood CA, Bellinger DL. Bidirectional communication between the brain and the immune system: implications for physiological sleep and disorders with disrupted sleep. Neuroimmunomodulation 13:357-374, 2006.
(16) Majde JA, Krueger JM. Links between the innate immune system and sleep. J Allergy Clin Immunol 116:1188-1198, 2005.
Saturday, December 19, 2009
The immune system (enteric, gender, seasonality)
The following blog posts will discuss basic immune function and the possible connections with CPPS.
The immune system is divided in two arms: innate and adaptive. Both of which contain cellular (macrophages, natural killer cells etc) and humoral (antibodies) immune components. Cellular immunity protects mainly against intracellular bacteria, protozoans, fungi and many viruses), while humoral immunity protects against multicellular parasites, extracellular bacteria, certain viruses, ceratin toxins and allergens. A popular concept of immunity is the Th1/Th2/Th17-hypothesis.(1-3) In additon to these two arms, an oft forgotten an very important part of the immune system is the enteric immune system.
Not only does the gut have a massive nervous system (see below), it is also the biggest immune system in the body. The gut-associated lymphoid tissue comprises about 70 percent of the mucosal barrier (most of the rest protects the lungs). And that is not suprising as the gut has to withstand an endless stream of pathogens and occasional toxins. Not only invaders from outside the body but also the about over 100 trillion organisms that live in the gut. The maternal intestinal microbiota (both organisms and a large number of “intestinally derived bacterial components”, N.B. not antibodies, but genetic material) is passed to the newborn trough the breast milk.(4) Ingested probiotics may modulate intestinal pain and the immune system by normalizing cytokine ratios.(5)
The brain and the viscera communicate with each other to coordinate behavior and emotional responses (due to evolutionary reasons like territorial marking, not stop to pee while hunted, panic, anxiety, and so on).and visceral activity. Pathological changes (e.g. bacterial infection, tissue damage, distension of the colon and others) in the viscera affect the forebrain.
Immune activity shows a circadian rhythm with cellular/Th1 prevalence during sleep (maximum activity coincides with nocturnal cortisol maximum) and humoral/Th2 prevalence during daytime. Diseases more common / worse during daytime are e.g. stroke, arrhythmias, seizures, sepsis and asthma.
A seasonal pattern of increased immune activity during winter with humoral bias, to counter wintertime stress induced immune suppression, and cellular bias during summer is also postulated.(6,7) Children (and especially foetuses) are more humoral/Th2 biased than adults (8) (and sex differences are minimal before puberty). Adult men generally have a more Th1-biased response, due to high androgen levels, that gets more Th2-biased with age as testosterone levels decrease. Female response is generally more Th2-biased due to the high levels of estrogens that are both pro-inflammatory (a pro-fibrotic response) and “immunosupportive”. Thus the same infectious (or adjuvant) insult may cause a stronger anti-inflammatory response in men.(9)
Estrogens correlate with increased incidence of depression, axiety and auto-immune disorders (women are 2-9 times more likely to suffer from pain disorders, RA and SLE). Female immune response varies with the different phases of the menstrual cycle, pregnancy and contraceptive usage.(10)
Much confusion casued by animals studies arises from the fact that acute and chronic phase response are not distinguished. These differences between acute and chronic phases and phases of the menstrual cycle are seldom considered in general research even if sex differences have been accounted for (which in itself is not done as much as it should).
Nocturia induced sleep disruption and androgen alterations may both lead to immune changes worsening CPPS and explain the sickness behaviour seen in CPPS sufferers. Also the fact that CPPS generally remits during summer (when sun-stimulated vitamin D production shift the immune response towards an anti-inflammatory response), may indicate that CPPS is an immune related disorder. Possibly a disorder of Th1-driven (cellular) inflammatory immunity.
CPPS, prostatit, kroniskt bäckenbottensmärtsyndrom, nokturi, trängningar, enteric, gender immune dimorphism, immunity, Th1/Th2, androgens, estrogens, nocturia, seasonality.
