How to Cook Broccoli

NF-Feb9 Second Strategy to Cooking Broccoli.jpeg

When I used to teach medical students at Tufts, I gave a lecture about this amazing new therapeutic called "iloccor-B." I'd talk about all the new science, all the things it could do, its excellent safety profile. Just as they were all scrambling to buy stock in the company and prescribe it to all their patients, I'd do the big reveal. Apologizing for my "dyslexia," I would admit that I'd got it backwards. All this time I had been talking about broccoli.

The main active ingredient in broccoli is thought to be sulforaphane, which may protect our brains, protect our eyesight, protect our bodies against free radicals, boost our detoxification enzymes, and help prevent and treat cancer.

In my videos The Best Detox and Sometimes the Enzyme Myth is the Truth, I talked about how the formation of sulforaphane is like a chemical flare reaction, requiring the mixing of a precursor compound with an enzyme, which is destroyed by cooking. This may explain why we get dramatic suppression of cancer cell growth from raw broccoli, cauliflower and Brussels sprouts, but hardly anything from boiled, microwaved or steamed (except for microwaved broccoli, which actually retains some cancer fighting abilities). But who wants to eat raw Brussels sprouts?

There is a strategy to get the benefits of raw in cooked form. In raw broccoli, the sulforaphane precursor, called glucoraphanin, mixes with the enzyme (myrosinase) when you chew or chop it. If given enough time--such as when sitting in your upper stomach waiting to get digested--sulforaphane is born. The precursor and sulforaphane are resistant to heat and therefore cooking, but the enzyme is destroyed. No enzyme = no sulforaphane.

That's why I described the "hack and hold" technique--if we chop the broccoli, Brussels sprouts, kale, collards, or cauliflower first and then wait 40 minutes, we can cook them all we want. The sulforaphane is already made; the enzyme has already done its job, so we don't need it anymore.

When most people make broccoli soup, for example, they're doing it wrong. Most people cook the broccoli first, then blend it. We now know it should be done the exact opposite way. Blend it first, wait, and then cook it.

What if we're using frozen broccoli, though? In my video, Second Strategy to Cooking Broccoli, you can see the amount of sulforaphane in someone's body after they eat broccoli soup made from fresh broccoli versus from frozen broccoli. The difference is dramatic. Commercially produced frozen broccoli lacks the ability to form sulforaphane because vegetables are blanched (flash-cooked) before they're frozen for the very purpose of deactivating enzymes. This prolongs shelf life in the frozen foods section, but the myrosinase is dead by the time you take it out of your freezer. It doesn't matter how much you chop it, or how long you wait, no sulforaphane is going to be made. This may be why fresh kale suppresses cancer cell growth up to ten times more than frozen.

The frozen broccoli is still packed with the precursor--remember that's heat resistant--and we could get lots of sulforaphane out of the frozen broccoli by adding some outside enzyme. Where do we get myrosinase enzyme from? Researchers just buy theirs from a chemical company. But we can just walk into any grocery store.

All cruciferous vegetables have this myrosinase. Mustard greens, a cruciferous vegetable, grow out of little mustard seeds, which we can buy ground up in the spice aisle as mustard powder. If we sprinkled some mustard powder on our cooked frozen broccoli, would it start churning out sulforaphane? We didn't know...until now.

Boiling broccoli prevents the formation of any significant levels of sulforaphane due to inactivation of the enzyme. However, researchers from the University of Reading found that the addition of powdered mustard seeds to the heat processed broccoli significantly increased the formation of sulforaphane. In the video I mentioned earlier, Second Strategy to Cooking Broccoli, you can see the amount of sulforaphane in boiled broccoli versus the amount after half a teaspoon or a teaspoon of mustard powder is added. Both a half teaspoon and a full teaspoon increase sulforaphane by the same amount, suggesting that we could use even use less mustard powder for the same effect. Therefore, although domestic cooking leads to the deactivation of myrosinase and stops sulforaphane formation, the addition of powdered mustard seeds to cooked cabbage-family vegetables provides a natural source of the enzyme such that it's practically like eating them raw.

So, if we forget to chop our greens in the morning for the day, or are using frozen, we can just sprinkle some mustard powder on top at the dinner table and we're all set. Daikon radish, horseradish, or wasabi--all cruciferous vegetables packed with the enzyme--work as well. Just a quarter teaspoon of Daikon radish root for seven cups of broccoli worked--just a tiny pinch can do it. Or you can add a small amount of fresh greens to your cooked greens, because the fresh greens have myrosinase enzyme that can go to work on the cooked greens.

I love kitchen chemistry--it totally revolutionized my daily greens prep. One of the first things I used to do in the morning is chop my greens for the day, so when lunch and supper rolls around they'd be good to go. But now with the mustard powder plan, I don't have to pre-chop.

