Positivity rate: ‘Backward’ states beat developed ones

Positivity rate: ‘Backward’ states beat developed ones These states are also screening a higher number compared to hotspots like Maharashtra and Kerala, indicating that while raising testing levels will result in more cases being detected, over time — when combined with diligent contact tracing and containment — the prevalence of infection can be brought down as officials zero in on nascent clusters and worrisome hotspots. https://ift.tt/eA8V8J
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Can a 2-Week ‘Circuit Breaker’ Lockdown Curb COVID-19? The U.K. May Be About to Try

The coronavirus is having its way with the United Kingdom—a fact that is told starkly by the numbers. The 21st most populous country in the world, the U.K. is 11th in total number of COVID-19 infections—and climbing fast. Its daily infection rate is doubling every seven to eight days in some regions, more people are now hospitalized there than on March 23 (when the country went into general lockdown), and in some regions, hospital beds and intensive care units are at 90% capacity. With cold weather coming on and flu season beginning, things look darker still.

“We could sleep-walk into a long and bleak winter,” warned Labor Party leader Sir Keir Starmer in an address last week.

The answer, hard as it may be to sell to a COVID-weary public, is another lockdown—sort of. British epidemiologists and policymakers are increasingly calling for what’s known as a “circuit-breaker” strategy: a short, sharp lockdown of just two to three weeks to get ahead of the virus and, if nothing else, buy a little time. The idea’s advocates argue that it has multiple advantages: It hits the brakes hard and fast on the pandemic’s spread; it eases the pressure on the National Health Service (NHS) and its hospitals; and it imposes restrictions with a known end date, making compliance among the general public far likelier than it was during the earlier quarantine period, which ran on indefinitely.

“The biggest difficulty people have is the uncertainty,” says Michael Tildesley, professor of infectious disease modeling at the University of Warwick. “If you can say to them, ‘O.K., you do this for two to three weeks and come hell or high water we’re going to lift the restrictions afterwards,’ you have a greater likelihood of compliance.”

It’s not just psychology in play here. It’s economics, too. “For businesses, the certainty of when and how long they will be closed gives room for planning, and for government to put in the appropriate financial support,” says Graham Medley, professor of infectious disease modeling at the London School of Hygiene and Tropical Medicine.

The biggest epidemiological goal of the circuit breaker approach is to reduce what’s known as the R of the pandemic—the number of people any one infected person goes on to infect in turn. When the R is above one, you’re in an exponential growth phase; when it’s below one you flip to a state of exponential reduction. Switching from above one to below one even for a short period is a powerful way to buy time.

“It’s doesn’t just put things on pause,” says Tildesley, “it hits the rewind button.”

Indeed it does. As a study by the Welsh government points out, trading two weeks of viral increase for two weeks of viral “decay” could put the pandemic back by 28 days or more. That could not only curb the infection rate, but save a lot of lives. According to estimates by Medley, a two-week lockdown would lower deaths from 79,800 at their current projected rate to 39,300.

“The rise in hospitalizations, and then deaths, is exponential,” says Medley. “Health systems cannot cope even with the early stages of these epidemics. Any kind of break or lockdown reduces transmission.”

If a circuit-breaker move is going to happen, it is likely to happen soon. British schools begin a mid-term vacation Oct. 26, meaning lockdown could come at a time when students wouldn’t be in class anyway. Parents should benefit as well, since they would not be scrambling for childcare alternatives. Most importantly, the children could benefit not just physically—reducing their risk of exposure to the virus—but psychologically.

“I believe strongly that there is long-term damage to kids from spending too much time out of school,” says Tildesley.

Key to making a national circuit-breaker period work is managing expectations and messaging smartly. The two-week period of any short-term quarantine is more or less the same as the incubation period for the virus, which means that throughout that entire fortnight, infection rates would keep right on rising, as people who contracted the virus before the lockdown begin testing positive. The government is thus well-advised to make it clear to Britons that they should not expect to see any benefits from the circuit-breaker approach until after the quarantine ends.

Epidemiologists, who know better how to read the numbers, may benefit from a short-term lockdown too. As the wildfire of national infections abates it can be easier to identify local brushfires, improving contact tracing and giving the NHS a better sense of how to mobilize its resources.

