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God väg till hälsa

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Ohälsa & Sjukdomar

Dans minskar psykisk ohälsa

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Örebroforskaren Anna Duberg prisades nyligen för sitt arbete med att förebygga psykisk ohälsa bland unga tjejer med hjälp av kravlös dans. Det handlar om att koppla på kroppsbaserad behandling som komplement till medicinering och samtal.

Priset, Guldskalpellen, delades nyligen ut av den medicinska tidsskriften Dagens medicin.

Anna Duberg är fysioterapeut och började forska vid Örebro universitet på dansens hälsoeffekter 2009. Och metoden ”dans för hälsa” som framförallt används inom elevhälsan har spridits till flera kommuner i landet och Anna Duberg utbildar ständigt nya instruktörer.

I Örebro heter verksamheten ”Bara dansa” och vänder sig till tjejer i högstadiet och gymnasiet som har olika typer av symptom på psykisk ohälsa. En av dem som fått hjälp är 19-åriga Jenny Scott. Hon mådde psykiskt dåligt en stor del av sin skoltid. Det handlade om mycket nedstämdhet, oro, allmän osäkerhet och social fobi. För Jenny började livet igen tack vare dansen. Därifrån orkade hon söka mer hjälp från psykiatrin. Idag har hon arbete inom förskolan och hon dansar tre gånger i veckan på en vanlig dansskola – med de krav som följer.

I de här dansgrupperna handlar det om ”kom som du är, du behöver inte prestera eller känna att du ska vara på topp innan du kliver in”. Här dansar man utifrån de förutsättningar som finns och jobbar med det friska. Och en av de saker som är bra med dans är att man kan öva på olika känslor, till exempel känna hur det känns att vara arg eller glad.

Dans för hälsa:
Grundförutsättningen för dansgrupperna är att krav på prestation är bortplockat. Dansgrupperna har olika namn i olika kommuner. Det vänder sig till unga tjejer med:

– oro

– stress

– höga krav på sig själv

– ont i magen

– trötthet

– nedstämdhet

– huvudvärk

Skolsköterskan eller kuratorn på skolan kan ge mer inormation. Det är gratis att delta.

Missa inte att vi pratat om detta mer utförligt i podcasten med Yogadoktorn https://4health.se/191-yogadoktorn-lakaren-yoga-som-medicin

https://www.svt.se/nyheter/lokalt/orebro/dans-raddningen-for-jenny

Vanliga besprutningsmedel ökar risk för ADHD

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En ny studie visar en koppling mellan exponering för besprutningsmedel och ADHD. När mammor utsätts för besprutningsmedel under graviditeten, och har högre nivåer av vanliga besprutningsmedel i urin, ökar sannolikheten att barnen har ADHD eller ADHD-symtom vid två till fyra års ålder.

Ur studien:

“Maternal urinary concentrations of pyrethroid and chlorpyrifos metabolites and attention deficit hyperactivity disorder (ADHD) symptoms in 2-4-year-old children from the Odense Child Cohort.”

“BACKGROUND: Pyrethroids and chlorpyrifos are widely used insecticides, but the potential impact of prenatal exposure on child neurodevelopment has only been addressed in few longitudinal studies.

OBJECTIVES: To investigate associations between prenatal exposure to pyrethroids and chlorpyrifos and traits of ADHD in 2-4-year-old children.

METHODS: Metabolites of chlorpyrifos and pyrethroids were measured in maternal urine collected at gestational week 28 among 1207 women from the Odense Child Cohort. Of these, 948 completed the Child Behavior Check List for ages 1.5-5 years (CBCL: 1½-5). Negative binomial and logistic regression models were used to estimate relative differences in ADHD problem scores (CBCL: 1½-5 subscale) expressed as the ratio of expected scores between exposure groups and the odds (OR) of scoring equal to or above the 90th percentile in relation to maternal urinary metabolite concentrations (continuous ln2-transformed or categorized into tertiles). The analyses were adjusted for maternal education level, parental psychiatric diagnosis, child age and sex.

