Berries for Inflammation and Osteoarthritis Treatment

How might berries improve human health, healthy aging, and quality of life?  Maybe, due to their anti-inflammatory effects, since inflammation can be an underlying contributing factor in the “development, progression, and complication” of a number of chronic diseases. Higher intake of anthocyanins, the brightly-colored pigments in berries, has been associated with anti-inflammatory effects, which may be “a key component” underlying the associated reduction in chronic disease risk. But these are all just associations. You can’t prove cause and effect until you put it to the test.

A double-blind, randomized, placebo-controlled trial found that blueberry smoothies could turn off inflammation genes. (This is measuring the expression of pro-inflammatory genes in white blood cells taken from individuals before and after six weeks of drinking placebo smoothies with no blueberries.) They got worse over time. Six weeks later, more inflammatory chemicals pouring out, whereas the blueberry group started out about the same at week zero, but six weeks of daily blueberries and, the expression of inflammatory genes went down.

“In addition to attenuating inflammation,” they demonstrate that “blueberry consumption was able to significantly decrease the levels of free radicals” in their bloodstream: no change in the placebo group, but after six weeks of blueberry smoothies, the amount of free radicals in their blood was  extinguished by half. Okay, but does all that antioxidant and anti-inflammatory power actually translate into clinical benefits? For example  what is the effect of blueberry consumption on recovery from excessive weight lifting-induced muscle damage?

A randomized crossover study: a blueberry smoothie or antioxidant-matched placebo smoothie five and 10 hours prior to, and then 12 and 36 hours after, exercise-induced muscle damage. The smoothies were about a cup and a half of frozen strawberries, a banana, and apple juice, or without the berries, but dextrose and vitamin C added to match it for calories and antioxidant power. Even so, the blueberries worked better at mopping up free radicals. Here’s the oxidative stress without the blueberries: it goes up and stays up. But, with the blueberries, it comes right down. Yeah, but what we care about is the recovery of muscle strength, so you can jump right back into training. Same drop in peak torque 12 hours later, but a day later, significantly faster restoration of peak muscle strength, demonstrating that the ingestion of blueberries can accelerate recovery — something that may be especially relevant to athletes who compete over successive days.

That’s all well and good, but what about using berries to treat inflammatory diseases like arthritis?  Yes, they may have protective effects against arthritis in a rat — significantly reducing “paw volume”— how swollen their paw gets when you inject it with some inflammatory irritant. But there had never been any human arthritis berry studies, until now.

Remember that amazing study where strawberries alone could reverse the progression of precancerous lesions? The strawberries were dramatically downregulating pro-inflammatory genes. Give strawberries to diabetics for six weeks, and not only does their diabetes get better, their C-reactive protein levels, a marker of systemic inflammation, drops 18%. Even just a single meal can help. Have people eat a largely unhealthy breakfast, and the level of inflammatory markers goes up over the next six hours, but less so if you added just five large strawberries to the meal.

So, can “strawberries improve pain and inflammation” in confirmed knee osteoarthritis? No fair that the title ruined the suspense, but yes, osteoarthritis patients randomized to get like a pint and a half of strawberries a day for 12 weeks and yeah, certain inflammatory markers plummeted on the strawberries. But did they actually feel any better? Significant reductions in constant pain, intermittent pain, and total pain. The “first clinical study on the effects of…berries” on human arthritis, and found that a “simple dietary intervention, the addition of berries to one’s diet, may have a significant impact on pain, inflammation, and overall quality of life in obese adults with [osteoarthritis].”

Source: https://www.youtube.com/watch?v=C6udzAvvacQ#action=share

Why hydrotherapy might work in COVID-19

Coronaviruses don’t like the heat. In fact at 38 deg C they have a massive drop in replication and infectivity. [1]  In the lab they are grown at 34 deg C. [2]

Coronaviruses inhibit the innate immune system: the first line of the body’s defence against viruses.  In particular they directly impair the release of the “distress beacon” cells send out to say they are infected (Interferon Type 1 “IFN Type 1”) and (either consequently or directly) inhibit the cell lines (eg monocytes and natural killer cells) in the innate immune system. [3,4] These messages and cells are essential to switch on a normal, healthy, adaptive immune response rather than the late, overactive and damaging immune response seen in hospitalised patients with COVID-19.

Cold temperatures impair the immune system’s ability to release IFN Type 1 when infected with a virus (in mice). [5]

So being cold both improves the growth of coronaviruses and impairs the body’s distress signal to show it is under attack, which is already being directly inhibited by the coronavirus.

Older people, and those with obesity (with or without the diseases associated with carrying extra weight) have impaired innate and adaptive immune systems, including a decreased ability to mount a fever to an infection. They also have decreased numbers and activity of cells such as natural killer cells and monocyte function [6-8].

So older and unwell/obese people are hit doubly hard by their own weakened innate immune response and the active attack of that area of the immune system by the virus that causes COVID-19.

Fever is a broad based stimulant to the whole of the innate and adaptive immune system [9].   In particular, in respect to COVID-19 infection, fever or hyperthermia increases the release of INF Type 1 and monocyte function [10-12] and directly inhibits viral replication [9]. There are similar results to the immune system if the body temperature is raised by external means eg sitting in a hot bath, as by internal means such as infection [9].

So inducing mild hyperthermia by water (also known as “hydrotherapy”) could directly

  • inhibit replication and activity of coronaviruses
  • overcome coronavirus inhibition of IFN Type 1, likely increasing the chances of normal immune resolution of COVID-19
  • Enhance immune function in those most vulnerable to immune complications of COVID-19

Hydrotherapy was used widely in Adventist hospitals in the Spanish Influenza pandemic with a mortality rate of 1% compared to 13% in the army-run “open air” hospitals considered state of the art at the time. Average mortality was 40% for hospitalised patients in traditional hospitals [13-15]. (NB these are old figures and not subject to the academic standards of research and trials of today. Nonetheless they are interesting to note.)

Hydrotherapeutic treatments have received little study since the advent of vaccination and effective antibiotic therapy.  Consequently there are no randomised controlled trials to support their use in coronaviruses of any sort, let alone COVID-19, but for the above reasons it is plausible to think it should be useful.   Early preparations are underway for a trial in Australia. In other cities around the world there is more urgency. 

It makes sense to use the time at home after diagnosis of COVID-19 to support the immune system to clear the virus, and increase the chance of a good resolution.  It feels like a better  alternative than to just cross your fingers and hope you are not one of the 20% who need to go to hospital, 5% who need ICU or 2.5% who do not survive.  There are multiple drugs and immunotherapies being trialled but most of these are being focused on the late stages of the illness and are not readily available now.  Besides hydrotherapy it makes sense to eat nutritious food, get enough rest, and manage stress. Quitting smoking and limiting your alcohol intake (if you do drink) are also great ideas for this time.

Hydrotherapy is a medical treatment like any other with risks and benefits. Please read the advice about contraindications and safety precautions carefully, and DO NOT USE HYDROTHERAPY INSTEAD OF APPROPRIATE MEDICAL CARE.  You should use the treatments outlined on this website only with the support of your local doctor, who can help you determine if it is safe for you, or help you modify them to make them safer for you.

(Written 10/04/20 by Dr Emma Campbell, BMed FRACGP)

Bibliography

(If you have little time, focus on numbers four and nine).