______________________
(1) Steinman L. A rush to judgment on Th17. J Exp Med 205(7): 1517–1522, 2008.
(2) Kidd P. Th1/Th2 balance: The hypothesis, its limitations, and implications for health and disease. Altern Med Rev 8(3):223-246, 2003
(3) Steinman L. A brief history of TH17, the first major revision in the TH1/TH2 hypothesis of T cell–mediated tissue damage. Nature medicine 13(2):139-145, 2007
(4) Perez PF, Dore J, Leclerc M, Levenez F, Benyacoub J, Serrant P, Segira-Roggero I, Schiffrin EJ, Donnet-Hughes A. Bacterial imprinting on the neonatal immune system: lessons from maternal cells? Pediatrics 119(3):E724-732, 2007.
(5) Marchesi J, Shanahan F. The normal intestinal microbiota. Curr Opin Infect Dis 20:508-513, 2007.
(6) Nelson RJ, GE Demas GE, Klein SL, Kriegsfeld LJ. Seasonal Patterns of Stress, Immune Function, and Disease. Cambridge University Press, 2002.
(7) Nelson RJ. Seasonal immune function and sickness responses Trends in Immunology 25(4):187-192, 2004.
(8) Petrovsky N. Towards a unified model of neuroendocrine–immune interaction. Immunol Cell Biol 79:350–357, 2001
(9) Fairweather D, Frisancho-Kiss S, Rose NR. Sex differences in autoimmune disease from a pathological perspective. Am J Pathol 173:600-609, 2008.
(10) Darnall BD, Suarez EC. Sex and gender in psychoneurimmunology research: past, present and future. Brain Behav Immun 23:595-604, 2009.
The immune system is divided in two arms: innate and adaptive. Both of which contain cellular (macrophages, natural killer cells etc) and humoral (antibodies) immune components. Cellular immunity protects mainly against intracellular bacteria, protozoans, fungi and many viruses), while humoral immunity protects against multicellular parasites, extracellular bacteria, certain viruses, ceratin toxins and allergens. A popular concept of immunity is the Th1/Th2/Th17-hypothesis.(1-3) In additon to these two arms, an oft forgotten an very important part of the immune system is the enteric immune system.
Not only does the gut have a massive nervous system (see below), it is also the biggest immune system in the body. The gut-associated lymphoid tissue comprises about 70 percent of the mucosal barrier (most of the rest protects the lungs). And that is not suprising as the gut has to withstand an endless stream of pathogens and occasional toxins. Not only invaders from outside the body but also the about over 100 trillion organisms that live in the gut. The maternal intestinal microbiota (both organisms and a large number of “intestinally derived bacterial components”, N.B. not antibodies, but genetic material) is passed to the newborn trough the breast milk.(4) Ingested probiotics may modulate intestinal pain and the immune system by normalizing cytokine ratios.(5)
The brain and the viscera communicate with each other to coordinate behavior and emotional responses (due to evolutionary reasons like territorial marking, not stop to pee while hunted, panic, anxiety, and so on).and visceral activity. Pathological changes (e.g. bacterial infection, tissue damage, distension of the colon and others) in the viscera affect the forebrain.
Immune activity shows a circadian rhythm with cellular/Th1 prevalence during sleep (maximum activity coincides with nocturnal cortisol maximum) and humoral/Th2 prevalence during daytime. Diseases more common / worse during daytime are e.g. stroke, arrhythmias, seizures, sepsis and asthma.