RESULTS: The chlorpyrifos metabolite, 3,5,6-trichloro-2-pyridinol (TCPY), the generic pyrethroid metabolite, 3-phenoxybenzoic acid (3-PBA), and the metabolite of trans-isomers of permethrin, cypermethrin, and cyfluthrin, trans-3-(2,2-dichlorovinyl)-2,2-dimethylcyclopropane-1-carboxylic acid (trans-DCCA), were detected in 90%, 94%, and 11%, respectively, of the urine samples. Each doubling in maternel 3-PBA concentration was associated with a 3% increase in the ADHD score (Ratio: 1.03 (95% CI: 1.00,1.07)) and a 13% higher odds of having a ADHD score ≥ the 90th percentile (OR: 1.13 (1.04,1.38)). Similar associations were seen for 3-PBA as categorical variable (p-trend=0.052 in negative binimoal regression, p-trend=0.007 in logistic regression). Furthermore, concurrent concentrations of 3-PBA and TCPY above their medians were associated with higher ADHD score (Ratio: 1.20 (1.04, 1.38)) and higher odds of scoring ≥ the 90th percentile (OR: 1.98 (1.26, 3.11)). Maternal trans-DCCA above the detection level increased the odds of ADHD symptoms (OR: 1.76 (1.08, 2.86)). The associations were not modified by sex.

CONCLUSIONS: Prenatal exposure to pyrethroids was associated with ADHD related traits at 2-4 years of age. Considering the widespread use of pyrethroids these results are of concern.”

https://www.ncbi.nlm.nih.gov/m/pubmed/31229776/

Våra tarmbakterier är en anledning till att vi reagerar så olika på läkemedel

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Bakterier i tarmen bryter ner det läkemedel som ges mot Parkinsons sjukdom. Detta är en förklaring till att läkemedel mot Parkinsons fungerar olika bra för olika personer, och varierande även för en och samma person över dagen.

Detta skulle också kunna vara en av förklaringarna till variationen i hur olika personer påverkas av olika läkemedel. En annan förklaring till dessa skillnader har att göra med vår genetik och hur effektiva vi är i att bryta ner olika substanser/läkemedel.

Personer med Parkinson har för lite av signalsubstansen dopamin i hjärnan, som bl.a. behövs för att kunna styra rörelser. De får ofta läkemedel som innehåller L-dopa. L-dopa är ett förstadium till dopamin. L-dopa kan ta sig förbi blodhjärnbarriären och inne i hjärnan omvandlas det till dopamin.

Men L-dopa fungerar som sagt olika bra för olika personer, och varierande även för en och samma person över dagen. Amerikanska forskare har visat att det kan bero på att redan i tunntarmen bryts L-dopa ned av bakterier, innan det hunnit ut i blodet och upp till hjärnan.

Den här nedbrytningen trodde man bara försegår i blodbanan. I blodet har L-dopa i läkemedlet skyddats av särskilda hämmare mot nedbrytning, så kallade dekarboxylashämmare. Men nu ser man alltså att vi har bakterier som kan göra samma sak.  De amerikanska forskarna har också hittat ett sätta att skydda L-dopa i tarmen, med en annan slags dekarboxylashämmare.

Ur studien:

“The efficacy of L-dopa treatment for Parkinson’s disease is hugely variable between individuals, depending on the composition of their microbiota. L-Dopa is decarboxylated into active dopamine, but if the gut microbiota metabolize L-dopa before it crosses the blood-brain barrier, medication is ineffective. Maini Rekdal et al. found that different species of bacterium are involved in L-dopa metabolism (see the Perspective by O’Neill). Tyrosine decarboxylase (TDC) from Enterococcus faecalis and dopamine dehydroxylase (Dadh) from Eggerthella lenta A2 sequentially metabolized L-dopa into m-tyramine. The microbial L-dopa decarboxylase can be inactivated by (S)-α-fluoromethyltyrosine (AFMT), which indicates possibilities for developing combinations of Parkinson’s drugs to circumvent microbial inactivation.”