This helps explain the results I presented in Raw Broccoli and Bladder Cancer Survival.

OK, but what's so great about this sulforaphane stuff? For a taste, see:

In health,
Michael Greger, M.D.

PS: If you haven't yet, you can subscribe to my free videos here and watch my live year-in-review presentations Uprooting the Leading Causes of Death, More Than an Apple a Day, From Table to Able, and Food as Medicine.

Image Credit: Jessica Spengler / Flickr

Original Link

Bile Binding Beets

NF-Jan21 Which Vegetable Binds Bile Best.001.jpeg

In my video Breast Cancer and Constipation, I discussed how fruits and veggies bind carcinogenic bile acids in our gut. Since bile acids are absorbed back into our systems, they may increase our risk of not only colon cancer but also other cancers as well. In light of this, researchers publishing in the journal, Nutrition Research, concluded that to "lower the risk of diet and lifestyle-related premature degenerative diseases and to advance human nutrition research, relative bile acid-binding potential of foods and fractions need to be evaluated."

They found that some vegetables bind bile acids better than others. We know that those eating more plant-based diets are at a lower risk of heart disease and cancer. This could partly be because of phytonutrients in plants that act as antioxidants and potent stimulators of natural detoxifying enzymes in our bodies. Veggies can also lower cholesterol and detoxify harmful metabolites, functions that can be predicted by their ability to bind bile acids.

A group of USDA researchers studying this topic discovered three important things. First, they found an over five-fold variability in bile acid binding among various vegetables that had similar fiber content, suggesting that bile acid binding is not just related to total dietary fiber content (as previously thought), but instead some combination of unique phytonutrients yet to be determined.

Second, they discovered that steaming significantly improves the bile acid binding of collards, kale, mustard greens, broccoli, peppers, cabbage, beets, eggplant, asparagus, carrots, green beans, and cauliflower, suggesting that in this way steaming vegetables may be more healthful than those consumed raw.

Finally, they ranked multiple vegetables for bile binding ability. Which vegetables kicked the most bile butt? (in my video, Which Vegetable Binds Bile Best?, you can see a visual comparison of bile binding ability.) Turnips turned up last. Then came cabbage, cauliflower, bell peppers, spinach, asparagus and green beans. Mustard greens and broccoli were better. Eggplant, carrots and Brussels sprouts basically tie for the #5 slot. Then collards at #4. Kale got the bronze, okra the silver, and beets the gold. Kale, surprisingly, got beet.

The researchers concluded that inclusion of all these vegetables in our daily diets should be encouraged. When consumed regularly, they concluded, these vegetables may lower the risk of premature degenerative diseases and improve public health.

More raw versus cooked comparisons in

Beets also have a number of other remarkable properties. Check out my video series on Doping with Beet Juice as well as Hearts Shouldn't Skip a Beet, and Whole Beets vs. Juice for Improving Athletic Performance.

In health,
Michael Greger, M.D.

PS: If you haven't yet, you can subscribe to my free videos here and watch my live year-in-review presentations Uprooting the Leading Causes of Death, More Than an Apple a Day, From Table to Able, and Food as Medicine.

Image Credit: Robert Couse-Baker / Flickr

Original Link

Which are More Anti-Inflammatory: Sweet Cherries or Tart Cherries?

NF-Oct6 Anti-inflammatory life is a bowl full of cherries.jpg

Haggis, the national dish of Scotland, is a savory pudding of heart, liver, lungs, and oatmeal traditionally stuffed inside of a stomach. When that stomach goes into our own stomach, our digestive enzymes and stomach acid have no problem digesting it away. How do our bodies digests the stomach lining of a sheep on our plate without digesting our own stomach linings? It's meat and we're meat, so why don't we digest our own stomach every time we eat?

Partly because we have an enzyme called cyclooxygenase (COX) that protects the lining of our stomach. There are two types, COX-1 and COX-2. COX-1 is thought to be the primary protector of our stomach, whereas COX-2 is an enzyme responsible for pain and inflammation. In fact, anti-inflammatory drugs like ibuprofen and naproxen work by inhibiting the COX-2 enzyme. But these are non-selective drugs, so in addition to inhibiting COX-2 they also inhibit COX-1, which is trying to protect our stomach linings. Thus, although drugs like ibuprofen are great at relieving pain and inflammation, they kill thousands every year due to ulcerations through the stomach wall that result in life-threatening bleeding and perforation.

What are the risks on an individual level? On average, one in about 1,200 people who take this class of drugs for at least two months will die as a result. To put this into perspective, we can compare the death rate from anti-inflammatory drug side-effects to the risks associated with some well-known events. For example, it may be safer to go bungee jumping a few hundred times.