  1. Chan KH, Peiris JS, Lam SY, Poon LL, Yuen KY, Seto WH. The Effects of Temperature and Relative Humidity on the Viability of the SARS Coronavirus. Adv Virol. 2011;2011:734690. doi: 10.1155/2011/734690. Epub 2011 Oct 1. PubMed PMID: 22312351; PubMed Central PMCID: PMC3265313.
  2. 2.Kaye M. SARS-associated coronavirus replication in cell lines. Emerg Infect Dis. 2006 Jan;12(1):128-33. doi: 10.3201/eid1201.050496. PubMed PMID: 16494729; PubMed Central PMCID: 
  3. R, Fehr AR, Zheng J, Wohlford-Lenane C, Abrahante JE, Mack M, Sompallae R, McCray PB Jr, Meyerholz DK, Perlman S. IFN-I response timing relative to virus replication determines MERS coronavirus infection outcomes. J Clin Invest. 2019 Jul 29;130:3625-3639. doi: 10.1172/JCI126363. eCollection 2019 Jul 29. PubMed PMID: 31355779; PubMed Central PMCID: PMC6715373.
  4. Prompetchara E, Ketloy C, Palaga T. Immune responses in COVID-19 and potential vaccines: Lessons learned from SARS and MERS epidemic. Asian Pac J Allergy Immunol. 2020 Mar;38(1):1-9. doi: 10.12932/AP-200220-0772. Review. PubMed PMID: 32105090.
  5. Prow NA, Tang B, Gardner J, Le TT, Taylor A, Poo YS, Nakayama E, Hirata TDC, Nakaya HI, Slonchak A, Mukhopadhyay P, Mahalingam S, Schroder WA, Klimstra W, Suhrbier A. Lower temperatures reduce type I interferon activity and promote alphaviral arthritis. PLoS Pathog. 2017 Dec;13(12):e1006788. Doi:
  6. Poland GA, Ovsyannikova IG, Kennedy RB, Lambert ND, Kirkland JL. A systems biology approach to the effect of aging, immunosenescence and vaccine response. Curr Opin Immunol. 2014 Aug;29:62-8. doi: 10.1016/j.coi.2014.04.005. Epub 2014 May 13. Review. PubMed PMID: 24820347; PubMed Central PMCID: PMC4119552
  7. Rao DV, Watson K, Jones GL. Age-related attenuation in the expression of the major heat shock proteins in human peripheral lymphocytes. Mech Ageing Dev. 1999 Feb 1;107(1):105-18. doi: 10.1016/s0047-6374(98)00143-2. PubMed PMID: 10197792.
  8. Parisi MM, Grun LK, Lavandoski P, Alves LB, Bristot IJ, Mattiello R, Mottin CC, Klamt F, Jones MH, Padoin AV, Guma FCR, Barbé-Tuana FM. Immunosenescence Induced by Plasma from Individuals with Obesity Caused Cell Signaling Dysfunction and Inflammation. Obesity (Silver Spring). 2017 Sep;25(9):1523-1531. doi: 10.1002/oby.21888. Epub 2017 Jul 14. PubMed PMID: 28707376
  9. Evans SS, Repasky EA, Fisher DT. Fever and the thermal regulation of immunity: the immune system feels the heat. Nat Rev Immunol. 2015 Jun;15(6):335-49. doi: 10.1038/nri3843. Epub 2015 May 15. Review. PubMed PMID: 25976513; PubMed Central PMCID: PMC4786079
  10. Postic B, DeAngelis C, Breinig MK, Monto HO. Effect of temperature on the induction of interferons by endotoxin and virus. J Bacteriol. 1966 Mar;91(3):1277-81. PubMed PMID: 5929756; PubMed Central PMCID: PMC316024.
  11. Manzella JP, Roberts NJ Jr. Human macrophage and lymphocyte responses to mitogen stimulation after exposure to influenza virus, ascorbic acid, and hyperthermia. J Immunol. 1979 Nov;123(5):1940-4. PubMed PMID: 489966.
  12. Knippertz I, Stein MF, Dörrie J, Schaft N, Müller I, Deinzer A, Steinkasserer A, Nettelbeck DM. Mild hyperthermia enhances human monocyte-derived dendritic cell functions and offers potential for applications in vaccination strategies. Int J  Hyperthermia. 2011;27(6):591-603. doi: 10.3109/02656736.2011.589234. PubMed PMID: 21846195.
  13. Hobday RA, Cason JW. The open-air treatment of pandemic influenza. Am J Public Health. 2009 Oct;99 Suppl 2:S236-42. doi: 10.2105/AJPH.2008.134627. Epub 2009 May 21. PubMed PMID: 19461112; PubMed Central PMCID: PMC4504358.
  14. WEAPONS AGAINST INFLUENZA. Am J Public Health (N Y). 1918 Oct;8(10):787-8. doi: 10.2105/ajph.8.10.787. PMID: 18009972; PMCID: PMC1362349
  15. W.A. Ruble, MD, Sanitarium Treatment of Influenza, Life & Health, 34 (5);114-115. May 1919. Graphics: Applied Physiology Lab WLCH ’09. BEB ibid.Accessed at: https://adventistdigitallibrary.org/adl-373944/life-and-health-may-1-1919 pg 20

 

Why Do Plant-Based Diets Help Rheumatoid Arthritis?

Rheumatoid arthritis is a chronic systemic autoimmune disease affecting millions, characterized by persistent pain and stiffness, and progressive joint destruction—particularly in the hands and feet, leading to crippling deformities. What can we do to prevent it and treat it?

In a famous 13-month long randomized controlled trial of plant-based diets for rheumatoid arthritis, patients were put on a vegan diet for three and a half months, and then switched to an egg-free lactovegetarian diet for the remainder of the study. Compared to the control group, who didn’t change their diet at all, the plant-based group had a significant improvement in morning stiffness within the first month, cutting the number of hours they suffered from joint stiffness in half. Pain dropped from five out of ten down to less than three out of ten. A drop in disability; they reported subjectively feeling better, significant improvement in their grip strength, fewer tender joints, less tenderness per joint, and less swelling, with the added benefit of losing about 13 pounds and keeping most of that weight off throughout the year. They also had a drop in inflammatory markers in their blood, sed rate, C-reactive protein, and white count. The question is why. What does diet have to do with inflammatory joint disease?

Well, rheumatoid arthritis is an autoimmune disease in which your body attacks the lining of your own joints. Why would it do that? Well, there’s a different autoimmune disease called rheumatic fever, in which your body attacks your own heart. Again, why would your body do that? It appears to be a matter of friendly fire.

Rheumatic fever is caused by strep throat, which is caused by a bacteria that has a protein that looks an awful lot like a protein in our heart. So when our immune system attacks the strep bacteria, it also attacks our heart valves, triggering an autoimmune attack by “molecular mimicry.” The protein on the strep bacteria is mimicking a protein in our heart, so our body gets confused and attacks both. That’s why it’s critical to treat strep throat early to prevent our heart from getting caught in the crossfire.

