Nutrition, evolution and thyroid hormone levels – a link to iodine deficiency disorders?

Denne nevner at jod mangel i befolkningen kommer mest av økt behov for jod, ikke pga mangel av jod i kosten. Et høykarbo kosthold krever mer jod enn et lavkarbokosthold. Derfor ser man jod-mangel problemer i befolkningen.

http://www.ncbi.nlm.nih.gov/pubmed/15142639

The higher iodine requirement exceeds the availability of iodine from environmental sources in many regions of the world, resulting in the development of IDD.

 

Physiopathology of intratendinous calcific deposition

Kalsium ansamlinger i sener eller andre strukturer i bevegelsesapparatet kan bidra til smertetilstander. Denne studien går igjennom hvordan disse oppstår slik at vi kan få en bedre forståelse av hva vi kan gjøre med det. Store ansamlinger kan sees på røntgen, men man kan også ha mikroskopiske ansamlinger som bidrar til plager uten å være synling på røntgen.

Det er spesielt vanlig blant de med diabetes (30%) og assosieres ofte med tyroidea problemer eller andre hormonproblemer. Genetisk predisposisjon er også en viktig faktor.

Ofte starter det med en skade, hvor det så skjer en kursendring i helbredelsesprosessen som gjør at kalsiumavleiringer eller andre problemer fremtrer og bidrar til smerteproblematikk.

http://www.biomedcentral.com/1741-7015/10/95

In calcific tendinopathy (CT) calcium deposits in the substance of the tendon. CT is particularly common in the rotator cuff tendons (RCTs) and supraspinatus tendon, and Achilles tendon and patellar tendon. CT of the rotator cuff is common in Caucasian populations, with a reported prevalence of 2.7% to 22%, mostly affecting women between 30 and 50 years. The most frequently involved tendon is the supraspinatus tendon, and in 10% of patients the condition is bilateral (Figure 1[1].

(kalsiumansamlinger vises ytterst og øverst på humerus)

(kalsiumansamling vises i ackillesenen)

Clinical manifestations of the calcific process within the tendons include chronic activity-related pain, tenderness, localized edema and various degrees of decreased range of motion (ROM). CT of the rotator cuff shows a tendency toward spontaneous resorption of the deposits and symptoms often resolve spontaneously, although some authors described persistent pain at long time follow-up and persistent reduction of ROM [5,6].

Microscopic calcifications which are not detectable at plain radiography can also occur in chronic tendinopathy. A histological study showed high incidence of small calcium deposits in tendinopathic supraspinatus tendons [8]. Microscopic calcium deposits are frequent also in diabetic patients [9].

Specimens of RCTs obtained during surgery consist of a gritty mass of sandy material or a toothpaste-like fluid, and the deposits were described as a white amorphous mass composed of many small round or ovoid bodies. Later, X-ray diffraction and infrared spectrometry and other techniques identified the material of calcific deposits as calcium carbonate apatite [1820].

Uhthoff and coworkers hypothesized that a favorable environment permits an active process of cell-mediated calcification, usually followed by spontaneous phagocytic resorption [28]. They describe four stages in the calcifying process of the rotator cuff: precalcific phase, calcific phase, resorptive phase, and repair phase. All phases may occur concomitantly in the same tendon.

Finally, bone is deposited and the spur is formed. No inflammatory cells or microtears were identified. The authors believe that the increased surface at the tendon-bone junction may represent an adaptive mechanism to increased mechanical loads.

An association between CT and diabetes and thyroid disorders has been shown, but the precise mechanism is still unknown [1]. Patients with associated endocrine disorders present earlier onset of symptoms, longer natural history, and they undergo surgery more frequently compared to a control population [61,62]. More than 30% of patients with insulin-dependent diabetes have tendon calcification [63]. The exposure of proteins to high levels of sugar moieties cause the glycosylation of several extra-cellular matrix proteins, which can modify the extracellular matrix by cross-linking proteins.

