Saturday, February 27, 2021

In Case You’re Still Equivocating?

Vaccinations have been responsible for the demise of polio, smallpox, and a host of pandemic diseases. Presently, it’s not known if once vaccinated, can you still be a carrier. Clearly, people who are attracted to Public Safety jobs have tamped down their aversion to risk. But, it also implies that you’re not stupid. 

Big data has consistently shown the value of Western Medicine. Below is a table of risk for hospitalization and death by age groups. The Latin term Rez Ipsa loquitur (the thing speaks for itself) should do the trick. 

Friday, February 26, 2021

Thursday, February 18, 2021

Coffee Gets a Boost


Coffee used to be blamed for everything from high blood pressure and high cholesterol (and thus heart disease) to pancreatic cancer, fibro-cystic breasts, and bone loss. But, better studies in more recent years have almost always refuted the older findings and have even suggested that this beloved beverage may have health benefits, including reduced risk of melanoma, colon cancer, endometrial cancer, liver disease, diabetes, and cognitive decline. 

Still, the findings are not robust enough to recommend that you start drinking coffee, but if you do already, science appears to back your habit. Here are the results of two observational studies from 2020 suggesting beneficial effects of your cup a joe—and one showing a quirkier consequence.

Less body fat. 

Women who regularly drink coffee have less total body and abdominal fat than their coffee- abstaining counterparts. The more coffee the women consumed, including decaf, the greater the effect, as seen on body scans. As has been the case in prior studies, no dose-response relationship was observed in men, possibly for reasons relating to differences in sex hormones, the researchers speculated.

Better heart health and longevity— especially when a filter is used in brewing. A 20-year study linked coffee consumption to overall reduced mortality, compared to abstaining. But, those who drank filtered coffee (one to four cups a day) had the lowest risk of premature death, including from cardiovascular disease. Brewing methods in which ground coffee comes in direct contact with hot water—such as French press or espresso—leave behind higher concentrations of diterpene compounds (kahweol and cafestol) that raise blood cholesterol, whereas a filter traps them, which could partly explain the better results seen in those drinking filtered coffee.

From: Aviation Medical

Tuesday, February 16, 2021

When is ‘dead’ really dead? What happens after a person ‘flatlines’

As an EMT and Paramedic, I’m sure you’ve faced your share of codes. I found this article to be informative (POD)

How long should doctors wait after a “flatline” appears before they can declare a person dead? How can they be sure that heartbeat and circulation will not return?

The most common way that people die is after their heart stops beating. However, there is limited evidence for how long to wait to determine death once the heart stops. This missing information has repercussions for clinical practice and for organ donation.

A fundamental principle of organ donation is the dead donor rule: donors must be dead prior to recovery of organs, and organ recovery must not be the cause of death. A lack of evidence about how long to wait before declaring death creates a tension: if doctors wait too long after the heart stops, the quality of organs begins to decline.

On the other hand, not waiting long enough introduces the risk of going ahead with organ recovery before death has actually occurred.

Our interdisciplinary team of doctors, bio-engineers and experienced clinical researchers has spent the past decade studying what happens when a person dies after their heart stops. We focused on patients in the intensive care unit who died after life support was withdrawn, since these patients may also be eligible for organ donation.

In particular, we were interested in understanding whether it is possible for the heart to restart on its own, without any interventions like cardiopulmonary resuscitation (CPR) or medication.
A closer look at end-of-life flatline

Our recent study, published in the New England Journal of Medicine, presents observations of the dying process of 631 patients across Canada, the Czech Republic and the Netherlands who died in an intensive care unit. All patients’ families consented to participate in the research.

In addition to collecting medical information about each patient, we built a computer program to capture and review heart rate, blood pressure, blood oxygenation level and respiratory patterns directly from bedside monitors. As a result, we were able to analyze end-of-life flatline patterns for 480 out of 631 patients — including looking at whether and when any circulation or heart activity returned after stopping for at least one minute.

Vital Signs @ 8X

This video shows arterial blood pressure and electrocardiogram signals stop for 64 seconds before resuming, and finally stopping nearly three minutes later. The video is sped up eight times.

As it turns out, the classic flatline of death is not so straightforward. We found that human heart activity often stops and restarts a number of times during a normal dying process.

Out of 480 “flatline” signals reviewed, we found a stop-and-start pattern in 67 (14 percent). The longest that the heart stopped before restarting on its own was four minutes and 20 seconds. The longest time that heart activity continued after restarting was 27 minutes, but most restarts lasted just one to two seconds. None of the patients we observed survived or regained consciousness.

We also found it was common for the heart to continue to show electrical activity long after blood flow or pulse stopped. The human heart functions as a result of electrical stimulation of nerves that causes the heart muscle to contract and contribute to blood flow — the pulse you can feel in your arteries and veins.