So researchers thought maybe rheumatoid arthritis might be triggered by an infection as well. A clue to where to start looking was the fact that women seem to get rheumatoid arthritis three times more frequently than men. What type of infection do women get more than men? Urinary tract infections, so researchers started testing the urine of rheumatoid arthritis sufferers, and lo and behold found this bacteria called Proteus mirabilis. Not enough to cause symptoms of a UTI, but enough to trigger an immune response. And indeed, there’s a molecule in the bacteria that looks an awful lot like one of our own molecules in our joints, so anti-Proteus antibodies against the bacteria may inadvertently damage our own joint tissues, leading eventually to the joint destruction. Therefore, therapeutic interventions aimed at the removal of this bacteria from the bodies of patients, with consequent reduction of antibodies against the organism, should lead to a decrease in inflammation.

Well, as we saw before, urinary tract infections originate from the fecal flora; the bugs crawl up from the rectum into the bladder. And so, how might one change the bugs in one’s colon? By changing our diet. Some of the first studies over 20 years ago on trying to fundamentally shift people’s gut flora were done using raw vegan diets, figuring that’s about as fundamental a shift from the standard Western diet as there is. And indeed, within days one could significantly change someone’s gut flora. And you put rheumatoid arthritis sufferers on that kind of diet, and they experienced relief, and the greater improvements were linked to greater changes in their gut flora. But the diet was considered so intolerable that half the patients couldn’t take it and dropped out–perhaps because they were trying to feed people things like buckwheat-beetroot cutlets buttered with a spread made out of almonds and fermented cucumber juice.

Thankfully, regular vegetarian and vegan diets work too, changing the intestinal flora and improving rheumatoid arthritis, but we didn’t specifically have confirmation that plant-based diets brought down anti-Proteus antibodies, until now. Those who responded to the plant-based diet showed a significant drop in anti-Proteus mirabilis antibodies compared to the control group. Maybe it just dropped immune responses across the board? No, antibody levels against other bugs remained the same, so the assumption is that the veg diet reduced urinary or gut levels of the bug.

A shift from an omnivorous to a vegetarian diet has a profound influence on the composition of the urine–for example, higher levels of lignans in the urine of those eating vegetarian. Up until now, it was just thought that lignans protected people eating more plant-based from getting cancer, but now we know lignans can also have antimicrobial properties as well, so may be helping to clear Proteus from the system. Either way, this suggests a new type of therapy for the management of rheumatoid arthritis. This new treatment includes anti-Proteus measures such as dietary manipulations in the forms of vegetarian diet.

Source:https://nutritionfacts.org/video/why-do-plant-based-diets-help-rheumatoid-arthritis/

Warum Hydrotherapie bei COVID-19 funktionieren könnte

Warum Hydrotherapie bei COVID-19 funktionieren könnte

Coronaviren mögen keine Hitze, tatsächlich kommt es bei 38°C zu einem massiven Rückgang der Replikation und Infektiosität. [1] Im Labor werden sie bei 34°C gezüchtet. [2]

Coronaviren hemmen das angeborene Immunsystem, welche die erste Linie der körpereigenen Abwehr gegen Viren sind. Insbesondere beeinträchtigen Sie die direkte Freisetzung der “Distress Beacon”-Zellen, die ausgesandt sind um zu indizieren, dass sie infiziert sind (Interferon Typ 1 “IFN Typ 1”) und (entweder konsequent oder direkt) die Zelllinien (z.B. Monozyten und natürliche Killerzellen) im angeborenen Immunsystem hemmen. [3,4] Diese Informationen und Zellen sind unerlässlich, um ein normales, gesundes, anpassungsfähiges Immunsystem einzuschalten, d.h. die erwünschte Reaktion zu starten statt der späten, überaktiven und schädlichen Immunantwort, wie bei den hospitalisierten Patienten mit COVID-19.

Kalte Temperaturen beeinträchtigen die Fähigkeit des Immunsystems IFN Typ 1 freizusetzen, wenn es mit einem Virus infiziert ist (bei Mäusen). [5] Kälte unterstützt also das Wachstum von Coronaviren und gleichzeitig entkräftet sie die Verbreitung des körperlichen Notsignals. Dieses Notsignal zeigt, dass der Körper angegriffen wird, und diese Funktion wird bereits durch das Coronavirus eingeschränkt.

Ältere Menschen und Menschen mit Übergewicht (mit oder ohne den Krankheiten, die mit dem zusätzlichen Gewicht zusammenhängen) haben ein beeinträchtigtes angeborenes und adaptives Immunsystem, einschließlich einer verminderten Fähigkeit, eine Infektion mit Fieber zu beschleunigen. Sie haben auch eine verminderte Anzahl und Aktivität von Zellen wie natürliche Killerzellen und Monozytenfunktion [6-8].

Ältere und kranke/fettleibige Menschen sind also doppelt so stark getroffen; von ihrer eigenen geschwächten angeborenen Immunantwort und dem aktiven Angriff auf diesen Bereich des Immunsystems durch das Virus, welches COVID-19 verursacht.

Fieber ist ein breit angelegtes Stimulans für das gesamte angeborene und adaptive Immunsystem [9].Insbesondere bei einer COVID-19-Infektion erhöht Fieber oder Hyperthermie die Freisetzung von INF Typ 1 und Monozytenfunktion [10-12] und hemmt dadurch  die virale Replikation [9]. Es gibt ähnliche Ergebnisse bezüglich des Immunsystems, sowohl wenn die Körpertemperatur durch äußere Mittel erhöht wird, z.B. Sitzen in einem heißen Bad, als auch durch innere Mittel wie Infektionen [9].

Die Induktion einer milden Hyperthermie durch Wasser (auch als “Hydrotherapie” bekannt) könnte:

● die Replikation und Aktivität von Coronaviren hemmen
● die Coronavirus-Hemmung von IFN Typ 1 überwinden und dadurch die Chancen einer
normalen Immunauflösung von COVID-19 erhöhen
● die Immunfunktion bei den am stärksten gefährdeten Komplikationen von COVID-19
verbessern

Die Hydrotherapie wurde in adventistischen Krankenhäusern bei der spanischen Grippepandemie eingesetzt und zwar mit eine Sterblichkeitsrate von 1% im Vergleich zu 13% in den von der Armee betriebenen “Freiluft”-Krankenhäusern, die damals als stark fortgeschritten galten.

In traditionellen Krankenhäusern lag die durchschnittliche Sterblichkeit bei 40% für hospitalisierte Patienten.  [13-15]. (Dies sind alte Zahlen und unterliegen nicht den akademischen Standards von Forschung und Testung von heute. Nichtsdestotrotz sind sie interessant zu beachten).

Hydrotherapeutische Behandlungen sind seit dem Aufkommen von Impfungen und wirksamen Antibiotika-Therapien nur wenig erforscht worden. Folglich gibt es keine randomisierten kontrollierten Studien zu ihrer Verwendung bei Coronaviren jeder Art, ganz zu schweigen von COVID-19, aber für die oben genannten Gründe ist es naheliegend, dass sie nützlich sein könnten. In Australien laufen die ersten Vorbereitungen für eine praktische Studie. In anderen Städten auf der ganzen Welt ist die Dringlichkeit größer.