The British public seems in favor of some kind of dramatic measure. According to The Telegraph, 54% of Britons surveyed on Oct. 13 said that the government should have imposed a lockdown in September, against just 28% who did not. A circuit-breaker, with its limited scope, would seem to be both a political and epidemiological winner—but only as long as that end point is honored.

“My worry,” says Tildesley, “is that the lockdown will keep getting extended and people will say, ‘I’m not doing this anymore.'” A circuit breaker with an off setting is no good at all if it doesn’t have an honest on as well.

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Coping with the loss of smell and taste

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As I cut a slice of lemon for my tea one morning last March, I found that I could not detect the familiar zing of citrus. Nor, it turned out, could I taste the peach jam on my toast. Overnight, my senses of smell and taste seemed to have disappeared. In the days prior to that I’d had body aches and chills, which I ascribed to a late-winter cold — nothing, I thought, an analgesic and some down time couldn’t take care of. But later that day I saw a newspaper article about the loss of smell and taste in patients with COVID-19, and I realized that I’d likely caught the virus. While I was fortunate enough to eventually recover from it without a trip to the hospital or worse, months after testing negative for COVID, my senses of both smell and taste are still not fully recovered.

In this, I know, I’m hardly alone. According to US News and World Report, 86% of patients with mild to moderate COVID-19 — over six million people, all told — reported problems with their sense of smell, while a similar percentage had changes in taste perception. (Taste and smell work together to create the perception of flavor.) This is in addition to the 13.3 million Americans diagnosed with anosmia — a medical term for the loss of smell — related to other respiratory viruses, head injuries, and other causes. For many of us, improvement has been slow.

Loss of smell affects our health and quality of life

Our senses — smell, vision, hearing, taste, and touch — are bridges that connect us to the world we live in, to life itself. Knock out two of the five bridges, and 40% of our sensory input is gone. Senses add richness and texture to everyday life; they are intricately tied in with our emotions. The loss of smell or taste might not seem as drastic as the shortness of breath or debilitating fatigue that many other people have experienced post-COVID, yet the impact can still be quite demoralizing. You can no longer smell the familiar scent of your loved ones, or taste your favorite dish. Author and poet Diane Ackerman describes these special tastes and smells as “the heady succulence of life” itself.

The loss of smell and taste can also affect our health, causing poor appetite and undesired weight loss. No longer able to enjoy food, patients with anosmia may no longer eat enough, or skip meals altogether. It can even pose an existential threat, by putting us at risk in detecting fires, gas leaks, or spoiled food.

All these impacts help explain why recent studies have linked post-COVID anosmia to depression and anxiety. The jury is still out on whether this has to do with the loss of smell or taste per se — or with the impact of the virus on the central nervous system. One thing we know for sure, however: mood and sense of smell are intricately related. The 5,000-plus members of the Facebook group for post-COVID anosmia sufferers can attest to that. Feelings expressed in their posts run the gamut from mere wistfulness to full-blown grief.

Recovering from the loss

The good news is that olfactory neurons are capable of regeneration. The bad news is that not everyone will return to his or her pre-COVID level of functioning. And, sadly, some of us might never regain our sense of smell or taste at all. According to some experts, patients with post-viral loss of smell have roughly a 60% to 80% chance of regaining some of their smell function within a year. Since the sense of smell usually diminishes due to age, the recovery could take longer and be less than complete for older adults.

Savor what you can experience and engage the mind

To reawaken the olfactory nerves, most specialists recommend smell training, a daily routine of sniffing essential oils such as lemon, eucalyptus, cloves, rose, and others. If you suffer from olfactory loss, don’t be discouraged if some of the essences smell different from what you expected: distortions associated with the loss of smell (troposmia) are not uncommon.

The principle of mindfulness plays an important role here. If you cannot smell the essence at all, try and remember the smell; in other words, engage your mind in evoking the sensation. When eating, if you cannot taste the full range of flavors of a dish, pay attention to the basic ones — sweet, bitter, sour, salty, or umami — as well as to the food’s texture and the sensation on your palate. This will help you focus on what you still can taste, rather than on what you cannot. When I eat dark chocolate, for example, I can taste only the bitter and the sweet; for the flavor of the cacao bean, I still have to rely on my memory.