What we need is a selective COX-2 inhibitor, inhibiting the pain and inflammation of COX-2 without inhibiting the stomach protection of COX-1. We thought we got it with Vioxx, a blockbuster drug that brought in billions in profits before it started killing tens of thousands of peoples. Internal emails reveal how the drug manufacturer responded to the revelation that they were killing people: They drew up a list of doctors who were trying to warn people to "neutralize" them. If that didn't work, they tried to discredit them (You can see the emails in the video, Anti-inflammatory Life Is a Bowl of Cherries).

We're left then with two options: death from internal bleeding from one type of drug or death from side effects from another type of drug. If only there was some sort of natural COX-2 inhibitor. There is: cherries, which unlike ibuprofen suppress COX-2 more than COX-1.

In videos I did on insomnia and reducing muscle soreness (See Tart Cherries for Insomnia and Reducing Muscle Soreness with Berries), I talked about the benefits of sour cherries, the types of cherries used in baking. But sweet cherries, the kind you eat fresh, seem to be the MVP for COX-2 inhibition. Tart cherries had less of an effect. Regular red sweet cherries (Bing sweet cherries) were shown to have a greater anti-inflammatory activity than tart cherries. This makes sense since we think it may be the anthocyanin phytonutrients, and there are much more in sweet red cherries than in tart, and nearly none in yellow Rainer cherries.

Because fresh cherries have limited availability, what about other cherry products? In terms of anthocyanin phytonutrients, fresh is best, but frozen would appear to be the second-best choice.

Here are two ways I incorporate cherries into my diet:

Other studies in which anti-inflammatory drugs were compared natural dietary remedies include: Turmeric Curcumin and Osteoarthritis and Turmeric Curcumin and Rheumatoid Arthritis.

Anti-inflammatory activity in a test tube is one thing, but can cherries actually be used clinically to treat inflammatory diseases? See Gout Treatment with a Cherry on Top.

In health,
Michael Greger, M.D.

PS: If you haven't yet, you can subscribe to my free videos here and watch my live year-in-review presentations Uprooting the Leading Causes of Death, More Than an Apple a Day, From Table to Able, and Food as Medicine.

Image Credit: Valdemar Fishmen / Flickr

Original Link

Living Longer by Reducing Leucine Intake

NF-June16 How What We Eat (And Don't Eat) Impacts How We Age.jpg

Many studies have shown that calorie restriction, without malnutrition, can increase lifespan and lower the risk of age-related diseases, such as cancer.

However, for many people, calorie restriction clearly has its drawbacks. In the classic Minnesota Starvation Study, many of the volunteers suffered a preoccupation with food, constant hunger, binge eating, and lots of emotional and psychological issues. Even researchers who study caloric restriction rarely practice it. There's got to be a better way to suppress the aging engine enzyme, TOR (see Why Do We Age? for more on TOR).

That's why researchers were so excited about rapamycin, a drug that inhibits TOR, thinking it could be caloric restriction in a pill. But like any drug, it a long list of potentially serious side effects. There's got to be a better way.

The breakthrough came when scientists discovered that the benefits of dietary restriction may be coming not from restricting calories, but from restricting protein intake (See my video Caloric Restriction vs. Animal Protein Restriction). If we look at the first comprehensive, comparative meta-analysis of dietary restriction, "the proportion of protein intake was more important for life extension than the degree of caloric restriction." In fact, just "reducing protein without any changes in calorie level have been shown to have similar effects as caloric restriction."

That's good news. Protein restriction is much less difficult to maintain than dietary restriction, and it may even be more powerful because it suppresses both TOR and IGF-1, the two pathways thought responsible for the dramatic longevity and health benefits of caloric restriction.

Some proteins are worse than others. One amino acid in particular, leucine, appears to exert the greatest effect on TOR. In fact, just cutting down on leucine may be nearly as effective as cutting down on all protein. Where is leucine found? Predominantly animal foods: eggs, dairy, and meat (including chicken and fish). Plant foods, such as fruits, vegetables, grains, and beans, have much less.

"In general, lower leucine levels are only reached by restriction of animal proteins." To reach the leucine intake provided by dairy or meat, we'd have to eat nine pounds of cabbage--about four big heads--or 100 apples. These calculations exemplify the extreme differences in leucine amounts provided by a conventional diet in comparison to a plant-based diet. The functional role of leucine in regulating TOR activity may help explain the extraordinary results reported in the Cornell-Oxford-China Study, "since quasi-vegan diets of modest protein content tend to be relatively low in leucine."