Es ist sinnvoll, die Zeit nach der Diagnose von COVID-19 zu Hause zu nutzen, um die Immunabwehr zu unterstützen, um das Virus zu beseitigen und die Chance auf eine kompletten  Wiederherstellung der Gesundheit zu erhöhen. Es fühlt sich an wie eine bessere Alternative, als einfach die Daumen zu drücken und zu hoffen, dass Sie nicht zu den 20 % gehören, die ins Krankenhaus gehen müssen, die 5 %, die eine Intensivstation benötigen, oder die 2,5 %, die nicht überleben. Es gibt mehrere Medikamente und Immuntherapien, die gerade getestet werden, aber die meisten davon konzentrieren sich auf die späten Stadien der Krankheit und sind jetzt nicht ohne weiteres verfügbar. Neben der Hydrotherapie macht es Sinn, nahrhaftes Essen einzunehmen, genügend Ruhe zu haben und Stress zu bewältigen. Es ist empfehlenswert mit dem Rauchen aufzuhören und auch den Alkoholkonsum  zu limitieren.

Die Hydrotherapie ist eine medizinische Behandlung wie jede andere mit Risiken und Nutzen. Bitte lesen Sie sorgfältig die Hinweise bezüglich Kontraindikationen und Sicherheitsvorkehrungen und VERWENDEN SIE HYDROTHERAPIE NICHT ANSTELLE EINER ANGEMESSENEN MEDIZINISCHEN VERSORGUNG. Die auf dieser Webseite beschriebenen Behandlungen sollten nur mit Unterstützung eines Arztes vor Ort durchgeführt werden, der bestimmen kann, ob es eine sichere Behandlung ist, oder er dieselbe modifizieren kann, um sie sicherer zu machen.

(Geschrieben am 10. April 2020 von Dr Emma Campbell, BMed FRACGP)

 

Quellenangabe

( wenn Sie wenig Zeit haben, dann empfehle Ich ihnen 4 und 9 zu lesen)

  1. Chan KH, Peiris JS, Lam SY, Poon LL, Yuen KY, Seto WH. The Effects of Temperature and Relative Humidity on the Viability of the SARS Coronavirus. Adv Virol. 2011;2011:734690. doi: 10.1155/2011/734690. Epub 2011 Oct 1. PubMed PMID: 22312351; PubMed Central PMCID: PMC3265313.2.
  2. Kaye M. SARS-associated coronavirus replication in cell lines. Emerg Infect Dis. 2006 Jan;12(1):128-33. doi: 10.3201/eid1201.050496. PubMed PMID: 16494729; PubMed Central PMCID: 
  3. R, Fehr AR, Zheng J, Wohlford-Lenane C, Abrahante JE, Mack M, Sompallae R, McCray PB Jr, Meyerholz DK, Perlman S. IFN-I response timing relative to virus replication determines MERS coronavirus infection outcomes. J Clin Invest. 2019 Jul 29;130:3625-3639. doi: 10.1172/JCI126363. eCollection 2019 Jul 29. PubMed PMID: 31355779; PubMed Central PMCID: PMC6715373.
  4. Prompetchara E, Ketloy C, Palaga T. Immune responses in COVID-19 and potential vaccines: Lessons learned from SARS and MERS epidemic. Asian Pac J Allergy Immunol. 2020 Mar;38(1):1-9. doi: 10.12932/AP-200220-0772. Review. PubMed PMID: 32105090.
  5. Prow NA, Tang B, Gardner J, Le TT, Taylor A, Poo YS, Nakayama E, Hirata TDC, Nakaya HI, Slonchak A, Mukhopadhyay P, Mahalingam S, Schroder WA, Klimstra W, Suhrbier A. Lower temperatures reduce type I interferon activity and promote alphaviral arthritis. PLoS Pathog. 2017 Dec;13(12):e1006788. Doi:
  6. Poland GA, Ovsyannikova IG, Kennedy RB, Lambert ND, Kirkland JL. A systems biology approach to the effect of aging, immunosenescence and vaccine response. Curr Opin Immunol. 2014 Aug;29:62-8. doi: 10.1016/j.coi.2014.04.005. Epub 2014 May 13. Review. PubMed PMID: 24820347; PubMed Central PMCID: PMC4119552.
  7. Rao DV, Watson K, Jones GL. Age-related attenuation in the expression of the major heat shock proteins in human peripheral lymphocytes. Mech Ageing Dev. 1999 Feb 1;107(1):105-18. doi: 10.1016/s0047-6374(98)00143-2. PubMed PMID: 10197792.
  8. Parisi MM, Grun LK, Lavandoski P, Alves LB, Bristot IJ, Mattiello R, Mottin CC, Klamt F, Jones MH, Padoin AV, Guma FCR, Barbé-Tuana FM. Immunosenescence Induced by Plasma from Individuals with Obesity Caused Cell Signaling Dysfunction and Inflammation. Obesity (Silver Spring). 2017 Sep;25(9):1523-1531. doi: 10.1002/oby.21888. Epub 2017 Jul 14. PubMed PMID: 28707376
  9. Evans SS, Repasky EA, Fisher DT. Fever and the thermal regulation of immunity: the immune system feels the heat. Nat Rev Immunol. 2015 Jun;15(6):335-49. doi: 10.1038/nri3843. Epub 2015 May 15. Review. PubMed PMID: 25976513; PubMed Central PMCID: PMC4786079
  10. Postic B, DeAngelis C, Breinig MK, Monto HO. Effect of temperature on the induction of interferons by endotoxin and virus. J Bacteriol. 1966 Mar;91(3):1277-81. PubMed PMID: 5929756; PubMed Central PMCID: PMC316024.
  11. Manzella JP, Roberts NJ Jr. Human macrophage and lymphocyte responses to mitogen stimulation after exposure to influenza virus, ascorbic acid, and hyperthermia. J Immunol. 1979 Nov;123(5):1940-4. PubMed PMID: 489966.
  12. Knippertz I, Stein MF, Dörrie J, Schaft N, Müller I, Deinzer A, Steinkasserer A, Nettelbeck DM. Mild hyperthermia enhances human monocyte-derived dendritic cell functions and offers potential for applications in vaccination strategies. Int J  Hyperthermia. 2011;27(6):591-603. doi: 10.3109/02656736.2011.589234. PubMed PMID: 21846195.
  13. Hobday RA, Cason JW. The open-air treatment of pandemic influenza. Am J Public Health. 2009 Oct;99 Suppl 2:S236-42. doi: 10.2105/AJPH.2008.134627. Epub 2009 May 21. PubMed PMID: 19461112; PubMed Central PMCID: PMC4504358.
  14. WEAPONS AGAINST INFLUENZA. Am J Public Health (N Y). 1918 Oct;8(10):787-8. doi: 10.2105/ajph.8.10.787. PMID: 18009972; PMCID: PMC1362349
  15. W.A. Ruble, MD, Sanitarium Treatment of Influenza, Life & Health, 34 (5);114-115. May 1919. Graphics: Applied Physiology Lab WLCH ’09. BEB ibid.Accessed at: https://adventistdigitallibrary.org/adl-373944/life-and-health-may-1-1919 pg 20

 

Book recommendation

Description

High Blood Pressure. Even if you haven’t received the diagnosis yet, as many as three-quarters of the Western world will have to contend with high blood pressure sometime in their lives. However you no longer need to be a victim. Drs. DeRose and Steinke along with Nurse Practitioner Li draw from cutting-edge medical research and their decades of clinical experience to guide you on an amazing 30-day journey. This remarkable book guides readers on a truly life-changing experience. This well-referenced book (over 400 footnotes) is far from a sterile medical treatise. Stories from real-life patients combined with over 100 figures, graphs, and tables, make the relevant medical science understandable for even lay readers. If you are looking for ways to control your high blood pressure without medications–or are trying to keep a normal blood pressure from creeping into a dangerous range–this book is for you.