“The human gut microbiota metabolizes the Parkinson’s disease medication Levodopa (L-dopa), potentially reducing drug availability and causing side effects. However, the organisms, genes, and enzymes responsible for this activity in patients and their susceptibility to inhibition by host-targeted drugs are unknown. Here, we describe an interspecies pathway for gut bacterial L-dopa metabolism. Conversion of L-dopa to dopamine by a pyridoxal phosphate-dependent tyrosine decarboxylase from Enterococcus faecalis is followed by transformation of dopamine to m-tyramine by a molybdenum-dependent dehydroxylase from Eggerthella lenta. These enzymes predict drug metabolism in complex human gut microbiotas. Although a drug that targets host aromatic amino acid decarboxylase does not prevent gut microbial L-dopa decarboxylation, we identified a compound that inhibits this activity in Parkinson’s patient microbiotas and increases L-dopa bioavailability in mice.”

“We have characterized an interspecies pathway for gut bacterial L-dopa metabolism and demonstrated its relevance in human gut microbiotas. Variations in these microbial activities could possibly contribute to the heterogeneous responses to L-dopa observed among patients, including decreased efficacy and harmful side effects. Our findings will enable efforts to elucidate the gut microbiota’s contribution to treatment outcomes and highlight the promise of developing therapies that target both host and gut microbial drug metabolism.”

https://science.sciencemag.org/content/364/6445/eaau6323

https://sverigesradio.se/sida/artikel.aspx?programid=406&artikel=7242119

Studie: Läkemedel mot sura uppstötningar – ökad risk för död

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En nyligen genomförd kohortstudie som publicerades i British Medical Journal har väckt alarmerande insikter gällande biverkningarna av läkemedel mot sura uppstötningar, så kallade PPI, läkemedel som klassas som protonpumpshämmare.

Denna långsiktiga observationsstudie genomfördes under en tioårsperiod med amerikanska veteraner. Den fördjupade studien använde omfattande data från databaserna. Forskarna använde också National Death Index-data för att analysera dödlighet och dödsorsak.

Resultaten visar tydligt att långsiktig användning av syradämpande läkemedel (PPI) har negativa hälsoeffekter. Biverkningar inkluderar ökad risk för dödlighet, kardiovaskulär sjukdom, kronisk njursjukdom och viss sorts cancer.

Bara i USA använder 15 miljoner människor läkemedel klassade som Proton Pump Inhibitors (PPI).

“Abstract
Objective To estimate all cause mortality and cause specific mortality among patients taking proton pump inhibitors (PPIs).

Design Longitudinal observational cohort study.

Setting US Department of Veterans Affairs.

Participants New users of PPIs (n=157 625) or H2 blockers (n=56 842).

Main outcome measures All cause mortality and cause specific mortality associated with taking PPIs (values reported as number of attributable deaths per 1000 patients taking PPIs).

Results There were 45.20 excess deaths (95% confidence interval 28.20 to 61.40) per 1000 patients taking PPIs. Circulatory system diseases (number of attributable deaths per 1000 patients taking PPIs 17.47, 95% confidence interval 5.47 to 28.80), neoplasms (12.94, 1.24 to 24.28), infectious and parasitic diseases (4.20, 1.57 to 7.02), and genitourinary system diseases (6.25, 3.22 to 9.24) were associated with taking PPIs. There was a graded relation between cumulative duration of PPI exposure and the risk of all cause mortality and death due to circulatory system diseases, neoplasms, and genitourinary system diseases. Analyses of subcauses of death suggested that taking PPIs was associated with an excess mortality due to cardiovascular disease (15.48, 5.02 to 25.19) and chronic kidney disease (4.19, 1.56 to 6.58). Among patients without documented indication for acid suppression drugs (n=116 377), taking PPIs was associated with an excess mortality due to cardiovascular disease (22.91, 11.89 to 33.57), chronic kidney disease (4.74, 1.53 to 8.05), and upper gastrointestinal cancer (3.12, 0.91 to 5.44). Formal interaction analyses suggested that the risk of death due to these subcauses was not modified by a history of cardiovascular disease, chronic kidney disease, or upper gastrointestinal cancer. Taking PPIs was not associated with an excess burden of transportation related mortality and death due to peptic ulcer disease (as negative outcome controls).