The old adage, “What doesn’t kill me makes me stronger,” acquires a fresh meaning when applied to the losses associated with COVID-19. These losses challenge us to become more mindful and self-aware, and ultimately, more resilient. We must also learn to be patient and appreciate incremental bits of progress. The other day, for the first time in months, I caught a whiff of citrus in my tea. Lemon never smelled so sweet.

Tips and coping strategies

In my practice with patients with post-COVID losses, and in my own recovery, I have found the following coping strategies helpful.

  • Acknowledge your feelings about the loss.
  • Consult with an ear, nose, and throat specialist for guidance.
  • Consider adjusting your cooking in favor of spicier foods.
  • Maintain hope for recovery.
  • Cultivate a sense of gratitude: you have survived a potentially lethal disease.
  • For additional help, see a counselor or join a support group.

The post Coping with the loss of smell and taste appeared first on Harvard Health Blog.

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After Months of Minimal COVID-19 Containment, Sweden Appears to Be Considering Local Lockdowns

Swedish authorities appear to be reconsidering their notoriously lax approach to COVID-19 containment, which has contributed to one of the world’s higher coronavirus death rates.

Starting Oct. 19, regional health authorities may direct citizens to avoid high-risk areas such as gyms, concerts, public transportation and shopping centers, the Telegraph reports. They may also encourage residents to avoid socializing with elderly or other high-risk individuals.

“It’s more of a lockdown situation—but a local lockdown,” Dr. Johan Nojd, who leads the infectious diseases department in the city of Uppsala, told the Telegraph.

A legal official from Sweden’s public health agency told the Telegraph the new policy is “something in between regulations and recommendations.” Violating the guidelines, for example, would not result in fines. Still, it’s a significant shift from Sweden’s previous handling of the coronavirus pandemic. While countries around the world implemented lockdowns once the virus began spreading, Swedish authorities largely let life continue as normal.

The Swedish government in March limited public gatherings to 50 people, but the policy left gaping loopholes—it doesn’t apply to private and corporate gatherings, nor to schools, shopping malls and plenty of other locations. Restaurants and bars never closed. Masks are not recommended in most places. There’s little to stop people from going to school or work if they come into contact with an infected person. Sweden’s testing and contact tracing capacities are lacking.

As of Oct. 18, Sweden’s per-capita death rate—58.6 per 100,000 people—was among the highest in the world. And from early September to early October, average daily cases nationwide rose by 173%, with particularly dramatic increases in cities such as Stockholm and Uppsala.

These hard-hit areas are the focus of Sweden’s shifting guidance, according to the Telegraph‘s report. Nojd told the outlet he is considering telling people in Uppsala not to visit the elderly and other vulnerable populations, and to avoid making unnecessary trips on public transportation. He also mentioned the possibility of imposing curfews on restaurants.

Neither representatives from the Public Health Agency of Sweden nor the city of Uppsala immediately responded to TIME’s request for further comment.

Swedish authorities appear to be conceding that reaching herd immunity—the threshold at which enough of a population is immune to the virus for it to stop spreading widely—is unlikely to be happen without a vaccine. While officials have avoided explicitly calling herd immunity the goal of their casual containment approach, emails obtained by journalists show high-level Swedish public-health officials discussing that strategy as early as March, apparently motivated by economic concerns.

National studies, however, show that far fewer people have developed natural immunity than officials hoped—as evidenced by the ongoing spike in infections. Sweden’s state epidemiologist Anders Tegnell acknowledged that reality last week.

“I think the obvious conclusion is that the level of immunity in those cities is not at all as high as we have, as maybe some people, have believed,” Tegnell said. “I think what we are seeing is very much a consequence of the very heterogeneous spread that this disease has, which means that even if you feel like there have been a lot of cases in some big cities, there are still huge pockets of people who have not been affected yet.”

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What the Conflicting Results on Promising COVID-19 Drug Remdesivir Really Mean

Treating any infectious disease is a high wire act—doctors must balance the risks and benefits of therapies with the risks of the disease. And those stakes are even higher for a new disease that doesn’t yet have a playbook for physicians to follow.