Author

Dr. David DeRose is a physician holding board certifications in both Internal Medicine and Preventive Medicine. He has a Master’s Degree in Public Health (MPH) with an emphasis in Health Promotion and Health Education. In addition to his conventional training, Dr. DeRose has three decades of experience in the alternative and complementary health field. He has worked at some of the nation’s most innovative health centers including over six years as a founding physician, and later Medical Director, of the Lifestyle Center of America. Please click below for his professional CV.

Dr. DeRose is a published scientific researcher, who is also known for his ability to take complex subjects and explain them in lay terms. His health communication skills have been honed by more than twenty years of radio and television work and a busy public speaking schedule. Dr. DeRose is currently heard on some 200 stations as host of the nationally syndicated health radio program, American Indian Living.

Dr. DeRose is known for his ability to make complex health subjects easily understood to people across educational and cultural lines. Dr. DeRose has worked in a variety of settings including the Midwest; Southern California; Orlando, Florida; New England; and New York City. His eclectic medical background provides a breadth of experience guaranteeing that all will relate to his compelling presentations of life-changing health information.

Proffessional CV: https://www.compasshealth.net/professional-cv/

With kind permission from compasshealth


https://www.compasshealth.net/product/30-days-to-natural-blood-pressure-control/
https://www.compasshealth.net/dr-derose-bio/

 

The book is available via:

https://www.compasshealth.net/product/30-days-to-natural-blood-pressure-control/

or

https://www.amazon.de/Thirty-Natural-Blood-Pressure-Control/dp/1942730020 

 

 

Exercise as a Treatment for Depression

Watch the video instead on ‘exercise vs. drugs for depression’.

We’ve known for decades that even a single bout of exercise can elevate our mood, but could it be enough to be used as a treatment for major depression?

We’ve known that physical activity has been associated with decreased symptoms of depression. For example, if you look at a cross-section of 8,000 people across the country, those that exercised regularly were less likely to have a major depression diagnosis. That’s just a snapshot in time, though. In that study, the researcher openly acknowledges this may be a case of reverse causation. Maybe exercise didn’t cut down on depression, maybe depression cut down on exercise. The reason depression may be associated with low physical activity is that people may feel too lousy to get out of bed. What we’ve needed was an interventional study where you take people who are already depressed and randomize them into an exercise intervention.

That is what researchers from Duke University Medical Center did. They randomized men and women over age 50 with major depression to two groups: one who did an aerobic exercise program for four months and another that took an antidepressant drug called Zoloft. In my video Exercise vs. Drugs for Depression, you can see a graph of their changes. Before exercise, their Hamilton Depression scores were up around 18 (anything over seven is considered depressed). Within four months, the drug group came down to normal, which is exactly what the drugs are supposed to do. What about the exercise-only group, though? Exercise had the same powerful effect.

The researchers concluded that an exercise training program may be considered an alternative to antidepressants for treatment of depression in older persons, given that they’ve shown that a group program of aerobic exercise is a feasible and effective treatment for depression, at least for older people.

Not so fast, though.

A “group program?” They had the exercise group folks come in three times a week for a group class. Maybe the only reason the exercise group got better is because they were forced to get out of bed and interact with people—maybe it was the social stimulation and had nothing to do with the actual exercise? Before you could definitively say that exercise can work as well as drugs, what we would need to see is the same study, but with an additional group who exercised alone with no extra social interaction. And those same Duke researchers did just that.

They created the largest exercise trial of patients with major depression conducted to date, and not just including older folks, but other adults as well with three different treatment groups this time: a home exercise group in addition to the supervised group exercise and the drug group as before.

And, they all worked about just as well in terms of forcing the depression into remission. So, we can say with confidence that exercise is comparable to antidepressant medication in the treatment of patients with major depressive disorder.

Putting all the best studies together, researchers indicate that exercise at least has a moderate antidepressant effect, and at best, exercise has a large effect on reductions in depression symptoms and could be categorized as a very useful and powerful intervention. Unfortunately, while studies support the use of exercise as a treatment for depression, exercise is rarely prescribed as a treatment for this common and debilitating problem.

https://nutritionfacts.org/2017/01/24/exercise-as-a-treatment-for-depression/

How Researchers Are Implementing Food To Treat Depression And Other Chronic Diseases

Ah, comfort food. Who doesn’t have a love/hate relationship with it? For me on a bad day, I find myself craving the perfect storm of fries, pizza, and ice cream. What I don’t realize as I’m dipping my fry into my ice cream is that I might experience an emotional low afterward that’s even worse than how I felt at the beginning. Actually, I’ve noticed that when I have fresh fruits and vegetables, I’m much more vibrant and happy and ready to accomplish the tasks throughout my day.

 That brings up the question: Can the food we eat have a drastic impact on our emotional health? More specifically, can a plant-based, vegan diet reverse symptoms of depression and improve emotional health?

There have been many studies done regarding the influence of diet on emotional health. For example, in January 2017, an issue of the medical journal BioMed Central (BMC) Medicine reported that a team of researchers led by Felice Jacka, an epidemiologist at Deakin University in Australia, studied the effect that diet had on the moods of individuals with major depression. The study had two groups: the initial group received counseling from a dietician and the second group received counseling from a positive social support caregiver.

The results indicated that those who ate a healthy diet were emotionally happier than those who received social support. Also shown was that an unhealthy diet high in processed and refined foods increased the risk for not only depression but other diseases as well. There have been many other studies revolving around this topic that support this research.

Nutritional psychiatry

“Nutritional psychiatry” is a recent development in the medical world, but it’s a rapidly growing research field. Understanding the effects that diet has on mental health is incredibly important – especially now – because there are so many chronic diseases that have become more prevalent because of the highly processed foods consumed by society.

Dr. Jacka is the co-founder of the International Society for Nutritional Psychiatry Research that aims to expand the field by using a multi-disciplinary approach to research connecting emotional and physical health on a new level. The Food and Mood Center was created by Dr. Jacka as a center for studies on how diet influences mental health. Because of the new studies that have been addressed, the American Psychiatric Association has begun to include presentations on nutritional psychiatry at their annual conferences.

Even though diet isn’t the only factor influencing mental health, researchers have found another way to prevent and treat depression. What is it? You guessed it, eating a plant-based diet. A plant-based diet doesn’t only promote good physical health, but it also shows promise in promoting emotional health and well-being. I think we can safely say that fruits and veggies should be the “happy food” to turn to when we’re having a bad day.

Here’s a recipe for a fruit smoothie from Nutriliving that is packed with fresh nutrition and will give you a bright boost to your day. Have a happy and healthy day!

Mood-Boosting Breakfast Blast 

Ingredients

  • ¼ cup blueberries
  • 1 banana
  • 5 walnuts
  • ½ cup oats
  • 1 ½ cups unsweetened almond milk

Instructions

  • Add all ingredients to your blender and blend for 30 seconds, or until smooth.
  • Enjoy!