A seasonal pattern of increased immune activity during winter with humoral bias, to counter wintertime stress induced immune suppression, and cellular bias during summer is also postulated.(6,7) Children (and especially foetuses) are more humoral/Th2 biased than adults (8) (and sex differences are minimal before puberty). Adult men generally have a more Th1-biased response, due to high androgen levels, that gets more Th2-biased with age as testosterone levels decrease. Female response is generally more Th2-biased due to the high levels of estrogens that are both pro-inflammatory (a pro-fibrotic response) and “immunosupportive”. Thus the same infectious (or adjuvant) insult may cause a stronger anti-inflammatory response in men.(9)
Estrogens correlate with increased incidence of depression, axiety and auto-immune disorders (women are 2-9 times more likely to suffer from pain disorders, RA and SLE). Female immune response varies with the different phases of the menstrual cycle, pregnancy and contraceptive usage.(10)
Much confusion casued by animals studies arises from the fact that acute and chronic phase response are not distinguished. These differences between acute and chronic phases and phases of the menstrual cycle are seldom considered in general research even if sex differences have been accounted for (which in itself is not done as much as it should).
Nocturia induced sleep disruption and androgen alterations may both lead to immune changes worsening CPPS and explain the sickness behaviour seen in CPPS sufferers. Also the fact that CPPS generally remits during summer (when sun-stimulated vitamin D production shift the immune response towards an anti-inflammatory response), may indicate that CPPS is an immune related disorder. Possibly a disorder of Th1-driven (cellular) inflammatory immunity.
CPPS, prostatit, kroniskt bäckenbottensmärtsyndrom, nokturi, trängningar, enteric, gender immune dimorphism, immunity, Th1/Th2, androgens, estrogens, nocturia, seasonality.
______________________
(1) Steinman L. A rush to judgment on Th17. J Exp Med 205(7): 1517–1522, 2008.
(2) Kidd P. Th1/Th2 balance: The hypothesis, its limitations, and implications for health and disease. Altern Med Rev 8(3):223-246, 2003
(3) Steinman L. A brief history of TH17, the first major revision in the TH1/TH2 hypothesis of T cell–mediated tissue damage. Nature medicine 13(2):139-145, 2007
(4) Perez PF, Dore J, Leclerc M, Levenez F, Benyacoub J, Serrant P, Segira-Roggero I, Schiffrin EJ, Donnet-Hughes A. Bacterial imprinting on the neonatal immune system: lessons from maternal cells? Pediatrics 119(3):E724-732, 2007.
(5) Marchesi J, Shanahan F. The normal intestinal microbiota. Curr Opin Infect Dis 20:508-513, 2007.
(6) Nelson RJ, GE Demas GE, Klein SL, Kriegsfeld LJ. Seasonal Patterns of Stress, Immune Function, and Disease. Cambridge University Press, 2002.
(7) Nelson RJ. Seasonal immune function and sickness responses Trends in Immunology 25(4):187-192, 2004.
(8) Petrovsky N. Towards a unified model of neuroendocrine–immune interaction. Immunol Cell Biol 79:350–357, 2001
(9) Fairweather D, Frisancho-Kiss S, Rose NR. Sex differences in autoimmune disease from a pathological perspective. Am J Pathol 173:600-609, 2008.
(10) Darnall BD, Suarez EC. Sex and gender in psychoneurimmunology research: past, present and future. Brain Behav Immun 23:595-604, 2009.
Some final words on androgens
As androgens, and especially testosterone, are important for male health they are an interesting field of research. Unfortunately the research is scant on the relation between androgens and CPPS. But it is definitively a good idea to try to minimize androgen disruption by trying to get enough sleep. Especially due to the fact that nocturia disrupts sleep in CPPS. A possible solution could be very small doses of desmopressin, to see if sleep improves leading to improved wellbeing and vigour. It would also be interesting to research thyroid and gonadal-pituitary function.
CPPS, prostatit, kroniskt bäckenbottensmärtsyndrom, nokturi, trängningar, androgens, erection, estrogens, nocturia, testosterone.
CPPS, prostatit, kroniskt bäckenbottensmärtsyndrom, nokturi, trängningar, androgens, erection, estrogens, nocturia, testosterone.