We found that the heart rate (electrical stimulation leading to movement of the heart muscle) and pulse (movement of blood in the veins) only stopped together in 19 percent of patients. In some cases, the electrical activity of the heart continued for over 30 minutes without resulting in any circulation of blood.
Why understanding death matters

The results of our study are important for a few reasons.

First, the observation that stops and restarts of heart activity and circulation are often part of the natural process of dying will be reassuring to doctors, nurses and family members at the bedside. Intermittent signals on bedside monitors can sometimes be alarming if observers interpret them as signs that life is unexpectedly returning. Our study provides evidence that stops and starts are to be expected during a normal dying process without CPR, and that they do not lead to regained consciousness or survival. Flatline resumption: heart activity stops and starts during the natural process of dying. Author provided

Second, our finding that the longest pause before heart activity restarted on its own was four minutes and 20 seconds supports the current practice of waiting five minutes after circulation stops before declaring death and proceeding to organ recovery. This helps to reassure organ donation organizations that practices of determination of death are safe and appropriate.

Our results will be used to better inform policy and guidelines for the practice of organ donation internationally. For donation systems to work, when someone is declared dead, there must be trust that the declaration is really true. Trust allows families to choose donation in a time of grief and allows the medical community to ensure the safe and consistent end of life care.

This study is also important for improving our broader understanding of the natural history of death. We have shown that figuring out when dead is really dead is perhaps not so simple. It requires careful observation and close physiologic monitoring of the patient. In addition, it requires an understanding that, just as in life, there are many patterns that the dying process can take.

Our work is a step towards appreciating the complexity of dying and suggests we must move beyond the idea of a straightforward flatline to indicate when death has occurred.

This article was co-authored by Laura Hornby, research manager and consultant at the Children’s Hospital of Eastern Ontario Research Institute and Canadian Blood Services, and Nathan Scales, a biomedical engineer and research associate at the Dynamical Analysis Lab at the Ottawa Hospital Research Institute.

Thursday, February 4, 2021

4 Theories About Overtraining

Maybe the debilitating effects of chronic overtraining syndrome are in your muscles after all, not your head or your hormones

From Outside Magazine
Alex Hutchinson

May 28, 2020

There’s no shortage of theories about overtraining syndrome, a state of pervasive fatigue and poor performance that lasts months or years and sometimes ends athletic careers. In fact, there are too many theories. It’s psychological, it’s neurological, it’s adrenal, it’s hormonal, it’s immunological, it’s cardiovascular—it seems to affect pretty much every system in the body, which makes it hard to pinpoint the cause.

A new paper from a group led by Johanna Lanner of the Karolinska Institute in Sweden presents the case for a seemingly obvious culprit: the muscles themselves. Writing in the journal Redox Biology, they explore four main theories for what might go wrong within your muscles after a prolonged period of heavy training that could lead to long-term changes like those seen in overtraining syndrome. If they’re right, it suggests some possible countermeasures against overtraining—but that’s a big if.

From the muscle’s perspective, training is a constant cycle of stress and recovery. A hard workout causes all sorts of metabolic and structural disruptions in your muscle fibers, which in turn trigger adaptations that occur during the recovery period and make you stronger and fitter. These perturbations are good when they’re temporary, but if they become chronic—for example, because you’re not recovering enough between workouts—then they make you weaker and more fatigued.

It’s not just your maximum strength that’s affected; even relatively light submaximal exercise like a jog feels harder. This effect can last for days or even weeks after a single killer workout, an effect known as “prolonged low-frequency force depression,” or PLFFD. Intriguingly, studies with single muscle fibers from rodents also exhibit PLFFD. These muscle fibers obviously aren’t depressed or hormonally imbalanced—there must be some sort of prolonged disruption within the muscle fiber itself. Since overtraining in some ways looks like a chronic version of PLFFD that won’t switch off, Lanner and her colleagues suggest that overtraining, too, may involve problems in the muscle.

Here are the four leading muscle-related explanations of overtraining they consider:
Glycogen Depletion

This one is pretty straightforward: maybe chronic depletion of glycogen, the form in which muscle fibers store carbohydrate, interferes with the ability of those fibers to generate force and ultimately leads to what we experience as overtraining. It almost seems too simple, but it’s actually quite plausible that athletes who are training at truly extreme levels—i.e. those most vulnerable to overtraining syndrome—have trouble keeping up with their bodies’ fuel needs. That’s what a study on ketone drinks suggested last year: the apparent ability of these drinks to ward off overtraining was linked to increased calorie intake.