When a cause cannot be found

Artikkel som nevner mye av problemen rundt behandling av f.eks. ikke-spesifikke ryggplager, IBS eller firbomyalgi. Dette er plager det ikke er noe tydelig årsak-virkning forhold, som ikke kan forklares med et molekyl eller anatomisk utgangspunkt som er felles for alle som har disse plagene, og hvor det ikke er noe klart skille mellom kropp og sinn.

https://raniblogsaboutcausation.wordpress.com/2014/08/14/when-a-cause-cannot-be-found/

This is not a small problem in medicine. By some estimates, such unexplained conditions amount to 30 percent of all symptoms reported to doctors, and they are linked to a 20-50% increase in outpatient costs and a 30% increase in hospitalisation.

This is, basically, what evidence based medicine means: statistical evidence from population studies are applied directly to a patient. This means that each patient is treated as a statistical average, not as a unique individual.

Rather than being dismissed as marginal, therefore, these unexplained conditions should be taken as exemplary for understanding health and disease in general.

A CLASSIFICATION-BASED COGNITIVE FUNCTIONAL APPROACH FOR THE MANAGEMENT OF BACK PAIN

Denne beskriver et ganske så komplett opplegg for behandling og undervisning av klienter med nesten alle typer muskel og leddplager.

Click to access OSullivanIFOMPT-Oct2012.pdf

Pathoanatomical factors: F.eks. funn på røntgen og MRI, som spiller liten rolle i kroniske muskel og leddplager.

Physical factors: muskelspenning og bevegelsesmønster endres ved smertetilstander. F.eks. kjermuskulatur spenner seg mer i bevegelser hos smertepasienter.

Lifestyle factors: interessant at mat og kosthold er det eneste av livsstilsfaktorer som ikke nevnes på denne listen. Ellers er trening, stress, søvn, røyk, overvekt, m.m. med.

Cognitive and psychosocial factors: angst, depresjon, frykt, katastrofering, og særlig ideen om at (f.eks.) ryggen må beskyttes pga smertene.

Social factors: trivsel i jobb, familie, forhold, og livssituasjon.

Neurophysiological factors: endringer i hjernen, som f.eks. mindre går materie, økt hjerneaktivitet i hvile, endres kroppsbilde, mindre nedregulering av smerte.

Individual factors: mål med behandling, forventninger, grunnleggende helsekunnskap, m.m.

Genetic factors: Visse gener gir økt disponering for smertetilstander.

Jeg likte spesielt dette sitatet:

Manual therapy is only used as a window of opportunity to change behaviors where movement impairments are present.

FORMIs Gule Flagg liste

Mange behandlere overser med vilje kostholdets forhold til smertetilstander. Av en eller annen grunn opplever de at mat spiller en svært lite rolle. Men dette er et blindfelt i deres persepsjonsevne som gjør at de ikke forholder seg til realitetene og snyter pasientene for mulig symptombedring.

Selv i de Nasjonale retningslinjene for korsryggsmerter sin liste over Gule Flagg (faktorer som bidrar til kroniske smertetilstander) står «problemer med mage» oppført. Dette i seg selv burde være nok til at ALLE behandlere som er i kontakt med smertepasienter setter seg inn i kostholdets betydning.

Gule flagg

Risikofaktorer (hovedsakelig psykososiale) for å utvikle mer langvarige ryggplager

• Arbeidsrelaterte problemer/sykmelding (bør tidsbegrenses)

• Emosjonelle problemer (f.eks depresjon og angst)

• Tilleggsymptomer i form av generaliserte smerter, hodepine, tretthet, svimmelhet og plager fra magen

• Pasienter med omfattende tidligere ryggplager og med nerverotaffeksjon

• Pessimistiske/negative holdninger/overbevisninger i forhold til smertene, f.eks uttalt engstelse for visse bevegelser og for å være i arbeid, og liten grad av forventning om å bli bra/komme tilbake i arbeid

Click to access Kortversjon.pdf

Fructose Administration Increases Intraoperative Core Temperature by Augmenting Both Metabolic Rate and the Vasoconstriction Threshold