This may also help explain the longevity of populations like the Okinawa Japanese, who have about half our mortality rate. The traditional Okinawan diet is only about 10% protein, and practically no cholesterol, because they ate almost exclusively plants. Less than one percent of their diet was fish, meat, eggs, and dairy - the equivalent of one serving of meat a month and one egg every two months. Their longevity is surpassed only by vegetarian Adventists in California, who have perhaps the highest life expectancy of any formally studied population in history.

This reminds of the study I profiled in The Benefits of Caloric Restriction Without the Actual Restricting.

Methionine is another amino acid that may be associated with aging. See Methionine Restriction as a Life Extension Strategy to find out which foods to avoid in that case. Both leucine and methionine content may be additional reasons why Plant Protein is Preferable.

Other reasons why those eating plant-based diets may live longer:

This all may help explain the results of Harvard's Meat and Mortality Studies.

-Michael Greger, M.D.

PS: If you haven't yet, you can subscribe to my free videos here and watch my live year-in-review presentations Uprooting the Leading Causes of Death, More Than an Apple a Day, and From Table to Able.

Image Credit: hslo / Flickr

Original Link

Exploiting Autophagy to Live Longer

NF-June11 Why do we age.jpg

Thanks to advances in modern medicine, we are living longer lives, but we're doing it by lengthening the morbidity phase. In other words, we live longer, but sicker, lives (see my video: Americans Are Live Longer, but Sicker Lives). So, traditional medicine increases the number of old people in bad health. Ideally, though, we'd extend lifespan by slowing aging to delay the onset of deterioration, rather than extending the period of deterioration.

That's exactly what a new compound appears to do. It sounds like science fiction. A bacteria in a vial of dirt taken from a mysterious island creating a compound that prolongs life. And not in the traditional medical sense. Researchers in a study profiled in my video, Why Do We Age?, called it rapamycin--named after the bacteria's home, Easter Island, which is known locally as Rapa Nui. Rapamycin inhibits an enzyme called TOR, or "target of rapamycin." TOR may be a master determinant of lifespan and aging. The action of TOR has been described as the engine of a speeding car without brakes.

Rather than thinking of aging as slowly rusting, a better analogy may be a speeding car that enters the low-speed zone of adulthood and damages itself because it does not and cannot slow down. Why don't living organisms have brakes? Because they've never needed them. In the wild, animals don't live long enough to experience aging. Most die before they even reach adulthood. The same used to be true for humans. For example, just a few centuries ago, average life expectancy in London was less than 16 years old.

Therefore, living beings need to grow as fast as possible to start reproduction before they die from external causes. The best evolutionary strategy may be to run at full speed. However, once we pass the finish line, once we win the race to pass on our genes, we're still careening forward at an unsustainable pace, all thanks to this enzyme TOR. In our childhood, TOR is an engine of growth, but in adulthood, it is the engine of aging. "Nature simply selects for the brightest flame, which in turn casts the darkest shadow."

Sometimes, though, even in our youth, our bodies need to turn down the heat. When we were evolving, there were no grocery stores; periodic famine was the norm. So sometimes even young people had to slow down or they might never even make it to reproductive age. So we did evolve one braking mechanism: caloric restriction. Caloric restriction may extend lifespan mainly through the inhibition of TOR.

When food is abundant, TOR activity goes up, prompting the cells in our body to divide. When TOR detects that food is scarce, it shifts the body into conservation mode, slowing down cell division and kicking in a process called autophagy, from the Greek auto meaning "self," and phagy meaning "to eat." Autophagy essentially means eating yourself. Our body realizes there isn't much food around and starts rummaging through our cells looking for anything we don't need. Defective proteins, malfunctioning mitochondria, stuff that isn't working anymore, and cleans house. Clears out all the junk and recycles it into fuel or new building materials, renewing our cells.

So caloric restriction has been heralded as a fountain of youth. The potential health and longevity benefits of such a diet regimen may be numerous, but symptoms may include dropping our blood pressure too low, loss of libido, menstrual irregularities, infertility, loss of bone, cold sensitivity, loss of strength, slower wound healing, and psychological conditions such as depression, emotional deadening, and irritability. And you walk around starving all the time! There's got to be a better way, and there is. Check out my video Caloric Restriction vs. Animal Protein Restriction.

More tips for preserving youthful health:

-Michael Greger, M.D.

PS: If you haven't yet, you can subscribe to my free videos here and watch my live year-in-review presentations Uprooting the Leading Causes of Death, More Than an Apple a Day, and From Table to Able.

Image Credit: Arian Zwegers / Flickr

Original Link

5 Ways To Enhance Nutrient Absorption

1. Use the magic of synergy by combining certain foods together (as seen in this graphic). Vitamin C-rich foods help absorb iron, so eat them together. Some ways to do so are to have a green salad with bell peppers or citrus dressing, drink a green smoothie with some fruit, or make hummus with beans …

Original Link