This summer, the U.S. Food and Drug Administration gave the drug remdesivir emergency use authorization for treating any patients hospitalized with COVID-19. But on Oct.15, researchers working on the World Health Organization’s (WHO) Solidarity trial published a preliminary report showing that nearly 3,000 people receiving the treatment were not more likely to survive infection with SARS-CoV-2 than those receiving standard of care.

The study involved more than 11,000 people hospitalized with COVID-19 who were randomly assigned to receive one of four different therapies—remdesivir, hydroxychloroquine, lopinavir, or interferon—for their infection, or standard of care. After following the patients for about a month, the researchers found that none of the drugs reduced mortality or cut down on hospital stays.

The remdesivir findings are in direct contrast to a report published Oct. 8 in the New England Journal of Medicine by a team led by researchers at the National Institute of Allergy and Infectious Diseases (NIAID), which found that remdesivir helped hospitalized COVID-19 patients to recover faster compared to placebo. While that study also did not find a statistically significant effect on mortality, the shorter hospital stays and shorter time on oxygen and ventilators suggest that the drug might provide some benefit for patients in overcoming their infections.

Remdesivir’s maker, Gilead, took issue with the findings, and in a statement quickly criticized the design of the study and the fact that the findings were preliminary and not published in a peer-reviewed journal: “The emerging data appear inconsistent with more robust evidence from multiple randomized, controlled studies published in peer-reviewed journals validating the clinical benefit of Veklury (remdesivir).”

So what do the conflicting results mean? Does remdesivir benefit COVID-19 patients or not? Experts are just as divided as the contrary results. “Here are the facts of this study,” Dr. Andre Kalil, professor of internal medicine at the University of Nebraska who was among the first to treat patients coming off the Diamond Princess cruise ship with remdesivir, says of the WHO Solidarity trial, “No data monitoring, no placebo, no double-blinding, no diagnostic confirmation of infection, no timing of symptom duration before treatment initiation, unknown baseline physiological severity, unknown supportive care provided, unknown health care capacity status of enrolling sites, and a large amount of missing data. Poor quality study design cannot be fixed by a large sample size, no matter how large it is.”

Dr. Eric Topol, director and founder of Scripps Research Translational Institute, on the other hand, notes that compared to the NEJM study, “This [Solidarity] is a much larger trial, done throughout the world at 400 hospitals. I think that gives this trial a little more weight.”

It turns out that the findings may not be as at-odds as they appear. There isn’t much detailed information on the hospitalized patients included in Solidarity, including, as Kalil notes, how long they were sick, why they were hospitalized and whether they had additional health conditions that could make them more vulnerable to severe COVID-19 disease. Dr. Roger Shapiro, associate professor of immunology and infectious diseases at Harvard T. H. Chan School of Public Health, and a practicing infectious disease physician, pointed out that, unlike the NIAID study, the Solidarity study did not break down people who needed oxygen by how much additional oxygen they needed. The Solidarity study grouped people by whether they did not need supplemental oxygen, whether they needed it or if they were on ventilators.

The difference could be important, as those needing less oxygen may be earlier in their infection than those needing more. Indeed, in the NIAID study, the scientists did look at the so-called low-flow and high-flow groups, and found that remdesivir provided more benefit for those needing less oxygen. And Shapiro notes that if the two groups in the NIAID study are combined, and treated as a single group like these patients were in Solidarity, the responses to remdesivir are pretty similar.

That suggests that it’s important to know how sick people are to determine how they might respond to remdesivir. Experts now believe that based on how remdesivir works, and how COVID-19 infections march along, the drug may be more effective earlier and soon after infection rather than later. Because remdesivir is an antiviral drug, it can thwart SARS-CoV-2’s ability to copy its genome and produce more virus. So it likely will have a more potent effect when there is less virus circulating during the early days of infection.

It’s also not clear from the preliminary Solidarity report how sick patients were when they were hospitalized. And because the trial involved 405 hospitals in 30 countries, the criteria for hospitalizing patients might have differed. “We have a lot of unknowns right now about who the patients in Solidarity were,” says Shapiro. “It’s really important to think about the diversity of what ‘hospitalization’ means in this study. In some places, people were hospitalized when they were near death’s door. In other places there may have been a tendency to hospitalize COVID-19 patients in order to isolate them, before they might have met certain criteria for requiring it.”