Mer om hvordan fruktose øker kroppvarme (termogenese). I denne er det snakk om å bruke det intravenøst for å unngå at pasienter blir kalde etter operasjoner. Det øker restitusjonsevnen etter operasjonen.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1473168/

Abstract

Background

We tested the hypothesis that intravenous fructose ameliorates intraoperative hypothermia both by increasing metabolic rate and the vasoconstriction threshold (triggering core temperature)

Methods

40 patients scheduled for open abdominal surgery were divided into two equal groups and randomly assigned to intravenous fructose infusion (0.5 g·kg−1·h−1 for 4 h, starting 3 h before induction of anesthesia and continuing for 4 hours) or an equal volume of saline. Each treatment group was subdivided: esophageal core temperature, thermoregulatory vasoconstriction, and plasma concentrations were determined in half, and oxygen consumption was determined in the remainder. Patients were monitored for 3 h after induction of anesthesia.

Results

Patient characteristics, anesthetic management, and circulatory data were similar in the four groups. Mean final core temperature (3 h after induction of anesthesia) was 35.7±0.4°C (mean ± SD) in the fructose group and 35.1±0.4°C in the saline group (P=0.001). The vasoconstriction threshold was greater in the fructose (36.2±0.3°C) than in the saline group (35.6±0.3°C; P<0.001). Oxygen consumption immediately before anesthesia induction in the fructose group (214±18 ml/min) was significantly greater than in the saline group (181±8 ml/min, P<0.001). Oxygen consumption was 4.0 L greater in the fructose patients during 3 hours of anesthesia; the predicted difference in mean-body temperature based only on the difference in metabolic rates was thus only 0.4°C. Epinephrine, norepinephrine, and angiotensin II concentrations, and plasma renin activity were similar in each treatment group.

Conclusions

Preoperative fructose infusion helped maintain normothermia by augmenting both metabolic heat production and increasing the vasoconstriction threshold.

Fructose is known to provoke the greatest thermogenesis among various carbohydrates.19,20 Fructose also provokes dietary-induced thermogenesis in awake healthy volunteers, and does so far better than glucose.15 We thus tested the hypothesis that intravenous fructose increases metabolic heat production in anesthetized humans. We also tested the hypothesis that fructose, like amino acids, increases the vasoconstriction threshold and thus has a thermoregulatory as well as metabolic contribution to maintaining perioperative normothermia.

CO2 production before infusion showed no significant difference between saline group (147+19 ml min−1) and fructose group (142+16 ml min−1) but increased significantly in the fructose group (201+26 ml min−1) just before induction of anesthesia, compared with the saline group (146+19 ml min−1)(p<0.001). This increased level was maintained for 135 min after induction of anesthesia.

Matoverfølsomhet – et paradigmeskifte

Artikkel skrevet i 2011 som nevner mange viktige poenger. Blandt annet at vagus svekkes ved IBS og at det gir andre plager, spesielt hudplager.

Click to access matoverfoelsomhet_aip_1_2011w_v2.pdf

Dessuten hadde mange pasienter ekstra-intesti- nale symptomer og skåret høyt på «Subjective Health Complaints» (1). Påfallende mange anga at de hadde kronisk tretthet samt leddsmerter med morgenstivhet uten påvisbar artritt. Livskvaliteten var til dels be- tydelig redusert (2).

Over 50% av pasientene tilfreds- stilte kravene til en psykiatrisk diag- nose. Men hvor mye av de psykologiske problemene kan være sekundære? Inntil for knapt 20 år siden ble også magesårsykdommen regnet som en psykosomatisk sykdom. De psykolo- giske problemene vi så hos ulcuspasi- entene var ganske like de vi nå finner hos de matoverfølsomme, og vi har enda friskt i minnet hvordan alle pro- blemene hos ulcuspasientene, in- kludert de psykologiske, «blåste bort» etter fjerning av magesårbakterien Helicobacter pylori (4).