Friday, November 27, 2009
Testosterone and sleep
This is very interesting for CPPS sufferers. As sleep is very important for health and for feeling well. And sleep disturbance is common in CPPS due to the need to void once or twice at night. Which can affect testosterone levels deeply.
Sleep is very important for testosterone levels. This is regardless of when you sleep as long as it is a good undisturbed period of about eight hours.(1) Shorter sleep in old age may be a cause of lower testosterone levels. Bad sleep, especially loss of REM sleep, will depress testosterone levels, but paradoxically high testosterone levels may cause bad sleep too by inducing apnea.(2) A vicious circle!
Individuals with obstructive sleep apnea (OSA) are an extreme example.(3) Sleep disruption will disturb all sleep-controlled endocrine rhythms, not only testosterone. "In conclusion, testosterone increased during sleep and fell during waking, whereas circadian effects seemed marginal. Individual differences were pronounced."(4) "During fragmented sleep, nocturnal testosterone rise was observed only in subjects who showed REM episodes. Our findings indicate that the sleep-related rise in serum testosterone levels is linked with the appearance of first REM sleep. Fragmented sleep disrupted the testosterone rhythm with a considerable attenuation of the nocturnal rise only in subjects who did not show REM sleep."(5)
As nocturia is a common cause of disrupted sleep addressing nocturia in CPPS patients is an important issue. The figure below shows normal sleep (no nightly awakenings) and disrupted sleep (nightly awakenings indicated by blue bars).
The following diagram shows normal nightly testosterone rise (left: A,C) and absence with disrupted rem sleep (right: B, D). Time zero is from onset of melatonin (upper: A,B) and start of sleep (lower: C,D). (Luboshitzky et al, 2001.)
Andra bloggar om CPPS, prostatit, kroniskt bäckenbottensmärtsyndrom, nokturi, trängningar, sömn, testosteron, androgener
___________________
(1) Axelsson J, Ingre M, Åkerstedt T, Holmbäck U. Effects of acutely displaced sleep on testosterone. J Clin Endocrinol Metab 90:4530-4535, 2005.
(2) Saaresranta T, Polo M. Sleep-disordered breathing and hormones. Eur Respir J 22:161-172, 2003.
(3) Luboshitzky R, Aviv A, Hefetz A, Herer P, Shen-Orr Z, Lavie L, Lavie P. Decreased pituitary-gonadal secretion in men with obstructive sleep apnea. J Clin Endocrin Metab 87(7):3394-3398, 2002.
(4) Axelsson J, Ingre M, Åkerstedt T, Holmbäck U. Effects of Acutely Displaced Sleep on Testosterone. J Clin Endocrin Metab 90(8):4530-4535, 2005.
(5) Luboshitzky R, Zabari Z, Shen-Orr Z, Herer P, Lavie P. Disruption of the nocturnal testosterone rhythm by sleep fragmentation in normal men. J Clin Endocrin Metab 86(3):1134-1139, 2001.
Sleep is very important for testosterone levels. This is regardless of when you sleep as long as it is a good undisturbed period of about eight hours.(1) Shorter sleep in old age may be a cause of lower testosterone levels. Bad sleep, especially loss of REM sleep, will depress testosterone levels, but paradoxically high testosterone levels may cause bad sleep too by inducing apnea.(2) A vicious circle!
Individuals with obstructive sleep apnea (OSA) are an extreme example.(3) Sleep disruption will disturb all sleep-controlled endocrine rhythms, not only testosterone. "In conclusion, testosterone increased during sleep and fell during waking, whereas circadian effects seemed marginal. Individual differences were pronounced."(4) "During fragmented sleep, nocturnal testosterone rise was observed only in subjects who showed REM episodes. Our findings indicate that the sleep-related rise in serum testosterone levels is linked with the appearance of first REM sleep. Fragmented sleep disrupted the testosterone rhythm with a considerable attenuation of the nocturnal rise only in subjects who did not show REM sleep."(5)
As nocturia is a common cause of disrupted sleep addressing nocturia in CPPS patients is an important issue. The figure below shows normal sleep (no nightly awakenings) and disrupted sleep (nightly awakenings indicated by blue bars).