By Raeann Leal

https://lifeandhealth.org/lifestyle/how-researchers-are-implementing-food-to-treat-depression-and-other-chronic-diseases/1010154.html

Source:

https://bmcmedicine.biomedcentral.com/articles/10.1186/s12916-017-0791-y?mod=article_inline

Corona – How to boost your mental health in times of social distancing during COVID-19

In this video, the ENAD team put together the most imporant things to enhance your mental health and help you to get through this coronavirus crisis during a time of social isolation…

Probably the most spoken word of the year. Starting in China this virus travelled from one person to another, to all over the world. In order to get rid of this disease again, we are all limited in our every day life. If you are staying at home for such a long time, it may be natural to get frustrated that you cannot do everything you want.
We as an ENAD team put together 7 things that will enhance your mental health in order to get through this crisis.

1. Get closer to people at home

When life is very busy, we tend to have little time for each other, especially for the ones that are closest to us. This crisis is a chance to connect to our loved ones that live in our homes. So set aside your devices and talk to each other. If you are alone, it is important to stay connected to those who are your emotional support.

2. Increase your physical activity for at least an hour a day.

In some places, hiking on trails in the open air is not yet forbidden. Take advantage of the extra time you have now. Moving your body does not only benefit your apearing, it also produces serotonin and therefore enhances your happiness an strenghten your immunsystem to fight against coronavirus

3. Re-organize your house

Since you are at home this is the perfect opportunity to start working on making every room enjoyable and clean. Get rid of clutter, catch up on your email, rearrange your furniture, and consider how to pare down where you have excess. Setting a timer for 15 minutes at a time can be a great way to get start.

4. Expand your skills

Use your time to learn how to perform enjoyable and brain enhancing activities every day. Try a new recipie, learn to play an instrument, start singing, drawing or learn a new language. Stay away from screens as much as possible.

5. Plant a garden

Try growing your own food. Spending time in nature is important for your mental health. You can get seedlings from grocery stores, or purchase them online. Also: A garden doesn’t have to be a raised bed – raising plants in pots is still rewarding.

6. Quit keeping up with the latest COVID-19 news

It is exhausting to see the changes hour-by-hour. Because you are already doing your part, there is nothing more you can usefully do by keeping up with the latest statistics or politics. Dont waste your time and go do one of the other 5 things of this video.

7. Explore your spirituality

So often we do not have or take the time needed to evaluate the state of our own spirituality. You now have this golden opportunity apart from the hustle and bustle of normal life. Spend a thoughtful hour reading the bible or a spiritual book, praying or spend time evaluating what you believe. You can also take an online bible-study course in the link below. Thoughtful moments will bolster your mental wellbeing.

Go and try one of those 7 things today, if you are not already doing it, and take care of your mental health. Also, check out our social media and other articles about coronavirus on our website.

www.joelmedia.de
www.amazing-discoveries.org

 

Corona – Lessons from the 1918 flu & Application to COVID-19

Can treatments used during the 1918 Spanish Flu outbreak be used to combat the pandemic we currently face? Learn from top medical professionals from the US for an online symposium as they share lessons learned that could be applied today!

Continuing education credits can acquired by attending this online symposium. For more information, go to awr.org/health.

Sponsored by AWR360 Health in partnership with GC Health, NAD Health, Your Best Pathway to Health, Weimar Institute, Oakhaven, and others.
Special Guest Speaker: President and CEO Loma Linda University Health
Host: Dr. Lela Lewis, Medical Director AWR360 Health and CEO/Founder Your Best Pathway to Health

Panelists in Order of Speaking:
Dr. Peter Landless, General Conference of Seventh-day Adventist Health Ministry Director
Dr. Richard Hart, President of Loma Linda University Health and CEO Loma Linda University Health,
Dr. Neil Nedley, President Weimar College
Dr. Roger Seheult Pulmonologist, Intensivist, Founder MedCram
Dr. John Kelly, President Oakhaven and Founder of the American College of Lifestyle Medicine
Dr. Charles Zeno Marcel, General Conference of Seventh-day Adventists – Assistant Director
Dr. Mark Finley, Assistant to the President, General Conference of Seventh-day Adventists
Dr. Duane McKey, President of AWR

Source: Youtube – Adventist World Radio

A New (Old) Treatment for COVID-19

Image

12/4/20

Pandemic COVID-19.  What can/should we do?

Having reached nearly 1.8 million reported cases globally, with reported deaths of nearly 110,000 this pandemic is reaching all corners of the globe and affecting all sections of society.

The impact on each population is profoundly affected by the decisions made by local and federal governments to promote handwashing and early social distancing and the extent to which a society is able to comply with that.  The ultimate solution to the pandemic, an effective vaccine is 12-18 months away. At the other end of the clinical course, hospital and ICU staff are either struggling to find adequate PPE, beds, ventilators and new treatments to minimise the substantial morbidity and mortality or preparing for the surge in clinical needs depending on where their city is in the course of the spread of the virus.  The resources that are able to be amassed to fight end stage COVID-19 are vastly different depending on the health system of the country affected.  

COVID-19 has a known clinical course (with the obvious variation of asymptomatic carriage). On average around day 5 become symptomatic, get tested (if testing available in patients region), then go home to wait and see what happens.  If they are lucky they become one of the 80% who recover without hospitalisation or if not, around day 12, they will need to go into a hospital with resources stretched beyond capacity, and will have significantly worse morbidity and mortality.  There is no active treatment in this middle stage of the clinical course, the outcome of which predominantly depends on whether their innate immune function is able to overcome SARS CoV-2’s direct impairment. Fever is well known to enhance innate and adaptive immunity.  

In Newcastle, Australia, we are proposing research into whether heat applied to the body as a proxy for fever can alter the clinical course of COVID-19 and decrease the likelihood of hospitalisation and poor clinical outcomes.  This sort of research is incumbent upon clinicians and countries that have the wherewithal, to support the global fight against COVID-19. In other countries, clinicians may choose to act on biological plausibility and clinical imperative alone.

Immune Pathophysiology of Coronaviruses causing SARS, MERS and COVID-19

Coronavirus infections that result in SARS, MERS and COVID-19 show the viruses are able to actively impair the innate immune response, in particular the Type 1 interferon (IFN) response from infected cells (such as Type 2 alveolar cells and likely macrophages and T cells).  They also (either directly or as a result of decreased IFN Type 1) impair monocytes and other innate immune cells (eg natural killer cells) which are required to phagocytose virus and present it to lymphocytes to switch on adaptive immunity [1-3].  