Kun sykdomspesifikk angst eller for- ventninger om plager var signifikante uavhengige prediktorer. Disse pre- diktorene forklarte dog til sammen ikke mer enn 10% av variansen i mageplagene, og alder var eneste signifikante prediktor av ekstra- intestinale plager. Det vil si at 90% av variansen i grad av somatiske plager ikke kunne forklares av psyko- logiske faktorer. Vi tror derfor nå at mange av de psykologiske problemene ved matoverfølsomhet er sekundære og at betydningen av psykologiske faktorer som årsak til matoverfølsomhet kan være betydelig overdrevet.

Vi kunne vise at et tungt fordøyelig, men fermenter- bart karbohydrat, som laktulose, ofte reproduserte pasientens plager (6). tester på klassisk IgE-sensitivisering mot spesifikke kostproteiner, deri- mot, var sjeldent positive. Det virker som om mageplagene først og fremst trigges av tungt fordøyelige karbo- hydrater og ikke spesielt av proteiner i kosten. Dessuten, at plagene kunne reproduseres av mat, viser at pasien- ten har rett – plagene kan skyldes maten! Det passer med at pasientene ikke har plager om natta, når de faster, etter tarm- skylling eller når de får tømt seg fullstendig.

Over 60% av pasientene hadde indikasjon på atopisk sykdom (Dette er hud- og slimhinnerelaterte sykdommer som allergi, tørr hud, kløe, m.m.)

Histamin øker sympatisk og redusert para- sympatisk (vagal) tonus, som også er karakteristisk for pasienter med funksjonelle mageplager (16, 17). Slik endret autonom aktivitet kan være et resultat av IgE-mediert histaminfrigjøring fra lokalt sensibili- serte mastceller (18).

Systemiske symptomer som kro- nisk tretthet og leddsmerter hos pasi- enter med IBS har tidligere ofte blitt forklart som somatisering av psykolo- giske problemer, men det finnes andre muligheter. For eksempel er det nylig rapportert at symptomer ved kronisk tretthetssyndrom kan behandles med en B-celle-antagonist (rituximab) (21). I likhet med de matoverfølsomme, har pasienter med kronisk tretthets- syndrom ofte IBS og endret mikro- flora som kan være av betydning for immunaktiveringen hos disse pasi- entene (22). Hos matoverfølsomme med IBS har vi nylig påvist økt nivå av B-celle aktiverende faktor (BAFF) i blod og tarmskyllevæske (23). BAFF er relatert til autoimmunitet og lokal immunaktivering i tarmen («lokal allergi») (24).

At karbohydrater kan reprodusere mageplagene hos pasienter med IBS og matoverfølsomhet, er verdt å merke seg, og mye tyder på at dette allerede nå bør få terapeutiske konsekvenser (27). Vi ser med andre ord for oss et paradigmeskifte når det gjelder utredning og behandling av pasienter med IBS og matoverfølsomhet.

Central sensitisation in visceral pain disorders

Nevner hvordan IBS skaper sentralsensitering og hyperalgesia andre steder enn bare tarmen, og bidrar til mange muskel- og ledd problemer. Nevner at dette spesielt skjer i korsryggen hvor sensoriske nerver fra tarmen treffer samme nerve i ryggmargen som de sensoriske nervene fra beina.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1856337/

The concept of visceral hyperalgesia has been examined in a variety of functional gastrointestinal disorders (FGIDs), including oesophagitis, gastro‐oesophageal reflux disease, non‐ulcer dyspepsia, gastroparesis, and irritable bowel syndrome (IBS). Visceral hypersensitivity has also been demonstrated in non‐gastrointestinal disorders such as interstitial cystitis and ureteric colic.1 Although the pathophysiological mechanisms of pain and hypersensitivity in these disorders are still not well understood, exciting new developments in research have been made in the study of the brain‐gut interactions involved in the FGIDs.

In this issue of Gut, Sarkar and colleagues2 address the phenomenon of temporal summation of pain, termed “wind‐up”, and its relationship to central sensitisation and secondary visceral pain hyperalgesia caused by acidification of the oesophagus (see page 920). Also in this issue of Gut, Drewes and colleagues3 examine peripheral and central sensitisation using both mechanical and thermal stimuli in patients with oesophagitis compared with control subjects (see page 926). They found that in patients with oesophagitis, the interaction between central and peripheral nociceptive input may help explain patient symptoms. Understanding the implications of these two studies requires examining the concept of central sensitisation in visceral pain disorders. Both of these studies have important clinical and research ramifications for the study of FGIDs.