Lanner and her colleagues aren’t convinced, though. They point out that a study in rats failed to prevent overtraining despite aggressive carbohydrate supplementation. Not getting enough carbohydrate may contribute to overtraining, but getting enough, on its own, doesn’t seem to prevent it.

Muscle Damage
This is the classic explanation for next-day soreness: a hard workout, especially something like downhill running or box jumps that involves a lot of eccentric contractions, causes little microtears and other physical damage to your muscle fibers. Normally this damage gets repaired and ultimately leaves you stronger—unless the balance between damage and repair is chronically tilted too far toward the former.

Not so fast, though. While the link between damaged muscle fibers and weaker muscles seems intuitively obvious, studies don’t seem to find a good correlation between the amount of visible damage and the decline in function, according to Lanner and her colleagues. The damage is there, but it doesn’t seem to directly cause the problems.

Inflammation and Cytokines
This may sound a little familiar from all the recent discussion of cytokine storms in                                                     COVID-19. A similar idea applies here: a limited amount of inflammation (which is induced by small proteins called cytokines) is a normal part of both immune responses and post-exercise muscle repair, but too much can inflict further damage. After repeated strenuous exercise with insufficient recovery, you can end up with chronically elevated cytokine levels and inflammation, which in turn interferes with muscle function.

Furthermore, this inflammatory response could start a vicious cycle: cytokines also lead to an increase in oxidative stress, which in turn triggers the release of more inflammation-promoting cytokines, which increases oxidative stress, and so on—which brings us to the heart of Lanner’s argument.
Oxidative Stress

There’s a reason this paper was published in Redox Biology, which is a rather specialized journal. Even though the authors present four theories, their main interest is in the idea that oxidative stress—the excessive presence of damaging molecules called reactive oxygen species—is a key driver of decreased muscle function in overtraining syndrome.

It’s true, according to at least some studies, that overtrained athletes display elevated levels of oxidative stress. You might think that there’s a simple solution to this: take antioxidant supplements, which neutralize reactive oxygen species. But it turns out that the role of oxidative stress in the body is fiendishly complicated. Like inflammation, oxidative stress also serves as a key signal telling your body to adapt and get fitter after exercise, so eliminating it can have negative effects. While the topic is still being debated among researchers, there’s considerable evidence that regular use of antioxidant supplements can blunt the gains you’d normally get from a training program.

Typically, rested muscle stays in a slightly “reduced” state. That’s the opposite of being oxidized, meaning it has gained rather than lost electrons. When you start exercising, that generates oxidative stress, which actually puts your muscle into an optimal balance between reduction and oxidation, maximizing the amount of force you can generate. But if you exercise too hard or too long, the amount of oxidation becomes too much and muscle performance decreases again.

Lanner and her colleagues provide a schematic diagram to illustrate this delicate balance between reduced and oxidized muscles:
(Photo: Courtesy Redox Biology)

Normally, you’re sitting slightly to the left on this diagram, at “Rested muscle.” If you start exercising, you move to the middle, at “Optimal exercise redox balance.” If you push too hard, you keep moving to the right, to “Exercise-induced fatigue.” Allow yourself to recover, then everything will be fine—but if you keep pushing, you’ll end up on the far right, at “Chronic disease and Overtraining.”

If you start popping a daily dose of vitamin C or other antioxidants, you move left on the curve. Under normal circumstances, you end up on the far left, at “Rested muscle + Antioxidants.” That’s not ideal, because then you can’t get to that optimal balance in the middle during workouts, which is why routine use of antioxidants isn’t a good idea for athletes. But if you’re on the border of overtraining, the risks and benefits may be different.

Lanner and her colleagues acknowledge the risks associated with supplementation, but suggest that if an athlete on the edge of overtraining syndrome is in a state of chronically elevated oxidative stress—the kind of thing you see in rheumatoid arthritis and Duchenne muscle dystrophy—then antioxidants may help. The same thing may apply to anti-inflammatory drugs: a bad idea under normal circumstances, but possibly helpful in the face of chronic inflammation.

Key caveat? Of the 122 references cited in the article, a majority seem to involve rats. That’s an important and useful way to figure out how muscle fibers work, but any real advice about how athletes should train needs to be based on studies of athlete's training. Still, I think the focus on what’s happening in the muscles is an interesting and perhaps underappreciated aspect of overtraining. And the idea that antioxidants are a bad idea on a routine basis but useful in times of unusually high stress—a training camp, a trip to altitude—has been floating around among elite athletes for a while.

For now, though, I think the most important weapon to keep in mind is the one Lanner and her colleagues mention at the start of their section on prevention and treatment: “carefully planned training programs that include regular monitoring by coaches and the athletes themselves to assess adaptation to training over both the short and long term.” Put more simply: if you’re really, really tired and seem to be getting slower, take a break rather than a pill.