…excessive type I IFN with the infiltrated myeloid cells are the main cause of lung dysfunction and negatively impact the outcome of the infection. It is speculated that upon SARS-CoV or MERS-CoV infection, delayed type I IFN compromises the early viral control, leading to influx of hyperinflammatory neutrophils and monocytes-macrophages. The increases in these innate immune cells yields deteriorating consequences to infected host that manifested in lung immunopathology, including pneumonia or acute respiratory distress syndrome. In SARS-CoV-2 infection, similar scenario is expected with varying degree of immune interference. Interestingly, transmission of virus is reported to occur even in asymptomatic infected individuals. This may be indicative of delayed early response of the innate immune response. Based on the accumulated data for previous coronavirus infection, innate immune response plays a crucial role in protective or destructive responses and may open a window for immune intervention. Active viral replication later results in hyperproduction type I IFN and influx of neutrophils and macrophages which are the major sources of pro-inflammatory cytokines. With similar changes in total neutrophils and lymphocytes during COVID19, SARS-CoV-2 probably induces delayed type I IFN and loss of viral control in an early phase of infection. Individuals susceptible to CoVID19 are those with underlying diseases, including diabetes, hypertension, and cardiovascular disease.2 In addition, no severe cases were reported in young children, when innate immune response is highly effective. These facts strongly indicate that innate immune response is a critical factor for disease outcome. [2]

Eighty percent of patients are able to overcome this direct innate immune suppression by the virus, mount a reasonable innate (and consequently a good adaptive) immune response and clear the virus. In about twenty percent of patients (predominantly those with impaired immunity to start with, for example – from age or obesity and it’s consequent diseases) this direct inhibition by the virus results in it being able to replicate relatively unchecked in the early days of the infection.  A few days to a week later, the body is confronted with large amounts of virus and there is an over exuberant immune response from the recruited neutrophils, monocytes and macrophages. The resultant hyperproduction of proinflammatory cytokines, the so-called “cytokine storm”, results in acute lung injury +/- ARDS +/- multi-organ failure +/- death [1-3]. See the diagram on the previous page.  

Early research has shown in vitro pretreatment of cells with IFN Type 1 in the days prior to infection shows a massive sustained reduction in viral replication and likely would result in a good in vivo result [4].   However IFN Type 1 is not yet an available experimental treatment. There are a number of other therapeutic trials showing promise with such treatments as vitamin C, plaquenil, zinc, even injection with natural killer cells etc but globally most patients are unable to access these as either in, or outpatients.   As for the case of the immune treatments like administered IFN or NK cells: what if we could do more than just increase one cytokine or cell line? What if we could activate the whole of the immune system?

How can we overcome immune inhibition by SARS CoV-2?

Fever is known to increase innate and acquired immune activity in multiple ways including:

  • increased release of heat shock proteins
  • increased phagocytic potential of dendritic cells and macrophages  
  • increased migration of APCs to regional lymph nodes, 
  • increased recruitment of neutrophils to lungs 
  • increased neutrophil activity
  • enhanced natural killer recruitment and activity  
  • increased numbers of lymphocytes. 

This is also true for induced hyperthermia eg  as created by injecting lipopolysaccharide (bacterial cell wall component) into mice or sitting in a warm bath for humans.[5,6] Hyperthermia not only optimises immune function it also directly inhibits viral replication [5].  Most importantly in the case of COVID-19, a number of studies have demonstrated that elevated body temperatures substantially augment Interferon Type 1 (IFNα) production/activity in response to viral infection [6-9] AND monocyte function[11] ie the immune processes that the virus directly inhibits.  By utilising induced hyperthermia to overcome the initial roadblocks that SARS-CoV-2 setup, the immune system is primed to proceed with a normal inflammatory response and clear the virus, rather than progress to inflammatory complications.

Fever is a good immune system enhancer as discussed above, however, there are two problems:  

  1. Not everyone mounts a good fever response to infection especially not the old and obese.  Immunosenescence (the decline in immune function with age, and obesity and its consequences) is mediated in part by impaired monocyte function[12,13]. 
  2. Fever is metabolically expensive with every degree of body temperature elevation requiring an increase in BMR of 10-12.5%.  

Mild hyperthermia induced by hydrotherapy potentially addresses both of these problems[5,11].

How can immune enhancement by hyperthermia help clinically?

The first week after diagnosis with COVID-19 infection is essentially being wasted at home.   If during that time we induced hyperthermia at home, with simple hydrotherapeutic techniques, we could directly stimulate the whole of the innate and adaptive immune response but in particular we may be able to partially or completely overcome the direct immune depressant effects of COVID-19 on INF and monocytes in the early days of infection.   If we are able to diminish the need for hospitalisation by even 5% of total infections that would be a 25% decrease in numbers requiring admission, substantially reducing the overstretched resources globally and will potentially save many lives. This potential treatment is even more important as an option for people in developing nations without a readily available hospital system, replete with ICU support.  

Hydrotherapy and COVID-19

Hydrotherapeutic hyperthermia can be induced in a number of ways, but one of the easiest  involves sitting in a warm to hot bath till sweaty, then having a douse of cold water to vasoconstrict the external vessels and keep the heat in, then resting in a warm bed for ½ an hour. The potential risks of this treatment include vasovagals due to vasodilation or arrhythmias induced by the cold water shock. Hydrotherapy is highly modifiable treatment   and can be performed with a patient in bed, in a chair or in a bath/shower with whatever is available to hand. It can also be adapted to suit the patients comorbidities and clinical status. Anecdotally, a physiotherapy colleague of mine has used therapeutic hyperthermia to good effect in many different situations around the globe. For example, by wrapping Karen refugees without access to any medical care, in black plastic to heat and then cooling off with a dip in the river for tropical PUO (likely Dengue or malaria).  When utilised in conjunction with standard medical care while working in a hospital in Bangkok, my colleague saw patients in hospital with Dengue fever fit to go home in 3 days when it usually took 7-10 days.

Could inducing a fever early just speed up the time to cytokine storm and not alter the clinical pathway at all?  

Reassuringly there is good evidence to suggest that early fever or induced hyperthermia plays a homeostatic role in managing the inflammatory course, and its outcomes, for good or ill. For example, thermal stress initially increases proinflammatory cytokine release from macrophages but, once they are activated, synthesis decreases. In addition, activated or “heat experienced” macrophages produce less TNF, IL6 and IL1beta in febrile temperatures, than heat inexperienced ones.[5]

What about those who are not infected but would like to optimise immune function today?  The evidence is a little less clear at a population rather than cellular level, (smaller studies, more observational, hard to blind people etc) but heat, then cold exposure has been shown to improve immune function, especially when used over longer periods [14,15,16]. 

A case report[17] followed the clinical course of a patient in Melbourne, Australia who recovered from COVID-19 after a brief hospitalisation.  There was a marked increase of adaptive immune cells around day 7, three days prior to alleviation of symptoms (still with noticeably low monocytes common to SARS CoV-2 infections).  It would be useful to have some comparative case studies showing what happens daily to the clinical course in COVID-19 with hydrotherapy. Taking a FBC at least on days 3 and 6 would show quickly whether immune suppression was taking place, or being overcome by the treatments and give a good prediction as to whether the patient was likely to need hospitalisation on day 12, or go on to make a good clinical resolution.  Case reports and historical records from when this treatment was used in the Spanish influenza pandemic suggest that the WCC should surge at day three (illustrating a rapid transition to acquired immunity) and bring about clinical resolution potentially around 4 days earlier than without hydrotherapy. 

It is worth noting that practicing Evidence Based Medicine is an excellent thing that helps keep us and our patients safe.  However during this pandemic ICUs and health care workers around the globe are just trying to figure out what works. There are no long term, multicentre RCTs to guide us at this stage, just clinical experience that guides expert opinion.  Once anecdotal evidence mounts, it is guiding smaller clinical trials and RCTs in regional centres. There are just too many lives to try to save to waste time waiting for someone else to deliver gold standard evidence. Not having an RCT to support a type of treatment is not stopping intensive care clinicians from trying any therapeutic modality that makes physiological sense and is available to hand.  I believe in this situation, primary care physicians, public health physicians and ID physicians should be following their lead. 