Conclusions Taking PPIs is associated with a small excess of cause specific mortality including death due to cardiovascular disease, chronic kidney disease, and upper gastrointestinal cancer. The burden was also observed in patients without an indication for PPI use. Heightened vigilance in the use of PPI may be warranted.“

Ketogen kost som behandling och förebyggande strategi för Alzheimers

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  • Försämrad glukosmetabolism i hjärnan, amyloida plack och celldöd är saker associerade med sjukdomspatologin i Alzheimers.
  • Ketoner är en alternativ metabol väg till glukos i hjärnan.
  • Ketogen kost reducerar sannolikt amyloidplack och kan minska deras neurotoxicitet.
  • Modern kost med högt innehåll av kolhydrater kan bidra till Alzheimers.
  • Den ketogena kosten (inklusive kolhydratrestriktion) kan vara användbar vid hanteringen av Alzheimers sjukdom.

Har skrivit och pratat om ketoner och dess effekt i Alzheimers sjukdom en hel del. Lyssna bl.a. på avsnitt 33  https://4health.se/33-forebygga-bromsa-och-reversera-alzheimers-demenssjukdomar samt avsnitt 12, och sök här på sidan eller använd taggen demens https://4health.se/tag/demens

Se även länken till en längre artikel i Health Impact News nedan

“The prevalence of Alzheimer’s disease, a chronic neurodegenerative condition, is increasing as is the need for effective treatments and preventions. The underlying pathology of Alzheimer’s is not yet fully understood, so existing research has focused on understanding the prominent features of the disease. These include amyloid plaques, which accumulate in the brains of those with Alzheimer’s disease; impaired glucose metabolism; and neuronal cell death. Emerging evidence suggests that a low-carbohydrate, high-fat ketogenic diet may help to mitigate the damage associated with these pathologies. The ketogenic diet could alleviate the effects of impaired glucose metabolism by providing ketones as a supplementary energy source. In addition, this diet may help to reduce the accumulation of amyloid plaques while reversing amyloid β toxicity. Research has begun to identify early underlying mechanisms in Alzheimer’s disease that could be targeted by new prevention strategies. Glycation of the ApoE protein leads to impaired transportation of important lipids, including cholesterol, to the brain, resulting in lipid deficiencies that could explain progression to the later pathologies of the disease. In this review, we hypothesize that the ketogenic diet could be an effective treatment and prevention for Alzheimer’s disease, but both ketone production and carbohydrate restriction may be needed to achieve this.”

https://www.sciencedirect.com/science/article/pii/S0899900718302764

http://healthimpactnews.com/2019/research-shows-high-fat-low-carb-diet-with-coconut-oil-can-prevent-or-cure-alzheimers/

Studie: Magnesium mot migrän, oro och depression

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Apropå ett av de populäraste och nyaste podcastavsnitten där vi pratar om hur nödvändigt magnesium är i nästan alla kroppens funktioner. https://4health.se/218-morley-robbins-magnesium-mineralerna-i-din-kropp-1 Det finns studier, som tex nedan studie, som visar god hjälp av magnesium vid bl.a. migrän. I den här studien gav det även effekt mot nedstämdhet, oro mm

“Magnesium is frequently used for pediatric migraine prophylaxis. The aim of this study was to evaluate to which extent the disability levels, quality of life (QOL), and anxiety and depressive symptoms change after 6-month magnesium prophylaxis in pediatric migraine. This is a follow-up study of 34 children aged 7-17 years with migraine treated with oral magnesium. Disability due to migraine was assessed by the Pediatric Migraine Disability Assessment tool (PedMIDAS), QOL was assessed by the KIDSCREEN-27, and anxiety and depressive symptoms were assessed by the Revised Child Anxiety and Depression Scale (RCADS). PedMIDAS scores significantly decreased from baseline to end-point (F(df, dferror) = 11.10 (1.63, 50.49), p<0.001), as well as anxiety (F(df, dferror) = 8.95 (1.64, 50.67), p = 0.001) and depressive symptoms (F(df, dferror) = 8.91 (1.59, 49.29), p = 0.001). Considering the KIDSCREEN-27, scores for physical and psychological well-being and social support domain significantly increased from baseline to end-point (p≤0.01). After 6 months of magnesium prophylaxis, disability due to migraine significantly decreased, whereas physical and psychosocial well-being improved. Children also reported fewer anxiety and depressive symptoms. More follow-up and randomized controlled clinical trials are needed to propose clinical recommendations for magnesium prophylaxis in pediatric migraine.”