If, for example, most of the patients in Solidarity were severely ill and further along in their disease, then they might not have benefited as much from an antiviral like remdesivir. And while the Solidarity data show that only 9% of participants in the study were on ventilators, that may, in part, reflect shortages in ventilators or hospital beds for those needing mechanical ventilation and not a true reading of how many people had severe enough disease to need the machines. “It raises the question about severity of illness, and how long people were sick before they started the study,” says Shapiro.

It’s also worth noting that Solidarity enrolled patients from March to October, over which time standards of care for COVID-19 changed dramatically. At the start of the pandemic, doctors had little to offer patients and were quick to intubate people and put them on ventilators if they complained of breathing problems. Now, doctors are advising patients to lie on their stomachs to reduce the burden on the lungs and know from other studies that ventilation can worsen symptoms rather than improve them.

“We have made so many changes in the last six months in the supportive care we provide for patients, and they are all incremental,” says Dr. Aruna Subramanian, professor of medicine at Stanford University who led a study sponsored by Gilead and released in April showing that remdesivir over a five-day period was as effective as a 10-day course. “Looking at one thing in isolation [like remdesivir] and saying that it doesn’t reduce mortality doesn’t make sense to me. It’s like the blind man feeling the elephant’s leg or trunk or tail and not being able to see the whole picture.”

Topol notes that given the conflicting results, it’s more likely that remdesivir may have a modest effect in mitigating COVID-19. “The Solidarity trial study is very short, and provides limited data,” he says. “Do I hope to see more data, yes. But I don’t know if that is going to change how it’s interpreted.”

The Solidarity study has not been peer reviewed, which means experts have not evaluated the methods and conclusions of the study yet. And the study was open-label, meaning patients knew they were receiving the drug. While the study authors argue this likely did not have an effect on the results given the size of the study, it’s not the scientific gold standard for evaluating drugs. The NIAID study, on the other hand, randomly assigned people to remdesivir or placebo and neither the doctors nor the patients knew which they received.

“I don’t think this study should be the death knell for remdesivir,” says Shapiro. “When we have a placebo controlled study like [the one from NIAID] that shows us a strong signal, you can’t poke a hole in that. That’s our gold standard. The size of Solidarity does give you pause but the signal we are seeing with the NIAID study is hard to explain away. We just can’t take Solidarity and say it supersedes what we saw with the [NIAID] trial. We just can’t do that because the quality of the [NIAID] trial is better.”

For Subramanian, “[Solidarity] doesn’t really change my standard of care at this time. I know based on our data that remdesivir helps people to leave the hospital quicker. And we are going into flu season when hospital beds are often very critical. Getting people better faster, and off of oxygen and home faster, is a very important outcome.”

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Young adults face higher risk of severe disease from infections than school-age children: New research suggests children aged 5-14 years are most resilient to infectious diseases, and immune aging may start in young adults, with implications for drug and vaccine design

Young adults face higher risk of severe disease from infections than school-age children: New research suggests children aged 5-14 years are most resilient to infectious diseases, and immune aging may start in young adults, with implications for drug and vaccine design submitted by /u/mubukugrappa
[link] [comments] https://ift.tt/eA8V8J October 19, 2020 at 09:01PM https://ift.tt/1R552o9
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Dear Mark: What’s With The Bean Protocol?

bean protocolFor today’s edition of Dear Mark, I’m answering a reader question about beans. But it’s not just about beans. It’s about something called the Bean Protocol, a rather new dietary approach that many of my readers have expressed interest in. The Bean Protocol is supposed to improve the liver’s ability to clear out toxins, thereby preventing them from recirculating throughout the body in perpetuity. Today, I’m going to discuss where it fits in a Primal eating plan.

Let’s go:

Hi Mark,

Have you heard about this “Bean Protocol”? From what I can tell people are eating tons of beans and getting great results. It’s supposed to remove toxins from the liver or something else that only beans can do.

What do you think?

Thanks,

Matt

I did some digging around. I read the Bean Protocol coverage over at PaleOMG, where Juli has been following the protocol for several months now and seeing great results. There’s a Bean Protocol E-course that I did not sign up for, but I think I have a decent handle on the topic.