“Hypersensitivity in IBS patients is not just limited to the gut and more widespread alterations in central pain processing may be involved in this chronic pain disorder”

The most pronounced hyperalgesia appears to occur at the lumbosacral level at which colon and lower extremity nociceptive afferents are likely to converge onto common spinal segments, explaining why patients had higher thermal hypersensitivity in the foot than in the hand (see fig 11).14,15,19

High Energy Diets-Induced Metabolic and Prediabetic Painful Polyneuropathy in Rats

Nevner hvordan høy-fett høy-karbo forværrer nevropati (ødelagte nerver), men høy-fett høy-karbo høy-salt ser ut til å dempe smertene noe.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3581455/

Conclusions

In the current study, early metabolic syndrome (hyperinsulinemia, dyslipidemia, and hypertension) and prediabetic conditions (IFG) could be induced by high energy (high-fat and high-sucrose) diets in rats which later developed painful polyneuropathy that was characterized by myelin breakdown and LMF loss in both peripheral and central branches of primary afferent neurons. However, SMF and UMF were far less damaged in the same rats. The phenomenon that the high energy diets only induce mechanical, but not thermal, pain hypersensitivity may reflect a selective damage to LMF, but not to the SMF and UMF. Moreover, dietary sodium (high-salt) deteriorates the neuropathic pathological process induced by high energy diets further, but paradoxically high salt consumption may improve, at least temporarily, chronic pain perception in these animals.

We have therefore established a strong link between high-energy/high-salt diet induced metabolic syndrome and prediabetes which results in relatively selective LMF damage in both the PNS and CNS that in turn can result in neuropathic pain. These results have a profound impact on patient welfare relative to diet choice, not just for T2DM onset, but also for its associated neuropathic symptoms.

Inflammatory Cytokine Concentrations Are Acutely Increased by Hyperglycemia in Humans

Denne viser hvordan selv de uten diabetes får økt cytokinverdi (betennelse) i blodet i 1-2 timer etter blodsukkerstigning. I denne studien var det snakk om blodsukker over 15 mmol/L. De sier at blodsukker økninger påvirker cytokinnivået mer enn et stabilt høyt blodsukker.

http://circ.ahajournals.org/content/106/16/2067.full

Control Subjects:

Plasma IL-6 levels rose from a basal value of 2.0±0.7 pg/mL to a peak of 3.1±0.9 pg/mL at 1 hour (P<0.01) and returned to basal level at 3 hours (Figure 2).

Fasting plasma TNF-α levels were 3.3±1.2 pg/mL; they peaked at 1 hour (4.9±1.4 pg/mL, P<0.01), and returned to baseline at 3 hours.

Plasma IL-18 levels rose from a basal value of 116±28 pg/mL to a peak of 140±31 pg/mL at 2 hours (P<0.01) and returned to basal levels at 3 hours (110±26 pg/mL).

The novel findings of the present study were that (1) acute hyperglycemia in control and in IGT subjects induces an increase in plasma IL-6, TNF-α, and IL-18 concentrations; (2) the effect of sustained hyperglycemia is reproduced by transient oscillations in plasma glucose and is amplified by the IGT status; and (3) the antioxidant glutathione completely prevents the rise in plasma cytokines induced by hyperglycemia. These results indicate that hyperglycemic spikes affect cytokine concentrations more than continuous hyperglycemia, at least in the short term, and suggest that an oxidative mechanism mediates the effect of hyperglycemia.

Another finding of the present study was that glutathione, a powerful antioxidant, completely prevented cytokine increase induced by oscillatory hyperglycemia in healthy humans. Hyperglycemia-induced oxidative stress, 32 along with soluble advanced glycation end products and products of lipid peroxidation, possibly serves as a key activator of upstream kinases, leading to induction of inflammatory gene expression.33