https://www.ncbi.nlm.nih.gov/pubmed/29637898

Studie: CoQ10 mot hjärtsjukdom

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Man har analyserat vidare data från den internationella studien Q-Symbio som först publicerades 2014 med goda resultat. Efter att forskarna nu specifikt studerat data från de europeiska studiedeltagarna, är resultaten än mer tydliga. Deltagare som tagit Q10 har en signifikant fördel.

Ur studien:

“Geographical differences in patient characteristics, management and outcomes in heart failure (HF) trials are well recognized. The aim of this study was to assess the consistency of the treat- ment effect of coenzyme Q10 (CoQ10) in the European sub-population of Q-SYMBIO, a randomized double-blind multinational trial of treatment with CoQ10, in addition to standard therapy in chronic HF.”

“Patients with moderate to severe HF were randomized to CoQ10 300 mg daily or placebo in addition to standard therapy. At 3 months the primary short-term endpoints were changes in New York Heart Association (NYHA) functional classification, 6-min walk test, and levels of N-terminal pro–B type natriuretic peptide. At 2 years the primary long-term endpoint was major adverse cardiovascular events (MACE).”

“The following secondary endpoints were significantly improved in the CoQ10 group compared with the placebo group: all-cause and cardiovascular mortality, NYHA classification and left ventricular ejection fraction (LVEF). In the European sub-population, when compared to the whole group, there was greater adherence to guideline directed therapy and similar results for short- and long-term endpoints. A new finding revealed a significant improvement in LVEF.”

“The therapeutic efficacy of CoQ10 demonstrated in the Q-SYMBIO study was confirmed in the European sub-population in terms of safely reducing MACE, all-cause mortality, cardiovascular mortality, hospitalization and improvement of symptoms.”

https://journals.viamedica.pl/cardiology_journal/article/view/62920

Vegetabiliskt fett istället för animaliskt minskar inte risk för hjärtsjukdom

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Att ersätta animaliskt fett med vegetabiliskt sänker inte risken för hjärtsjukdomar enligt en större analys som publiceras i British Medical Journal.

Det har länge funnits en allmän uppfattning om att vegetabiliska oljor sänker kolesterolhalterna i blodet och på så sätt minskar risken för hjärt-kärlsjukdomar. Men det vet ju du som läser och lyssnar här att så inte är fallet. (https://4health.se/139-kolesterol-van-eller-fiende)

Men nu har amerikanska forskare gått igenom en av de större studierna på området, Minnesota coronary experiment, som pågick mellan 1968 och 1973. När studien publicerades visade den att en kost rik på vegetabiliska oljor minskade kolesterolhalten och kom på så sätt att bli en hörnsten i uppfattningen att fleromättat fett är bättre för hjärtat än mättat fett, som främst kommer från djurriket.

Men den nya analysen visar att överlevnaden inte alls var bättre för de deltagare som fick en kost rik på vegetabiliskt fett. Forskarna har även gått igenom ett antal andra studier där deltagarna lottats till olika dieter. Men dessa visade inte heller på någon minskad risk att dö med en kost rik på vegetabiliska oljor, jämfört med en kost rik på animaliskt fett.

Deras resultat får ytterligare stöd i form av tidigare opublicerat material från en annan stor studie på området, Sydney diet heart study. Även här hade deltagarna en ökad risk för kranskärlsjukdom om de fick vegetabilisk olja och linolsyra, jämfört med mättat fett.