How to Do the Bean Protocol

Here’s the gist:

  • No caffeine
  • No sugar
  • No dairy
  • No gluten
  • No processed food
  • No factory-farmed meats; no fatty meats
  • Eat 6-8 half-cup servings of beans or lentils a day.
  • Fill the rest of the food with lean meat, leafy green vegetables, alliums (onion, garlic, leek, etc), and cruciferous vegetables (broccoli, cabbage, cauliflower).

What’s Supposed to Happen on the Bean Protocol

The soluble and insoluble fiber in the beans binds to toxins which the body can then flush out more easily. Without the fiber from the beans, your body can’t process and excrete the toxins, so they simply recirculate, stay in the body, and sometimes express themselves in the form of acne and other diseases. Adherents credit the bean protocol for fixing longstanding issues like acne, Crohn’s, and many other conditions.

Is this true? Is there any evidence of this in the scientific literature?

Well, there isn’t much direct evidence for beans improving liver clearance of toxins, but there is circumstantial evidence. For one, prebiotic fiber is good for liver health. There are plenty of studies to support this.

Synbiotics (a combination of probiotics and prebiotics) and BCAAs taken together improve hepatic encephalopathy, a feature of liver failure where the liver fails to detoxify excess ammonia.1 However, it does not do so directly. The fiber isn’t necessarily “binding” to the lead and excreting it. Instead, it does so by increasing levels of lead-binding gut bacteria which in turn bind and excrete it, shoring up the gut lining so that lead can’t make it into circulation, increasing bile acid flow, and increasing the utilization of healthy essential metals (like zinc and iron). The bacteria are essential for the effect; pre-treatment with antibiotics abolishes the benefits. So we can’t say for sure that the fiber itself is “binding” to the toxins.

Allium, Inulin

The Bean Protocol is also rich in allium vegetables like garlic and onions, another source of prebiotic fibers shown to improve liver health and toxin clearance. For instance, inulin given to rats prevents acute cadmium toxicity.2 Inulin also increases bile flow.3 Moreover, compounds found in garlic improve glutathione activity in the liver and enhance its ability to metabolize toxins.4

Cruciferous Vegetables

The Bean Protocol also emphasizes cruciferous vegetable consumption. The crucifers, which include cabbage, broccoli, cauliflower, and kale, can exert beneficial effects on liver health. Sulforaphane, one of the most prominent compounds in cruciferous vegetables, has well-established effects on toxin clearance. It can speed up the clearance of airborne pollutants and counter the carcinogens formed from high-heat cooking.56

Back to Basics

By emphasizing lean meats and eliminating sugar, alcohol, and industrial food, you are eliminating the major causes of fatty liver in the diet: sugar, seed oils, and alcohol.

My point is not to disparage the Bean Protocol. I think it has some merit. My point is to point out that beans alone probably don’t explain the benefits people are seeing. There’s a lot more going on than just beans.

Lectins and Phytic Acid in Beans

Okay, okay. So while beans aren’t the only (or even necessarily the best) way to obtain prebiotic fiber to modulate gut bacteria and improve liver health and therefore toxin clearance and metabolism, they are promising. But aren’t beans bad for you? Aren’t they neolithic foods full of lectins and anti-nutrients that are anything but Primal?

Lectins are anti-nutrients and beans do have them. Studies show that they can damage the intestinal lining, prey upon already-damaged intestinal lining, and prevent the body from repairing that damage.7 If they make it into the bloodstream, they can bind to cell membranes throughout the body, trigger autoimmune reactions, and cause real havoc.8 People have actually been hospitalized from lectin poisoning.9

But here’s the thing: cooking and soaking deactivates the majority of legume lectins.

  • In one study, navy and kidney beans showed 0.1% lectins leftover after cooking.10
  • One study found that pressure cooking kidney beans for 30 minutes eliminated all hemagglutinin activity.11
  • In another, a combo of soaking and cooking white beans completely eliminated activity of the most pernicious lectin, the one responsible for kidney bean poisoning: phytohemagglutinin.12

Most of the research indicting legume lectins used animals consuming large amounts of raw lectins. Those people who got lectin poisoning ate undercooked kidney beans. Don’t eat raw or undercooked beans and make sure they’re soaked overnight. Canned beans are also prepared pretty well.

