Coronaviruses don’t like the heat. In fact at 38 deg C they have a massive drop in replication and infectivity.  In the lab they are grown at 34 deg C. 
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). 
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 . 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 . 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 .
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)
(If you have little time, focus on numbers four and nine).
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.  Im Labor werden sie bei 34°C gezüchtet. 
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).  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 .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 . 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 .
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
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 Alkoholkonsumzu 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)
( wenn Sie wenig Zeit haben, dann empfehle Ich ihnen 4 und 9 zu lesen)
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
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. 
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 . 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 .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 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:
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].
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.
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 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.
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:
help keep patients out of hospital (more acute care for those who really need it)
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
optimise our own immune function to help keep us all working safely as long as is required..
Author:Dr Emma Campbell BMed FRACGP
Highlighted in bold are the two most useful resources, if you only have time to look at a couple of papers.
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.
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
In medicine, there is often the concern that a patient will not respond to a particular treatment, but in a turn for the books, physicians are now worried that a new cancer treatment might be so effective at eliminating tumors that it does more harm than good.After receiving a single treatment of a novel combination therapy, a woman’s tumor seemingly “dissolved” from her chest in just three weeks, leaving her with a gaping hole in its place. The patient received the same cocktail of skin cancer drugs as almost 150 individuals enrolled in a clinical trial designed to test whether one of the therapies worked better on its own or when combined with another. While most patients did significantly better on the combination therapy, researchers were left gobsmacked by this woman’s rapid and dramatic response and have consequently described her case in the New England Journal of Medicine, alongside the trial results.The therapies the scientists were investigating were the FDA-approved melanoma drugs Yervoy (ipilimumab) and Opdivo (nivolumab), which are both antibodies …
CHURCH PLACES STRONG EMPHASIS ON HEALTH AND WELLBEING
March 16, 2015 | Silver Spring, Maryland, United States | Andrew McChesney/Adventist Review
The Seventh-day Adventist Church has issued an official statement on vaccines, saying it “encourages responsible immunization” and has no faith-based reason to discourage believers from participating in immunization programs.
Image courtesy Wikimedia Commons
The full statement, titled, “Immunization,” says:
“The Seventh-day Adventist Church places strong emphasis on health and well-being. The Adventist health emphasis is based on biblical revelation, the inspired writing of E.G. White (co-founder of the church), and on peer-reviewed scientific literature. As such, we encourage responsible immunization/vaccination, and have no religious or faith-based reason not to encourage our adherents to responsibly participate in protective and preventive immunization programs. We value the health and safety of the population, which includes the maintenance of ‘herd immunity.’
“We are not the conscience of the individual church member, and recognize individual choices. These are exercised by the individual. The choice not to be immunized is not and should not be seen as the dogma nor the doctrine of the Seventh-day Adventist Church.”
Erectile dysfunction is the recurrent or persistent inability to attain and/or maintain an erection in order for satisfactory sexual performance. It is present in up to 30 million men in the U.S. and approximately 100 million men worldwide. The U.S. has less than 8% of the world’s population, yet up to 30% of the impotence? We’re #1!
But hey, we’ve got red, white, and blue pills like Viagra. The problem is that the pills just cover up the symptoms of vascular disease and don’t do anything for the underlying pathology. Erectile dysfunction and our #1 killer, coronary artery disease, are just two manifestations of the same disease: inflamed, clogged, and crippled arteries, regardless of which organ it affects (See Survival of the Firmest: Erectile Dysfunction and Death).
Atherosclerosis is considered a systemic disorder that uniformly affects all major blood vessels in the body. Hardening of the arteries can lead to softening of the penis because stiffened arteries can’t relax, open wide, and let the blood flow. Thus erectile dysfunction may just be the flaccid “tip of an iceberg” in terms of a systemic disorder. For two-thirds of men showing up to emergency rooms for the first time with crushing chest pain, their penis had been trying to warn them for years that something was wrong with their circulation.
Why does it hit the penis first? Because the penile arteries in the penis are half the size of the coronary artery in our heart. So the amount of plaque we wouldn’t even feel in the heart could clog half the penile artery, causing symptomatic restriction in blood flow. That’s why erectile dysfunction has been called “penile angina.” In fact, by measuring blood flow in a man’s penis we can predict the results of his cardiac stress test with an accuracy of 80%. Male sexual function is like a penile stress test, a “window into the hearts of men.”
Forty percent of men over age forty have erectile dysfunction. 40 over 40. Men with erection difficulties in their 40s have a 50-fold increased risk of having a cardiac event (like sudden death). I said before that various things increase heart disease risk by 20% or 30%. That’s nearly 5000%, leading the latest review to ask, “is there any risk greater?” That’s because it’s not so much a risk factor for atherosclerosis as atherosclerosis itself. A man “with erectile dysfunction (even if he doesn’t have cardiac symptoms) should be considered a cardiac patient until proven otherwise.”
Erectile dysfunction is considered to be a cardiac equivalent; it’s a marker of the coronary artery one likely already has. Thus, there’s more to treating ED than establishing an erect penis; it offers an opportunity for reducing cardiovascular risk. The reason even young men should care about their cholesterol is because itpredicts erectile dysfunction later in life, which in turn predicts heart attacks, strokes, and a shortened lifespan.