Forskarna bakom analysen har även gått igenom fem andra randomiserade studier som testat att ersätta mättat fett med vegetabiliska oljor för att minska risken för hjärtsjukdom. Men ingen av dessa kunde visa att risken att dö minskade med en diet som var hög på linolsyra.

Den bristfälliga publiceringen från främst Minnesota coronary experiment ligger troligtvis bakom en överskattad tro på att fleromättat fett bör ersätta mättat fett, skriver forskarna.

“Results The intervention group had significant reduction in serum cholesterol compared with controls (mean change from baseline −13.8% v −1.0%; P<0.001). Kaplan Meier graphs showed no mortality benefit for the intervention group in the full randomized cohort or for any prespecified subgroup. There was a 22% higher risk of death for each 30 mg/dL (0.78 mmol/L) reduction in serum cholesterol in covariate adjusted Cox regression models (hazard ratio 1.22, 95% confidence interval 1.14 to 1.32; P<0.001). There was no evidence of benefit in the intervention group for coronary atherosclerosis or myocardial infarcts. Systematic review identified five randomized controlled trials for inclusion (n=10 808). In meta-analyses, these cholesterol lowering interventions showed no evidence of benefit on mortality from coronary heart disease (1.13, 0.83 to 1.54) or all cause mortality (1.07, 0.90 to 1.27).

Conclusions Available evidence from randomized controlled trials shows that replacement of saturated fat in the diet with linoleic acid effectively lowers serum cholesterol but does not support the hypothesis that this translates to a lower risk of death from coronary heart disease or all causes. Findings from the Minnesota Coronary Experiment add to growing evidence that incomplete publication has contributed to overestimation of the benefits of replacing saturated fat with vegetable oils rich in linoleic acid.”

https://www.bmj.com/content/353/bmj.i1246

https://www.dagensmedicin.se/artiklar/2016/04/13/vegetabiliskt-fett-skyddar-inte-hjartat/

https://www.corren.se/nyheter/vaxtfett-skyddar-inte-hjartat-om4093967.aspx

Tack till Annika Dahlqvist som hittade studien.

Tarmfloran/ studie: Autism minskade med 50% !

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Hur är tarmfloran involverad i Autism? VÄLDIGT mycket! Det finns egentligen i min erfarenhet (och kunskap/ vad studierna säger) alltid 3 områden som är involverade i Autism:

  1. problem på cellnivå, med näringsobalanser/ energiproduktion/ oxidativ stress
  2. toxisk belastning / problem med kroppens egen detox
  3. problem med tarm/tarmflora

Nu har man studerat nr 3 genom att göra avföringstransplantationer vid autism – och minskat symtom med hela 50% (!)

Läsvärt (saxat ut det viktigaste):

“Autism symptoms reduced nearly 50% two years after fecal transplant”

[autism spectrum disorder (ASD))]

“Currently, effective treatments for ASD include behavioral therapy, speech and social therapy, psychiatric medications, and dietary and nutritional approaches. However, no medical treatments have been approved to treat core symptoms of ASD such as social communication difficulties and repetitive behaviors.

One promising avenue of autism research involves the gut microbiome, which is the collection of microbes that lives in our intestines and helps us in many ways including digestion of our food, training our immune system and preventing overgrowth of harmful bacteria. Recent research suggests our gut microbiomes also affect brain communication and neurological health. Worldwide, interest is growing in the idea that changes in normal gut microbiota may be responsible for triggering a vast range of diseases.”

In a new study, “Long-term benefit of Microbiota Transfer Therapy in Autism Symptoms and Gut Microbiota,” published in Scientific Reports, Arizona State University researchers Rosa Krajmalnik-Brown, Ph.D., James Adams, Ph.D, and lead author Dae-Wook Kang, Ph.D, demonstrate long-term beneficial effects for children diagnosed with ASD through a revolutionary technique known as Microbiota Transfer Therapy (MTT), a special type of fecal transplant […]. Remarkably, improvements in gut health and autism symptoms appear to persist long after treatment.