The following diagram shows normal nightly testosterone rise (left: A,C) and absence with disrupted rem sleep (right: B, D). Time zero is from onset of melatonin (upper: A,B) and start of sleep (lower: C,D). (Luboshitzky et al, 2001.)
Andra bloggar om CPPS, prostatit, kroniskt bäckenbottensmärtsyndrom, nokturi, trängningar, sömn, testosteron, androgener
___________________
(1) Axelsson J, Ingre M, Åkerstedt T, Holmbäck U. Effects of acutely displaced sleep on testosterone. J Clin Endocrinol Metab 90:4530-4535, 2005.
(2) Saaresranta T, Polo M. Sleep-disordered breathing and hormones. Eur Respir J 22:161-172, 2003.
(3) Luboshitzky R, Aviv A, Hefetz A, Herer P, Shen-Orr Z, Lavie L, Lavie P. Decreased pituitary-gonadal secretion in men with obstructive sleep apnea. J Clin Endocrin Metab 87(7):3394-3398, 2002.
(4) Axelsson J, Ingre M, Åkerstedt T, Holmbäck U. Effects of Acutely Displaced Sleep on Testosterone. J Clin Endocrin Metab 90(8):4530-4535, 2005.
(5) Luboshitzky R, Zabari Z, Shen-Orr Z, Herer P, Lavie P. Disruption of the nocturnal testosterone rhythm by sleep fragmentation in normal men. J Clin Endocrin Metab 86(3):1134-1139, 2001.
Sunday, May 17, 2009
Nocturia and neurological health
Two interesting studies by Asplund and Asplund et al. showed that self-reported poor somatic and mental health, pain, sick leave and visual impairement all increased with increasing nocturnal voids, while quality of life decreased.(1,2) This is very interesting in view of the importance of sleep for immune function (see below) and the possibility of neurological causes. Hypercalciuria has been implicated with nocturia in children and with concomitant hypokalemia also with diabetes insipidus, while in adults hypertension has been associated with nocturia. Sugaya et al. (7) have also shown that patients with nocturia have higher levels of serum catecholamines (adrenaline, noradrenaline and dopamine) which indicates that nocturia is stressful per se, or caused by a disorder of or affecting the adrenal gland. Other causes are: heart disease, sleep apnea, bladder and prostate problems, diabetes mellitus, HPA dysfunction (nocturnal polyuria and diabetes insipidus).
Nocturia is the leading cause of sleep disruption in adults. It is not a sickness of old age but afflicts young adults, 35+, too. "Nocturia patients are sleeping on average only 2-3 hours before waking for the first void." Traditionally nocturia has been indicated if two or more voids per night, but nocturia once a night is almost as disruptive as twice a night. Especially if the void occurs during slow wave sleep (during the first 4 hours of sleep).(3) "This results in disruption of the restorative sleep period with physiological consequences such as mood disturbance, cognitive and memory impairment and reduced performance at work. In addition, it is accountable for increased morbidity and mortality, increased risk of falling, cardiovascular disease, depression and lowered immune response." Sleep disruption also causes lowered testosterone and LH levels. Especially if disruption occurs during REM sleep.(8) It is more bothersome for younger people especially as they have work and families to care for and cannot take a nap or two during the day.(4) (Notice that lack of sleep causes daytime tiredness, mood disturbances, memory impairment, increased falling, accidents, more often sick, decreased life expectancy, depression, diabetes, obesity etc.) Nocturia affects QoL as much or even more as prostate cancer (except terminal cancer) and cardio-vascular disease regardless whether it is one or more nightly voiding.(5)
The preferred treatment for nocturia is desmopressin as it ensure the longest uninterrupted sleep period. Time to first void is on average 4-5 hours. Desmopressin increaes mean initial sleep period with about 100 minutes while indiplon and temazepam only with about 45-50 and 65-70 minutes.(6)
Andra bloggar om CPPS, kroniskt bäckenbottensmärtsyndrom, kronisk abakteriell prostatit, NIHIIIb, nokturi, överaktiv blåsa
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(1) Asplund R, Marnetoft S-U, Selander J, Åkerström B. Nocturia in relation to somatic health, mental health and pain in adult men and women. BJU Int 95:816-819, 2005.