Okay, what about phytic acid?

Phytic acid is the primary storage form of phosphorus in plants. When you eat a food containing phytic acid, it can bind to several other minerals, like calcium, magnesium, and zinc, and prevent their absorption. Diets based entirely in high-phytate foods can thereby lead to nutrient deficiencies. As legumes are one such high-phytate food, people are justifiably cautious about basing their diet on them.

Soaking legumes is really good at reducing phytic acid. In one study, cooking straight up without soaking reduced phytate by 20%, cooking after soaking in the soaking water reduced it by 53%, and cooking after soaking in fresh water reduced it by 60%.13 Another study found that cooking in fresh water after 16 hours of soaking with a 3:1 water:bean ratio eliminated 85% of phytate.14 That basically takes care of the problem.

If you want to really eliminate phytic acid you can sprout your legumes. You can also buy pre-sprouted beans.

What about the carb content of beans?

Legumes are higher in carbs than many other Primal foods but not as high as you might think. The musicality of the legume partially offsets its carbohydrate density. All those sugars and fibers being digested by gut bugs and producing the farts are carbs that you aren’t consuming as glucose. If you pay attention to “net carbs,” you’ll love legumes—at least compared to something like potatoes or bread.

Which, by the way, is why legumes appear to be so helpful in the Bean Protocol.

A half cup of cooked black beans has 20 grams of carbs with 7.5 coming from fiber.

A half cup of cooked chickpeas has 30 grams of carbs with 5 coming from fiber.

A half cup of cooked pinto beans has 22 grams of carbs with 7.7 coming from fiber.

A half cup of cooked lentils has 20 grams of carbs with 7.8 coming from fiber.

And much of that fiber, remember, comes in the form of galactooligosaccharides, that same prebiotic shown in studies to improve gut health and even increase lead excretion. But these are also FODMAPs, which, depending on your gut biome, can be helpful or painful. Some people won’t be able to handle the gas, some will get downright painful bloating, while others will get huge prebiotic benefits. Your mileage may vary, so just figure out what works.

Are beans actually nutritious, though?

Legumes aren’t nutrient-dense compared to something like liver or oysters, but they’re more nutrient-dense than grains and many other foods.

Again, a half cup of beans isn’t very many carbs. Maybe 20 grams, with only two thirds of that turning into glucose. You’ll get a lot of food for your gut and a decent whack of some important nutrients like folate, copper, magnesium, and manganese. That half cup of black beans provides 32% of your daily folate requirements, 20% of copper, 14% of magnesium, and 17% of manganese. A half cup of lentils provides 45% of your daily folate requirements along with 28% of copper and 21% of manganese. Not bad for a measly 20 grams of carbs.

A Plea: Lentils

If you want to try the Bean Protocol and insist on doing the 8 servings a day version, I’d recommend you go with lentils.

A cup of standard lentils gets you:

  • 40 grams carbs, almost 16 g fiber.
  • 230 calories.
  • 18 grams protein. Legume protein can’t replace animal protein, but it can offset some of your requirements.
  • 90% of folate.
  • 28% of vitamin B1 (thiamine), 25% of vitamin B5 (pantothenic acid), and 21% of B6 (pyridoxine). B vitamins generally aren’t issues for folks eating Primal, but they can’t hurt.
  • 55% of copper.
  • 17% of magnesium.
  • 43% of manganese.

Lentils added to a meal slow gastric emptying, which should keep a person fuller longer.15 This is in contrast to most sources of refined carbs, which increase a person’s hunger.

Another benefit is that lentil prep is simple. They contain less phytic acid than most other legumes and require less soaking (or none at all) and cooking time than other legumes to reduce it. If you want to sprout lentils, they sprout much quicker than beans.

All in all, I’d say the Bean Protocol is worth trying if you’re interested or intrigued. I don’t know that the “8 servings of beans” is more important than the other stuff you’re eating or omitting, but I also know that sometimes things just work a certain way even if the hard clinical evidence hasn’t been established. After all, people used to say the same thing about Primal or keto.

If you do try out the Bean Protocol, be sure to keep us all informed and up to date on your progress. I’d be really curious to hear about it.

The post Dear Mark: What’s With The Bean Protocol? appeared first on Mark's Daily Apple.

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