At two years post-treatment, most of the initial improvements in gut symptoms remained. In addition, parents reported a slow steady reduction of ASD symptoms during treatment and over the next two years. A professional evaluator found a 45% reduction in core ASD symptoms (language, social interaction and behavior) at two years post-treatment compared to before treatment began.

“We are finding a very strong connection between the microbes that live in our intestines and signals that travel to the brain,” said Krajmalnik-Brown, a professor at the Biodesign Swette Center for Environmental Biotechnology at the Biodesign Institute and ASU’s School for Sustainable Engineering and the Built Environment. “Two years later, the children are doing even better, which is amazing.”

“Many kids with autism have gastrointestinal problems, and some studies, including ours, have found that those children also have worse autism-related symptoms,” said Krajmalnik-Brown. “In many cases, when you are able to treat those gastrointestinal problems, their behavior improves.”

Roughly 30-50% of all people with autism have chronic gastrointestinal (GI) problems, primarily constipation and/or diarrhea that can last for many years. That chronic discomfort and pain can cause irritability, decreased attention and learning, and negatively impact behavior.

An earlier study with only vancomycin (an antibiotic) had found major temporary improvements in GI and autism symptoms, but the benefits were lost a few weeks after treatment stopped despite use of over-the-counter probiotics.

So, the question at hand was what’s going on in the gut, and how does it affect both physical and behavioral symptoms of autism, and how can we develop a long-lasting treatment?

Krajmalnik-Brown, Kang and Adams have shown that by transferring healthy microbiota to individuals lacking certain gut bacteria, it is possible to “donate” a more diverse set of bacteria into the patient and improve gut health.

[…] Only one dose of FMT is usually enough to cure C. Difficile infections, but his patients with autism were far harder to treat. He discovered that three months of daily FMT was required to treat his autism patients, but eventually resulted in significant improvements in both GI and autism symptoms.

Based on his experience with his patients, Borody led the design of the clinical treatment used at ASU for this study. The MTT approach involves 10 weeks of treatment, including pre-treatment with vancomycin, a bowel cleanse, a stomach acid suppressant, and fecal microbiota transfer daily for seven to eight weeks.

[…]  Improvements in GI symptoms, ASD symptoms, and the microbiome all persisted for at least eight weeks after treatment ended, suggesting a long-term impact.” The present study now shows the benefits are extended beyond eight weeks to at least two years post-treatment.

The ASU team compared differences in the microbiome of children with autism compared to typically developing children. At the start of the study, children with autism were found to have lower diversity in their respective gut microbes and were depleted of certain strains of helpful bacteria, such as Bifidobacteria and Prevotella. “Kids with autism are lacking important beneficial bacteria, and have fewer options in the bacterial menu of important functions that bacteria provide to the gut than typically developing kids,” Krajmalnik-Brown said.

FMT treatment substantially increased microbial diversity and the presence of helpful bacteria in the gut, such as Bifidobacteria and Prevotella. After two years, diversity was even higher and the presence of beneficial microbes remained.

“We originally hypothesized that our therapy would be efficient to transform the dysbiotic gut microbiome toward a healthy one. In our original paper in 2017, we reported an increase in gut diversity together with beneficial bacteria after MTT, and after two years, we observed diversity was even higher and the presence of beneficial microbes remained,” Kang said. He added that this may be one of the reasons for success in improving the gut health, but further mechanistic studies are warranted to define specific roles of gut microbes in the context of autism.

The work done at ASU is not only about treating patients but also about learning from the treatment in order to develop better formulations and optimize dosing.

“Understanding which microbes and chemicals produced by the microbes are driving these behavioral changes is at the heart of our work,” Krajmalnik-Brown said. The team’s new publication reports that the study demonstrated that two years after treatment stopped the participants still had an average of a 58% reduction in GI symptoms compared to baseline. In addition, the parents of most participants reported “a slow but steady improvement in core ASD symptoms.”

“Every family completed the study, and every family returned two years later for a follow-up evaluation,” said Adams, citing the families’ dedication to the research. “The treatment was generally well-tolerated with minimal adverse effects.”