(2) Asplund R. Visual impairment, sleep and nocturia in the elderly. Arch Gerontol Geriatr. 41(1):61-67, 2005.
(3) N Stanley, Sleep, is it a waste of time and is nocturia causing relevant problems?, EUA 2009 Congress
(4) JP Norgaard, Nocturia: a disease or a natural consequence of ageing, EUA 2009 Congress
(5) T Holm-Larsen Why treat nocturia... EUA 2009 Congress
(6) van Kerrebroeck et al Eur Urol 52:221-229, 2007
(7) Sugaya K, Nishijima S, Miyazato M, Ogawa Y. Central nervous control of micturition and urine storage. J Smooth Muscle Res 41(3):117-132, 2005.
(8) In papers by Luboshitzky and Axelsson. Additional detail in post about testosterone.
Nocturia is the leading cause of sleep disruption in adults. It is not a sickness of old age but afflicts young adults, 35+, too. "Nocturia patients are sleeping on average only 2-3 hours before waking for the first void." Traditionally nocturia has been indicated if two or more voids per night, but nocturia once a night is almost as disruptive as twice a night. Especially if the void occurs during slow wave sleep (during the first 4 hours of sleep).(3) "This results in disruption of the restorative sleep period with physiological consequences such as mood disturbance, cognitive and memory impairment and reduced performance at work. In addition, it is accountable for increased morbidity and mortality, increased risk of falling, cardiovascular disease, depression and lowered immune response." Sleep disruption also causes lowered testosterone and LH levels. Especially if disruption occurs during REM sleep.(8) It is more bothersome for younger people especially as they have work and families to care for and cannot take a nap or two during the day.(4) (Notice that lack of sleep causes daytime tiredness, mood disturbances, memory impairment, increased falling, accidents, more often sick, decreased life expectancy, depression, diabetes, obesity etc.) Nocturia affects QoL as much or even more as prostate cancer (except terminal cancer) and cardio-vascular disease regardless whether it is one or more nightly voiding.(5)
The preferred treatment for nocturia is desmopressin as it ensure the longest uninterrupted sleep period. Time to first void is on average 4-5 hours. Desmopressin increaes mean initial sleep period with about 100 minutes while indiplon and temazepam only with about 45-50 and 65-70 minutes.(6)
Andra bloggar om CPPS, kroniskt bäckenbottensmärtsyndrom, kronisk abakteriell prostatit, NIHIIIb, nokturi, överaktiv blåsa
____________________
(1) Asplund R, Marnetoft S-U, Selander J, Åkerström B. Nocturia in relation to somatic health, mental health and pain in adult men and women. BJU Int 95:816-819, 2005.
(2) Asplund R. Visual impairment, sleep and nocturia in the elderly. Arch Gerontol Geriatr. 41(1):61-67, 2005.
(3) N Stanley, Sleep, is it a waste of time and is nocturia causing relevant problems?, EUA 2009 Congress
(4) JP Norgaard, Nocturia: a disease or a natural consequence of ageing, EUA 2009 Congress
(5) T Holm-Larsen Why treat nocturia... EUA 2009 Congress
(6) van Kerrebroeck et al Eur Urol 52:221-229, 2007
(7) Sugaya K, Nishijima S, Miyazato M, Ogawa Y. Central nervous control of micturition and urine storage. J Smooth Muscle Res 41(3):117-132, 2005.
(8) In papers by Luboshitzky and Axelsson. Additional detail in post about testosterone.
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