Treatment/Research Plans…

As we are making good progress in “flattening the curve” in Australia we have the opportunity to formally assess whether immune stimulation by mild hyperthermia from hydrotherapy can alter clinical outcomes.  Not every country or city is in our position. Some clinicians may choose to trial this old/new treatment for infectious disease without recent trials. This therapy is scientifically plausible, at little to no cost, readily available, and can be safely utilised by patients in their own homes with a little education and common sense.  Like all treatments hydrotherapy is not without risks eg falls from postural hypotension or arrythmias triggered by cold stimulation. If clinicians and patients are aware of the risks and contraindications to this therapy it can be considered on a case by case basis.

Detailed protocols, as well as precautions/contraindications, are available at hydro4covid.com.  This information is based on clinical experience and historical textbooks/records of treatment of the Spanish Influenza pandemic.   These protocols, used with care, can be utilised to possibly:

  1. help keep patients out of hospital (more acute care for those who really need it) 
  2. diminish asymptomatic and presymptomatic shed in the community (slow community spread) especially in the young who are at least risk from this illness and are the most likely to share it without knowing it
  3. optimise our own immune function to help keep us all working safely as long as is required..

Author: Dr Emma Campbell BMed FRACGP

 

Bibliography

Highlighted in bold are the two most useful resources, if you only have time to look at a couple of papers.

  1. Channappanavar R, Fehr AR, Zheng J, Wohlford-Lenane C, Abrahante JE, Mack M, Sompallae R, McCray PB Jr, Meyerholz DK, Perlman S. IFN-I response timing relative to virus replication determines MERS coronavirus infection outcomes. J Clin Invest. 2019 Jul 29;130:3625-3639. doi: 10.1172/JCI126363. eCollection 2019 Jul 29. PubMed PMID: 31355779; PubMed Central PMCID: PMC6715373.
  2. Prompetchara E, Ketloy C, Palaga T. Immune responses in COVID-19 and potential vaccines: Lessons learned from SARS and MERS epidemic. Asian Pac J Allergy Immunol. 2020 Mar;38(1):1-9. doi: 10.12932/AP-200220-0772. Review. PubMed PMID: 32105090.
  3. Channappanavar R, Perlman S. Pathogenic human coronavirus infections: causes and consequences of cytokine storm and immunopathology. Semin Immunopathol. 2017 Jul;39(5):529-539. doi: 10.1007/s00281-017-0629-x. Epub 2017 May 2. Review. PubMed PMID: 28466096; PubMed Central PMCID: PMC7079893.
  4. Lokugamage KG, Schindewolf C, Menachery VD. SARS-CoV-2 sensitive to type I interferon pretreatment. unpublished.Forthcoming;
  5. Evans SS, Repasky EA, Fisher DT. Fever and the thermal regulation of immunity: the immune system feels the heat. Nat Rev Immunol. 2015 Jun;15(6):335-49. doi: 10.1038/nri3843. Epub 2015 May 15. Review. PubMed PMID: 25976513; PubMed Central PMCID: PMC4786079
  6. El-Radhi AS. Fever management: Evidence vs current practice. World J Clin Pediatr. 2012 Dec 8;1(4):29-33. doi: 10.5409/wjcp.v1.i4.29. eCollection 2012 Dec 8. Review. PubMed PMID: 25254165; PubMed Central PMCID: PMC4145646.
  7. Postic B, DeAngelis C, Breinig MK, Monto HO. Effect of temperature on the induction of interferons by endotoxin and virus. J Bacteriol. 1966 Mar;91(3):1277-81. PubMed PMID: 5929756; PubMed Central PMCID: PMC316024.
  8. Manzella JP, Roberts NJ Jr. Human macrophage and lymphocyte responses to mitogen stimulation after exposure to influenza virus, ascorbic acid, and hyperthermia. J Immunol. 1979 Nov;123(5):1940-4. PubMed PMID: 489966.
  9. Knippertz I, Stein MF, Dörrie J, Schaft N, Müller I, Deinzer A, Steinkasserer A, Nettelbeck DM. Mild hyperthermia enhances human monocyte-derived dendritic cell functions and offers potential for applications in vaccination strategies. Int J  Hyperthermia. 2011;27(6):591-603. doi: 10.3109/02656736.2011.589234. PubMed PMID: 21846195.
  10. Prow NA, Tang B, Gardner J, Le TT, Taylor A, Poo YS, Nakayama E, Hirata TDC, Nakaya HI, Slonchak A, Mukhopadhyay P, Mahalingam S, Schroder WA, Klimstra W, Suhrbier A. Lower temperatures reduce type I interferon activity and promote alphaviral arthritis. PLoS Pathog. 2017 Dec;13(12):e1006788. doi: 10.1371/journal.ppat.1006788. eCollection 2017 Dec. PubMed PMID: 29281739; PubMed Central PMCID: PMC5770078
  11. Zellner M, Hergovics N, Roth E, Jilma B, Spittler A, Oehler R. Human monocyte stimulation by experimental whole body hyperthermia. Wien Klin Wochenschr. 2002 Feb 15;114(3):102-7. PubMed PMID: 12060966
  12. Rao DV, Watson K, Jones GL. Age-related attenuation in the expression of the major heat shock proteins in human peripheral lymphocytes. Mech Ageing Dev. 1999 Feb 1;107(1):105-18. doi: 10.1016/s0047-6374(98)00143-2. PubMed PMID: 10197792.
  13. Parisi MM, Grun LK, Lavandoski P, Alves LB, Bristot IJ, Mattiello R, Mottin CC, Klamt F, Jones MH, Padoin AV, Guma FCR, Barbé-Tuana FM. Immunosenescence Induced by Plasma from Individuals with Obesity Caused Cell Signaling Dysfunction and Inflammation. Obesity (Silver Spring). 2017 Sep;25(9):1523-1531. doi: 10.1002/oby.21888. Epub 2017 Jul 14. PubMed PMID: 28707376
  14. Brenner IK, Castellani JW, Gabaree C, Young AJ, Zamecnik J, Shephard RJ, Shek PN. Immune changes in humans during cold exposure: effects of prior heating and exercise. J Appl Physiol (1985). 1999 Aug;87(2):699-710. doi: 10.1152/jappl.1999.87.2.699. PubMed PMID: 10444630.
  15. Dugue B, Lappanen E, Grasbeck R. Effect of thermal stress (sauna + swimming in ice-cold water) in man on the blood concentration and production of pro-inflammatory cytokines and stress hormones. Pathophysiology. 1998; 1001(5):149.
  16. Ernst E, Pecho E, Wirz P, Saradeth T. Regular sauna bathing and the incidence of common colds. Ann Med. 1990;22(4):225-7. doi: 10.3109/07853899009148930. PubMed PMID: 2248758.
  17. Thevarajan I, Nguyen T, Koutsakos M, Druce J, Caly L, van de Sandt C, Jia X, Nicholson S, Catton M, Cowie B, Tong S, Lewin S, Kedzierska K. Breadth of concomitant immune responses prior to patient recovery: a case report of non-severe COVID-19. Nature Medicine. 2020/03; doi: 10.1038/s41591-020-0819-2