“This is a world-first discovery that when we treated the gut bacteria in these children during our clinical trial two years ago to reset their microbiome with FMT, positive results are still continuing to be improving two years from the original treatments. I would call it the highest improvement in a cohort that anyone has achieved for autism symptoms,” said Borody.

Professional evaluation revealed a 45% decrease in ASD symptoms compared to baseline. Researchers note that although there may be some placebo effect, much of that effect appears to be real. At the start of the study, 83% of participants were rated as “severe” autism. At the end of the study, only 17% were “severe,” 39% were “mild/moderate,” and 44% were below the cut-off for mild ASD.

[…]

All of the participants in the study exhibited chronic GI symptoms from infancy, including chronic constipation and/or chronic diarrhea. The treatment benefits extended beyond their physical symptoms, even causing some parents to note how much their children’s behavior had improved over time.

“It is very unusual to see steady gradual improvement after the conclusion of any treatment,” said Adams. “We only conducted the long-term follow-up study after several families told us that their child was continuing to improve significantly.” Krajmalnik-Brown stated that the data suggests that the MTT intervention transformed the gut environment into a healthier status, leading to long-term benefit on both GI and ASD symptoms.

Adams said many of the participants in the trial shared common traits, including birth by C-section, reduced breastfeeding, increased antibiotics, and low fiber intake by the mother and child, all of which lead to limited biodiversity in their gut bacteria. Due to the open label nature of the study and the small sample size used, more research is needed in order to verify the usefulness of MTT as a therapeutic.

[…]

The microbiota formulation used in the original study was developed at the University of Minnesota by Alexander Khoruts and Michael Sadowsky, who developed innovative methods for collecting microbiota from healthy, carefully-screened donors and purifying and freezing them. They licensed their technology to Finch Therapeutics, who provided financial support for the manufacturing of the therapeutic microbiota used for the study.”

Mer via taggen microbiome

https://eurekalert.org/pub_releases/2019-04/asu-asr040819.php

Statiner (kolesterolsänkande) ökar risken för ALS

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Signifikant högre förekomst ALS och ALS-symtom hos personer som tar kolesterolsänkande medicin, statiner!

ALS, amyotrofisk lateral skleros, är neurodegenerativa sjukdomar där nervceller i centrala nervsystemet (hjärnan, hjärnstammen och ryggmärgen) dör. ALS angriper de motoriska nervcellerna, det vill säga de nervceller i hjärnan och ryggmärgen  som styr musklernas rörelser. Detta leder i sin tur till muskelförtvining och förlamning.

Missa inte att lyssna på de ingående avsnitten på temat kolesterol och statiner, 139 och 140: https://4health.se/139-kolesterol-van-eller-fiende

“Apparent elevations in reporting of amyotrophic lateral sclerosis (ALS)-like conditions associated with statin use have been previously described from data obtained via US and European databases.”

“The aim of this study was to examine US FDA Adverse Event Reporting System (FAERS) data to compare reporting odds ratios (RORs) of ALS and ALS-like conditions between statins and other drugs, for each statin agent.”

“We assessed for disproportional rates of reported ALS and ALS-related conditions for each statin agent separately by using the ROR formula. FAERS data were analyzed through September 2015.”

“RORs for ALS were elevated for all statins, with elevations possibly stronger for lipophilic statins. RORs ranged from 9.09 (6.57–12.6) and 16.2 (9.56–27.5) for rosuvastatin and pravastatin (hydrophilic) to 17.0 (14.1–20.4), 23.0 (18.3–29.1), and 107 (68.5–167) for atorvastatin, simvastatin, and lovastatin (lipophilic), respectively. For simvastatin, an ROR of 57.1 (39.5–82.7) was separately present for motor neuron disease.”

“These findings extend previous evidence showing that significantly elevated ALS reporting extends to individual statin agents, and add to concerns about potential elevated occurrence of ALS-like conditions in association with statin usage.”

https://link.springer.com/article/10.1007/s40264-017-0620-4